Anatomy of the Pharynx PDF

 Part 2 section 1 THE PHARYNX Page Chapter 1 Examination of the pharynx 3 Chapter 2 Sore Throut 10 Chapter 3 Suppurration of parapharyngeal spaces 25 Chapter 4 Sleep...

 Part 2 section 1 THE PHARYNX Page Chapter 1 Examination of the pharynx 3 Chapter 2 Sore Throut 10 Chapter 3 Suppurration of parapharyngeal spaces 25 Chapter 4 Sleep Disorders 34 Chapter 5 Dysphagia 40 Part 2 section 2 THE LARNX Page Chapter 1 Clinical examination of the larynx 61 Chapter 2 Stridor 64 Chapter 3 Hoarseness 78 Chapter 4 Air way restoration 85 "‫إرىم بعصا إلس نوإر‬ Page | 2  ANATOMY OF THE PHARYNX ❖ It is a fibro-muscular tube lined with mucosa ,which In the midline of the neck. ❖ Length About 12.5 cm ( 5 inches ) in adults. ❖ Extends from the base of the skull superiorly to be continuous with the oesophagus inferiorly. ❖ In front of the upper six cervical vertebrae. ❖ Behind the nose, mouth and larynx; from above downwards. ▪ Its wall consists of four layers; from within outwards. 1. Mucous membrane: ✓ Lined by stratified squamous epithelium, except the nasopharynx which is lined by pseudo- stratified ciliated columnar epithelium. 2. Pharyngeal aponeurosis: ✓ layer of loose connective tissue. ✓ Contains abundant sub-epithelial lymphoid tissue. ✓ This lymphoid tissue aggregates in some areas to form tonsils. ✓ These tonsils collectively form Waldeyer’s ring. 3. Muscle layer: Formed mainly of three constrictor muscles; superior, middle and inferior. 4. Bucco-pharyngeal fascia: A thin connective tissue investing layer which surrounds the pharynx. Page | 3 ▪ What is Waldeyer’s ring? ✓ A ring of lymphoid tonsils which lies in the Pharyngeal submucosal connective tissue layer of The Pharyngeal aponeurosis. ✓ It surrounds the upper part of the aero-digestive Tract. ✓ This ring consists mainly of: 1- One pharyngeal ( nasopharyngeal ) tonsil In the Roof of the nasopharynx. 2- Two tubal tonsils around ET orifices. 3- Two palatine ( faucial ) tonsils In the oropharynx. 4- Two lingual tonsils In the base of the....... LYMPH DRAINAGE OF THE PHARYNX: 1) The nasopharynx Retropharyngeal→ upper deep Cervical lymph nodes. 2) The oropharynx Upper deep cervical lymph nodes. 3) The hypopharynx Upper and lower deep cervical lymph nodes. NERVE SUPPLY OF THE PHARYNX: 1- Motor nerve supply: The vagus nerve through the pharyngeal plexus. 2- Sensory nerve supply: A) The nasopharynx: The trigeminal nerve. B) The oropharynx: The glossopharyngeal Nerve. C) The hypopharynx: The vagus nerve. Parts of the pharynx It is divided into three parts : 1. Naso-pharynx Behind the nose. 2. Oro-pharynx Behind the mouth ( oral cavity ). 3. Laryngo-pharynx ( hyp pharynx ) Behind the larynx. Page | 4 A) Nasopharynx: ▪ Lies behind the nasal cavities & in Front of the 1st Cervical vertebra. ▪ Extends from the base of the skull Superiorly to the level of the soft Palate inferiorly. ▪ Communicates anteriorly with the Nasal cavities through the nasal Choanae & inferiorly with the Oropharynx through the vel Pharyngeal sphincter. ▪ This sphincter lies between the Soft palate ( velum ) and the Posterior wall of the pharynx. B) Oropharynx: ▪ Lies behind the oral cavity & in front of The 2Nd And 3rd Cervical vertebrae. ▪ Extends from the level of the soft palate Superiorly to the level of the tip of the Epiglottis inferiorly. ▪ Communicates anteriorly with the oral Cavity superiorly with the nasopharynx. The anterior and posterior pillars ( fauces ) are Mucosal folds that extend from the soft Palate to each side of the tongue. ▪ The palatine tonsils lie in its lateral walls ( one on each side ), between the anterior and posterior pillars. C) Laryngopharynx ( Hypopharynx ): ▪ Lies behind the larynx & in front of the 3rd to 6th cervical vertebrae. ▪ Extends from the level of the tip of the epiglottis cartilage superiorly to the level of the lower border of the cricoid cartilage inferiorly. ▪ Communicates anteriorly with the larynx through the laryngeal inlet, superiorly with the oropharynx & inferiorly with the oesophagus. ▪ Features It lies not only behind the larynx, but also projects forwards to form a recess on each side of the larynx. Therefore, it consists of three parts: a. a middle part behind the larynx → called the post-cricoid area. b. &c. a lateral recess on each side of the larynx → called the pyriform fossa. Page | 5  THE PHARYNGEAL TONSIL ▪ A mass of sub-epithelial lymphoid Tissue which forms part of Waldeyer’s ring. ▪ Its free surface is covered with Pseudo-stratified ciliated columnar Epithelium. ▪ It lies at the junction of the roof and Posterior wall of the nasopharynx. ▪ it is similar to a truncated pyramid. ▪ Has no capsule. ▪ Its free surface has 5 – 6 vertical Projections; called folds. They project Outside the substance of the tonsil. ▪ LYMPHATIC DRAINAGE: The retro-pharyngeal → upper deep cervical lymph nodes THE PALATINE TONSILS ▪ Two; ovoid masses of sub epithelial lymphoid tissue, forming part of Waldeyer’s ring, one on each side Of the oropharynx. Between two mucosal palatal folds → called the anterior and Posterior pillars. ▪ Its upper pole reaches the soft palate. ▪ Its lower pole reaches the base of The tongue. ▪ Its lateral surface is related to the Superior constrictor muscle of the Pharynx. This muscle forms → the bed Of the tonsil. ▪ Its free medial surface has 12 – 15 Blind invaginations; called crypts. They Dip inside the substance of the tonsil. Page | 6 ▪ The largest crypt lies near the upper Pole of the tonsil and is called crypta Magna. ▪ Its free medial surface is covered with Stratified squamous epithelium. ▪ It extends to line the crypts. ▪ Its lateral surfaces is covered with a fibrous tissue capsule. A connective tissue space ( called peri-tonsillar space ) separates the capsule of the tonsil from its bed i.e. the superior Constrictor muscle. ▪ ARTERIAL SUPPLY: From the external carotid artery and Its branches; 1- Tonsillar artery ( from the facial artery ) → mainly. 2- Ascending palatine artery (from the Facial artery) 3- Descending palatine artery (from the Maxillary artery). 4- Dorsalis lingulae artery (from the Lingual artery). 5- Ascending pharyngeal artery (from the External carotid artery). ▪ LYMPHATIC DRAINAGE: The jugulo-digastric lymph nodes ( of the upper deep cervical lymph nodes ), Which lie just below the angle of the mandible. PHYSIOLOGY OF THE PHARYNX 1) SWALLOWING (DEGLUTITION) FUNCTION: ❖ The pharynx acts as a swallowing ( deglutition ) pathway. How? It transfers the food bolus from the mouth to the oesophagus. ❖ What is swallowing? Swallowing is the process by which the food bolus is transferred from the mouth → to the stomach. ❖ It occurs in three phases: Page | 7 A- Oral phase: Voluntary passage of the food bolus from the oral cavity →to the oropharynx. How? 1. The mouth is closed. 2. The bolus is positioned on the middle 1/3 of the tongue. 3. The tongue is elevated against the palate pushing the bolus to the oropharynx. B– Pharyngeal phase: Involuntary passage of the food bolus from the oropharyn→ to the oesophagus. How ? ▪ The pharynx transfers the bolus to the oesophagus. How? Peristaltic waves propel the bolus from the pharynx to the oesophagus. The peristaltic waves consist of successive contraction and relaxation of the superior, middle and inferior constrictor muscles. ▪ Escape of the bolus to the nasal cavities ( i.e. nasal regurge ) is prevented. How? The soft palate moves upwards and backwards →to separate the nasopharynx from the oropharynx i.e. closes the velo-pharyngeal sphincter. ▪ Escape of the bolus to the airway is prevented ( i.e. airway protection ).How? 1. Cessation of respiration. 2. Closure of the laryngeal sphincters i.e. the ary- epiglottic ( mainly ), ventricular and vocal folds. 3. Elevation of the larynx →the laryngeal inlet is hidden by base of the tongue. 4. Backward tilt of the epiglottis→ to cover the laryngeal inlet. 5. Reflex coughing →when a foreign body enters the larynx. C– Oesophageal phase: Involuntary passage of the food bolus from the oesophagus→ to the stomach. How? Physiology of the oesophagus. Page | 8 2) RESPIRATORY FUNCTION: The pharynx acts as a respiratory airway. How? ▪ It transfers air from the nasal cavities to the larynx. ▪ The pharyngeal muscles have a tonic dilator activity. ▪ This tonic dilator activity is essential for continuous easy breathing. Why? ✓ Inspiration→ creates a negative pressure within the upper airway & ✓ the oropharynx is collapsible, because it has no rigid skeletal support. This leads to→ tendency of the oropharynx to collapse inwards during inspiration. Therefor, the tonic dilator activity of the pharyngeal muscles is essential to keep the lumen of the pharynx patent during inspiration. 3) SPEECH FUNCTION: The pharynx helps in speech resonance. How? ▪ During speech → the soft palate moves upwards and backwards to separate the nasopharynx from the oropharynx ( i.e. closes the velo-pharyngeal sphincter). ▪ This occurs during production of all speech sounds except m and n. 4) PROTECTIVE FUNCTION: The submucosal lymphoid tissues of Waldeyer’s ring act as a defense line at the entrance of the air and food passages. How? ▪ They have a rich reservoir of lymphocytes. ▪ The surface epithelial cells of the pharyngeal mucosa collect samples from the antigens and organisms present in the inhaled air and swallowed food→ transport them to the submucosal lymphocytes. ▪ These lymphocytes reinforce immunity of the aero-digestive tract by formation of antibodies against these antigens and organisms. ▪ This function is especially important during the first years of life because the child is subjected to many antigens and infections. Therefore, these tonsils undergo physiological hypertrophy during the first decade of life. Page | 9  SORE THROAT Sore throat is a symptom of many pharyngeal conditions as: 1- Acute pharyngitis. ✓ Acute simple pharyngitis. ✓ Vincent Angina. ✓ Infectious mononucleosis. ✓ Moniliasis. ✓ AIDS. 2- Chronic pharyngitis. ✓ Chronic simple pharyngitis. ✓ Tuberculosis. 3- Infection of the pharyngeal spaces. ✓ Quinsy. ✓ Parapharyngeal abscess. ✓ Retropharyngeal abscess. ✓ Ludwig’s angina. 4- Pharyngeal manifestations of systemic diseases. ✓ Agranulocytosis. ✓ Acute leukaemia. ✓ Recurrent aphthous ulcers. ✓ Behcet’s disease. 5- Acute tonsillitis. 6- Chronic tonsillitis. Page | 10  Acute simple pharyngitis AETIOLOGY: Causative organisms: ▪ Mostly primary viral infection. In association with common cold and Influenza. ▪ May be followed by bacterial infection with Streptococcus haemolyticus )commonest)Streptococcus pneumoniae and Haemophilus influenzae. Mode of transmission: Droplet infection. SYMPTOMS: General symptoms: Rapid onset of fever headache, anorexia and malaise. Pharyngeal symptoms: Rapid onset of severe sore throat and referred otalgia. SIGNS: General signs: High fever and flushed face. Pharyngeal signs: ▪ Diffuse hyperaemia of the pharyngeal mucosa. ▪ The mucosa may be covered with a non-adherent yellowish true membrane Cervical signs: Enlarged tender upper deep cervical lymph nodes. COMPLICATIONS: Spread of infection→ otitis media and laryngitis. TREATMENT: 1. Antibiotics therapy. 2. Supportive and symptomatic measures Rest, ample fluid intake, analgesics, antipyretics and gargles ( as warm tea with lemon ) Vincent’s angina AETIOLOGY: Causative organisms: Two anaerobic organisms which act in symbiosis →Borrelia vincentii and Spirochaeta denticolata. Predisposing factor : Carious teeth. SYMPTOMS: General symptoms: Gradual onset of fever, headache, anorexia and malaise. Pharyngeal symptoms: ▪ Severe sore throat and referred otalgia. ▪ Bad mouth odour ( halitosis ). Page | 11 SIGNS: 1. General signs: Mild fever. 2. Pharyngeal signs: Necrotic ulceration & false membrane formation on the oral and pharyngeal mucosa. 3. Cervical signs: Enlarged tender upper deep cervical lymph nodes. INVESTIGATIONS: A swab from the membrane is examined by direct film for the causative organisms. TREATMENT: 1- Antibiotics therapy The drug of choice is penicillin. 2- Mouth wash and gargle with hydrogen peroxide Provide an oxygenated medium which is not suitable for growth of the causative anaerobic organisms. Moniliasis( candidiasis or thrush ) AETIOLOGY: Causative organism: Candida albicans. Predisposing factors: Debilitating diseases(as AIDS, malignancy & diabetes mellitus ) and prolonged use of systemic antibiotics or steroids. SYMPTOMS: General symptoms: No fever. Pharyngeal symptoms: Mild sore throat. SIGNS: General signs: No fever. Pharyngeal signs: ▪ Diffuse hyperaemia of the pharyngeal mucosa. ▪ The oral and pharyngeal mucosa is covered with multiple small milky white patches. Removal of these patches reveals superficial mucosal ulcers. Cervical signs No enlarged cervical lymph nodes. TREATMENT: 1- Local anti-fungal drugs as miconazole and nystatin. 2- Treatment of the cause Page | 12  Infectious mononucleosis AETIOLOGY: Causative organism: Epstein Barr virus. SYMPTOMS: General symptoms: Rapid onset of fever, headache, anorexia and malaise. Pharyngeal symptoms: Severe sore throat and referred otalgia. SIGNS: General signs: ▪ High fever ▪ Generalized lymphadenopathy & splenomegaly. Pharyngeal signs: Formation of a false membrane ( pseudo- membrane )→which is bilateral. Cervical signs: Enlarged tender deep cervical lymph nodes. INVESTIGATIONS: 1) Blood picture Monocytosis and lymphocytosis with atypical lymphocytes. 2) Serological tests Positive monospot test and positive Paul-Bunnell’s test i.e. patient’s serum can agglutinate sheep’s red blood cells. Why? Due to presence of abnormal antibodies. TREATMENT: 1) Antibiotics therapy To avoid secondary bacterial infection. N.B. Avoid ampicillin→because it may cause a skin rash. 2) Supportive and symptomatic measures: Rest, ample fluid intake, analgesics, antipyretics and gargles ( as warm tea with lemon ). 3) Systemic steroids in severe cases. Acquired immuno-deficiency syndrome ( AIDS ) AETIOLOGY Causative organism Human immuno-deficiency virus ( HIV ). CLINICAL PICTURE: 1- General manifestations Poor general condition. 2- Pharyngeal manifestations a. Hypertrophy of the pharyngeal tonsils. B. Recurrent and severe candidiasis, viral pharyngitis and aphthous ulcers. Page | 13  C. Hairy leukoplakia: White mucosal patches. It consists of localized epithelial hyperplasia. The basement membrane remains intact. D. Kaposi’s sarcoma: Red plaque or nodule. It is a malignan mesenchymal tumour. It consists of aberrant slitlike vascular spaces surrounded by atypical spindle cells Cervical manifestations Enlarged deep cervical lymph nodes. INVESTIGATION: Enzyme-linked immuno-sorbent assay ( ELISA ) To detect antibodies to HIV. TREATMENT: The patient should be referred to a specialized hospital. Chronic simple pharyngitis AETIOLOGY: 1- Recurrent attacks of acute pharyngitis. 2- Mouth breathing ( due to nasal obstruction ). 3- Smoking, spirits and spices. 4- Gastro-oesophageal reflux. SYMPTOMs: a) History of repeated attacks of acute pharyngitis b) Sensation of throat irritation →frequent hawking and hemming to clear the throat. 1- Catarrhal chronic pharyngitis Mild hyperaemia of the pharyngeal mucosa. 2- Hypertrophic chronic pharyngitis Scattered small nodules on the posterior pharyngeal wall ( due to hypertrophy of the subepithelial lymphoid tissues ) → granular appearence TREATMENT: Of predisposing factors. Page | 14  Tuberculous pharyngitis AETIOLOGY: Most commonly secondary to pulmonary tuberculosis. CLINICAL PICTURE: 1- Pallor of the pharyngeal mucosa. 2- Painful shallow ulcers, with undermined edges and caseous pale yellowish floor. TREATMENT Anti-tuberculous therapy Pharyngeal suppuration ❖ Severe unilateral sore throat and referred otalgia.. ❖ On pus formation → the pain becomes throbbing. ❖ Severe dysphagia →the patient is unable to swallow even his own saliva →drooling of saliva from his mouth. Page | 15  4- Pharyngeal manifestations of systemic diseases. DEFINITIO: Inflammatory disorders of the mucosal lining of the pharynx due to systemic diseases. TYPES: 1- Blood Diseases a) Agranulocytosis. B) Acute leukaemia. 2- Diseases of Unknown Aetiology c) Recurrent aphthous ulcers D) Behcet’s disease. Agranulocytosis AETIOLOGY: Depression of the bone marrow, which may be idiopathic or due to drugs→ antibiotic as chloramphenicol, anti-mitotic as methotrexate, antiemetic as chlorpromazine. CLINICAL PICTURE: 1- General manifestations: Recurrent infections →due to leucopenia. 2- Pharyngeal manifestations: a) Sore throat and referred otalgia. B) Extensive necrotic ulceration & false membrane formation on the pharyngeal mucosa. The ulcers are not surrounded by red inflammatory reaction. INVESTIGATIONS: 1- Blood picture Marked leucopenia particularly the granulocytes. 2- Bone marrow aspirate ( sternal puncture ) Diagnostic. TREATMENT: 1- Immediate withdrawal of the causative drug. 2- Hospitalization, isolation and systemic antibiotics →to prevent secondary infection. 3- Repeated fresh blood transfusion. Page | 16  Acute leukaemia AETIOLOGY: Neoplastic proliferation of the precursors of the white blood cells in the bone marrow. CLINICAL PICTURE 1- General manifestations a) Pallor →due to anaemia. b) Bleeding tendency→ due to thrombocytopenia. c) Recurrent infections →because most leucocyte are non-functioning immature cells. d) Generalized lymphadenopathy and splenomegaly. e) Sternal tenderness. 2- Pharyngeal manifestations: a) Sore throat and referred otalgia. b) Extensive necrotic ulceration & false membrane formation on the pharyngeal mucosa. C) Multiple haemorrhagic petechiae on the pharyngeal mucosa. INVESTIGATIONS: 1- Blood picture Marked leucocytosis ( with many immature blast cells ), anaemia and thrombocytopenia. 2- Bone marrow aspirate ( sternal puncture ) Diagnostic. TREATMENT: 1- Hospitalization, isolation and systemic antibiotics→ to prevent secondary infection. 2- Repeated fresh blood transfusion. 3- Chemotherapy and bone marrow transplantation. Recurrent aphthous ulcers INCIDENCE: Commonest cause of oral and pharyngeal ulceration. AETIOLOGY: Unknown. May be vitamin deficiency, immunological disturbance or stress. CLINICAL PICTURE: 1- General manifestations: Good general condition. 2- Pharyngeal manifestations: a) Recurrent single or multiple variable sized painful oral and pharyngeal ulcers which are surrounded with marked hyperaemia. b) They heal spontaneously within 1 – 2 weeks. TREATMENT: Local corticosteroids. Page | 17  Behcet’s disease AETIOLOGY: Unknown. Most probably→ an auto-immune disease. CLINICA PICTURE: 1) General manifestations ▪ Iridio-cyclitis. ▪ Genital ulcers. ▪ Progressive sensorineural hearing loss. 2- Pharyngeal manifestations ▪ Recurrent multiple small painful oral and pharyngeal ulcers which occur in groups Acute Tonsillitis DEFINITION: Acute inflammation of the palatine tonsils. INCIDENCE: Age Any, but much more common in children. AETIOLOGY: Causative organisms Streptococcus beta-haemolyticus ( commonest ), Streptococcus pneumoniae and Haemophilus influenzae. Mode of transmission Droplet infection. SYMPTOMS: 1) General symptoms: Rapid onset of fever, headache, anorexia and malaise. 2) Pharyngeal symptoms: ▪ Rapid onset of severe sore throat and referred otalgia. ▪ Bad mouth odour ( halitosis ). Page | 18 SIGNS 1) General signs ▪ High fever and flushed face. Febrile convulsions may occur in children. 2) Pharyngeal signs ▪ Acute follicular tonsillitis The crypts are full of purulent exudate →the surface of the tonsil has yellowish spots → characteristic spotted appearance. ▪ Acute membranous tonsillitis These yellowish spots may coalesce →form a non- adherent yellowish true membrane ▪ Acute parenchymatous tonsillitis Marked hyperaemia and enlargement of the tonsils. 3) Cervical signs ▪ Enlarged tender jugulo-digastric lymph nodes ( just below the angle of the mandible. COMPLICATIONS: 1- Local complications ▪ Pharyngeal suppuration→ peri-tonsillar abscess, para-pharyngeal abscess and retro- pharyngeal abscess ▪ Laryngitis. ▪ Otitis media How? Spread of infection. 2- Systemic complications: Rare and almost confined to childhood. ▪ Rheumatic fever →carditis and arthritis. ▪ Acute glomerulo-nephritis. How? They are due to an auto-immune reaction i.e. the antibodies produced against Streptococcus beta-haemolyticus cross-react with the patient’s own tissues Page | 19 TREATMENT: 1- Antibiotics therapy for 10 days. 2- Supportive and symptomatic measures Rest, ample fluid intake, analgesics, antipyretics and gargles ( as warm tea with lemon ). Chronic Tonsillitis DEFINITION: Chronic inflammation of the palatine tonsils. AETIOLOGY: It follows acute tonsillitis →as a result of 1- Organism factor Repeated attacks of acute tonsillitis. 2- Treatment factor Inadequate dose or short course of antibiotics therapy. 3- Patient factor Low patient’s resistance e.g. malnutrition. SYMPTOMS: 1- History of repeated attacks of acute tonsillitis. 2- Sense of throat irritation →frequent hawking and hemming to clear the throat. 3- Bad mouth odour ( halitosis ) →due to accumulation of pus in the crypts. 4- Difficult swallowing → if hypertrophic. 5- Snoring and obstructive sleep apnea →if hypertrophic. SIGNS: A. Pharyngeal signs: 1- Size; Inequality of the size of both tonsils. 2– Shape; ▪ Hyperaemia of the anterior pillars→ in the absence of acute infection. ▪ Irregularity of the surface of the tonsils → due to fibrosis. B. Squeezing: The crypts ooze pus on pressure by a tongue depressor. Cervical signs: Persistent enlargement of the jugulo-digastric lymph nodes. TREATMENT: Tonsillectomy operation when chronic tonsillitis is symptomatic. Page | 20  Tonsillectomy Operation DEFINITION: Excision of the palatine tonsils. INDICATIONS: 1) Symptoms of chronic tonsillitis: ▪ Recurrent attacks of acute tonsillitis → 4 - 6 / year. ▪ Snoring and obstructive sleep apnea→ due to tonsils hypertrophy. ▪ Difficult swallowing→ due to tonsils hypertrophy. ▪ Bad mouth odour ( halitosis ) →due to accumulation of pus in the crypts. 2) Signs of chronic tonsillitis: ▪ Size: a) Bilateral hypertrophic tonsils. B) Inequality of the size of both tonsils. ▪ Shape: a) Hyperaemia of the anterior pillars→ in the absence of acute infection. b)irregularity of the surface of the tonsils →due to fibrosis. ▪ Squeezing: The crypts ooze pus on pressure by a tongue depressor. ▪ Cervical: Persistent enlargement of the jugulo-digastric lymph nodes. 3) Complications of tonsillitis: ▪ Febrile convulsions. ▪ Peri-tonsillar abscess ( quinsy ). ▪ Auto-immune diseases i.e. rheumatic carditis, rheumatic arthritis and glomerulonephritis → when the patient does not comply with prophylactic penicillin therapy. 4) Other indications: ▪ Tonsillar tumours. ▪ Tuberculous cervical lymphadenopathy → because the tonsils are the portal of entry of the tubercle bacilli. ▪ As a part of other operations as uvulo-palato-pharyngoplasty. CONTRAINDICATIONS: 1) Local contraindications: ▪ Acute tonsillitis and acute upper respiratory infection ( within 3 weeks ). Why? To avoid bleeding and infection of the wound. 2) Systemic contraindications: ▪ Active rheumatic fever. Why? To avoid bacterial endocarditis. ▪ Bleeding tendency as haemophilia and purpura. Why? To avoid bleeding. ▪ Uncontrolled systemic diseases as anaemia and diabetes mellitus. Why? To avoid their complication. Page | 21 POST-OPERATIVE CARE: 1) Extubation: ▪ The endotracheal tube is removed after return of the coughing and swallowing reflexes. Why? To prevent inhalation of blood and vomitus. 2) Position: The patient is put in the post-tonsillectomy position until he regains full consciousness. a) to allow proper observation by the nurse, b) to allow blood to trickle out of the mouth → easily detected, c) to prevent inhalation of blood and vomitus & d) to prevent rolling of the patient on his face or his back. 3) Observation of signs of respiratory obstruction: a) noisy breathing i.e. stridor b) bluish discoloration of the lips i.e. cyanosis. 4) Observation of signs of bleeding : a) frequent swallowing ( normally once / 3 - 5 minutes ), b) spitting of fresh blood, c) vomiting of dark blood, d) rising pulse rate e) falling blood pressure ( late ). 5) Feeding: a) Starts after few hours. b) In the first day → the diet consists of cold fluids and semi-solids. c) From the 2nd to the 7th days → normal diet but avoid hard, spicy and hot food. 6) Medications: a) Antibiotics for one week. B) Analgesics for pain in the throat and referred otalgia. Page | 22 COMPLICATIONS: 1) Complications of general anaesthesia: a) Anaphylactic shock. B) Succinyl choline apnoea. C) Cardiac arrest. 2) Respiratory obstruction: May be due to a) Extubation laryngeal spasm: Treatment: Suction of blood over the vocal cords and oxygen inhalation. B) Falling back of the tongue: Treatment: Pull the mandible forwards or insert an oral airway. C) Inhalation of a foreign body: As blood clot or vomitus. Treatment: Bronchoscopic removal. 3) Haemorrhage: ❖ Primary haemorrhage: ▪ Definition: Excessive bleeding during the operation. ▪ Cause: ✓ Bad patient selection ( bleeding tendency or during acute infection) and ✓ bad surgeon technique ( incomplete removal of the tonsils ). ▪ Treatment: ✓ Ligation or diathermy of the bleeding vessels. ✓ Remove the remnants. ❖ Reactionary haemorrhage: ▪ Definition: Bleeding during the first 24 hours after the operation. ▪ Cause: ✓ Slippage of a loose ligature or ✓ rise of blood pressure to its normal level ( during recovery from anaesthesia ) →dislodgment of a blood clot. ▪ Treatment: ✓ Local haemostatic measures e.g. apply cotton swab soaked with hydrogen peroxide. ✓ If this fails →re-anaesthetize the patient ligate the bleeding vessels. ❖ Secondary haemorrhage: ▪ Definition: Bleeding after 24 hours; usually between the 5th and 10th days. ▪ Cause: Wound infection →slough of vessels and tissues. ▪ Treatment: ✓ Antibiotics. Page | 23  ✓ Sedatives. ✓ If this fails ( rare ) → re-anaesthetize the patient → pack the tonsillar bed with an absorbable haemostatic material →suture the pillars over it. ✓ Do not try to ligate the bleeding points. Why? Because the tissues are friable 4) Surgical trauma: a. Injury of the teeth. B. Injury of the soft palate→ hyper-nasal speech and nasal regurgitation of fluids. 5) Infection: a. Wound infection. B. Para-pharyngeal abscess. C. Bronchitis and broncho-pneumonia. D. Sub-acute bacterial endocarditis; if the patient has a rheumatic heart valve disease. 6) Incomplete removal : Primary post-operative haemorrhage. Infection of the remnants. TREATMENT: Local and systemic corticosteroids. Page | 24  INFECTIONS OF THE PHARYNGEAL SPACES 1) Peri-tonsillar absces (quinsy ). 2) Para-pharyngeal abscess. 3) Acute retro-pharyngeal abscess. 4) Chronic retro-pharyngeal abscess. 5) Ludwig’s angina. Peri tonsillar Abscess (Quinsy) DEFINITION: Collection of pus in the peri-tonsillar space. The peri-tonsillar space is a connective tissue space. ✓ Lies between the capsule of the tonsil and its bed ( which is formed of the superior constrictor muscle of the pharynx ). INCIDENCE: ▪ Age Adults. ▪ Side Unilateral. ▪ Site Above and lateral to the tonsil. AETIOLOGY: ✓ Acute tonsillitis. ✓ The infection passes outside the tonsil through crypta magna. SYMPTOMS ▪ General symptoms: Fever, headache, anorexia and malaise. ▪ Pharyngeal symptoms: After an attack of acute tonsillitis ;the patient develops: a. Severe unilateral sore throat and referred otalgia.  On pus formation →the pain becomes throbbing. b. Severe dysphagia→ the patient is unable to swallow even his own saliva→drooling of saliva from his mouth. c) Bad mouth odour ( halitosis ). Page | 25  SIGNS: ▪ General sign: High fever. ▪ Pharyngeal signs: a) A pharyngeal swelling:  in the soft palate, above and lateral to the tonsil,  pushes the adjacent tonsil downwards and medially, pushes the uvula to the opposite side & on pus formation → the swelling pits on blunt probing. B) Trismus i.e. inability to open the mouth→ due to spasm of the pterygoid muscle. ▪ Cervical signs a) Enlarged tender upper deep cervical lymph nodes. B) Torticollis i.e. neck tilt to the diseased side →due to spasm of the neck muscles. COMPLICATIONS: 1- Spread of infection to a) the para-pharyngeal space →par-pharyngeal abscess b) the larynx→ laryngea edema. 2- Rupture of the abscess into the pharynx→ aspiration of bus→ broncho-pneumonia. TREATMENT: 1. Medical treatment ✓ When? Before pus formation:→ i.e. in the stage of peri-tonsillar cellulitis. ✓ How? Massive antibiotic therapy. 2. Surgical treatment: Drainage of the abscess. ✓ When? After pus formation → i.e. in the stage of peri-tonsillar abscess. as indicated by throbbing pain‚ pitting oedema or pointing abscess. ✓ How?  Anaesthesia: Commonly surface with the patient sitting.  The incision: Is performed with a guarded scalpel or better a quinsy knife in one of points Page | 26  1) Most pointing point. 2) Midway between the last upper molar Tooth and base of the uvula. 3) 1/2 cm lateral to the meeting point of two lines→ a vertical line along the anterior pillar & a horizontal line along the base of the uvula.  The drainage: Is performed by a quinsy forceps;using Hilton’s method i.e. the forceps is introduced closed→ opened in the abscess →withdrawn out open. 3. Tonsillectomy operation: When? After 4 - 6 weeks. Why? To avoid recurrence of quinsy. Para pharyngeal Abscess DEFINITION: Collection of pus in the para-pharyngeal space. The para-pharyngeal space is a connective tissue space. ✓ Lies on the lateral side of the nasopharynx and oropharynx. ✓ Extends from the base of skull, to the level of hyoid bone. ✓ Limited laterally by the mandible superiorly and the sterno-mastoid muscle inferiorly. ✓ Contains the internal carotid artery, internal jugular vein, last four cranial nerves, deep cervical lymph nodes and deep lobe of the parotid gland. AETIOLOGY: ▪ Acute tonsillitis, peritonsillar abscess and infection after tonsillectomy. ✓ The infection passes through the superior constrictor muscle of the pharynx. ▪ Infection of the last lower molar tooth. Page | 27 SYMPTOMS: ▪ General symptoms: Fever, headache, anorexia and malaise. ▪ Pharyngeal symptoms: ✓ Severe unilateral sore throat and referred otalgia. On pus formation→ the pain becomes throbbing. ✓ Severe dysphagia. →the patient is unable to swallow even his own saliva → drooling of saliva from his mouth. SIGNS: ▪ General sign: High fever. ▪ Pharyngeal signs: ✓ A pharyngeal swelling which pushes the lateral pharyngeal wall and tonsil medially. ✓ Trismus i.e. inability to open the mouth → due to spasm of the pterygoid muscle. ▪ Cervical signs: ✓ A unilateral diffuse tender swelling below & behind the angle of the mandible, deep to the anterior border of the sterno- mastoid muscle. ✓ Torticollis i.e. neck tilt to the diseased side →due to spasm of the neck muscles. N.B. The pharyngeal swelling, cervical swelling and trismus →constitute Boeck’s triad, which is diagnostic of para-pharyngeal abscess. INVESTIGATIONS: CT scan Diagnostic. COMPLICATIONS: 1- Spread of infection to: ✓ the base of skull → meningitis, ✓ the carotid sheath→ thrombosis of internal jugular vein and rupture of carotid artery, ✓ the mediastinum ( along the carotid sheath ) → mediastinitis. ✓ the larynx →laryngeal oedema. 2- Rupture of the abscess into the pharynx → aspiration of pus → broncho-pneumonia. Page | 28 TREATMENT: 1- Medical treatment: Massive antibiotic therapy. 2- Surgical treatment: Drainage of the abscess by a vertical cervical incision along theanterior border of the sterno-mastoid muscle. Acute Retro pharyngeal Abscess DEFINITION: Collection of pus in the retropharyngeal space. The retro-pharyngeal space is a connective tissue space. ✓ Lies behind the pharynx. ✓ Lies between the buccpharyngeal fascia & the prevertebral fascia. ✓ The two fasciae are attached in the midline by a strong median raphe→there is right & left spaces. ✓ Each space contains one lymph node called the lymph node of Henle.These nodes drain the upper respiratory tract. They atrophy before the age of 5 years. AETIOLOGY: 1- Suppuration of the retro-pharyngeal nodes, secondary to upper respiratory infection. 2- Infection after adenoidectomy. AGE: Children, below the age of 5 years. SYMPTOMS 1- General symptoms: Fever, headache, anorexia and malaise. 2- Pharyngeal symptoms: a. Severe unilateral sore throat and referred otalgia. On pus formation→ the pain becomes throbbing. b. Severe dysphagia→the patient is unable to swallow even his own saliva →drooling of saliva from his mouth. Page | 29  c. Severe dyspnoea i.e. difficult breathing. Why? Because ✓ collection of pus behind the nasopharynx→ nasal obstruction ✓ collection of pus behind the hypopharynx →laryngeal obstruction and stridor. SIGNS 1) General sign Fever. 2) Pharyngeal signs A pharyngeal swelling pushes the posterior pharyngeal wall forwards. The swelling is limited to one side of the midline; due to midline attachment of the bucco-pharyngeal and pre-vertebral fasciae. 3) Cervical signs Torticollis i.e. forward flexion of the neck. Why? Because neck extension → stretching of pre-vertebral muscles →pressure on the abscess →increase of pain. INVESTIGATIONS: Plain x-ray&CT scan Widening of the pre-vertebral space with normal vertebral bodies. COMPLICATIONS: 1- Spread of infection to: ✓ the mediastinum →mediastinitis. 2- Rupture of the abscess into the pharynx→ aspiration of pus → broncho-pneumonia. TREATMENT: 1- Medical treatment: Massive antibiotic therapy. 2- Surgical treatment: A. Drainage of the abscess by an incision in the posterior pharyngeal wall, with the patient in Trendlenburg’s position i.e. the head is lower than the chest in order to avoid aspiration of pus. B. Tracheostomy when necessary. Page | 30  Chronic Retro pharyngeal Abscess SYNONYM: Pre-vertebral abscess. DEFINITION: Formation of a cold abscess in the pre-vertebral space. The pre-vertebral space is a connective tissue space. ✓ Lies behind the pharynx. ✓ Lies between the pre-vertebral fascia and the cervical vertebrae. AETIOLOGY: Tuberculous caries of the cervical vertebrae ( Pott’s disease ). It starts as a cold abscess in the pre-vertebral space. It reaches the retro-pharyngeal space when the abscess ruptures through the pre- vertebral fascia. AGE: Adults. SYMPTOMS 1) General symptoms: Tuberculous toxaemia i.e. night fever, night sweating & loss of weight 2) Pharyngeal symptoms: Mild sore throat. 3) Cervical symptoms: Painful limited neck movements. SIGNS 1) General signs: Tuberculous toxaemia→ pallor and loss of weight. 2) Pharyngeal signs: ✓ A pharyngeal swelling pushes the posterior pharyngeal wall forwards. ✓ The swelling lies in the midline of the posterior pharyngeal wall. 3) Cervical signs: Tenderness over the cervical spine. INVESTIGATIONS: Plain x-ray&CT scan: Widening of the pre-vertebral space with destruction of the vertebral bodies TREATMENT: 1) Medical treatment: Anti tuberculous therapy. Page | 31 2) Surgical treatment: a. Drainage of the abscess by vertical cervical incision along the posterior border of the sterno-mastoid muscle b. Orthopedic management of the cervical spine. Ludwig’s Angina DEFINITION: ✓ Bilateral diffuse cellulitis of the floor of the mouth. ✓ Suppuration seldom occurs. ✓ The floor of the mouth is a connective tissue space. ✓ It is divided by the mylo-hyoid muscle to→ submandibular and sublingual spaces. AETIOLOGY: Infection of the floor of the mouth e.g. lower teeth ( commonest ), mandible, tongue, submandibular or sublingual salivary gland. SYMPTOMS: a) General symptoms: Fever, headache, anorexia and malaise. b) Local symptoms: a. Severe dysphagia. Why? Because the tongue is pushed upwards and backwards →may obstruct the food passage. b. Severe dyspnoea. Why? Because the tongue is pushed upwards and backwards →may obstruct the air passage SIGNS: a)General signs: Fever. Page | 32 B) Pharyngeal signs ✓ A swelling in floor of the mouth→ pushes the tongue upwards and backwards. ✓ Trismus i.e. inability to open the mouth→ due to spasm of the pterygoid muscles. C) Cervical signs ✓ Tender indurated swelling of both submandibular regions. ✓ Suppuration seldom occurs. COMPLICATION: Spread of infection to → the larynx →laryngeal oedema ( common ). TREATMENT: 1) Medical treatment ✓ Massive antibiotic therapy. ✓ Bed rest, in the semi-sitting position→ to avoid airway obstruction. 2) Surgical treatment ✓ Drainage by a horizontal cervical incision below the mandible. ✓ Usually there is no or little frank pus → because suppuration seldom occurs. ✓ Tracheostomy when necessary. Page | 33 Chapter 4 SNORING AND OBSTRUCTIVE SLEEP APNEA SYNDROME The pharyngeal muscles have Tonic Dilator Activity to keep the lumen of the pharynx patent during inspiration. At the end of this chapter you should be able to This tone is essential to overcome the negative pressure A- Describe the causes , clinical created during inspiration and prevent collapse symptoms and signs of snoring & of the pharynx. OSAS and its complications During sleep the muscle tone of pharyngeal muscles decreases B- Determine the appropriate ➡️ the pharyngeal lumen becomes diagnostic tools and therapeutic lines SNORING Definition: Noisy breathing during sleep Etiology: 1. Narrowing of the nasal cavities: All causes of bilateral nasal obstruction 2. Narrowing of the pharyngeal cavities: - Nasopharyngeal: Adenoid, tumors. - Palate: redundant soft palate. - Lateral pharyngeal wall: hypertrophied tonsils, fat deposition. - Tongue: - Large tongue base - Posterior tongue position in micrognathia and retrognathia. Pathogenesis: Supralaryngeal obstruction➡️ negative pressure in the oropharynx during inspiration ➡️partial collapse of the oropharynx➡️ vibration of the soft palate and lateral pharyngeal wall with the base of the tongue➡️ noisy breathing. Page | 34  OBSTRUCTIVE SLEEP APNEA (OSA) Definition : cessation of respiration during sleep for more than 10 seconds , or 5 or more apnea attacks per one sleep hour. Etiology: the same as snoring Pathogenesis: - Supralaryngeal obstruction➡️ negative pressure in the oropharynx during inspiration ➡️ collapse of the oropharynx➡️ complete collapse ( also due to decreased muscle tone during sleep) cessation of respiration (Apnea). - Apnea leads to decrease of O2 pressure and increase of CO2 pressure ➡️ stimulation of CNS ➡️ arousal of the Patient➡️ return of muscle tone of the pharynx and resumption of pharyngeal patency, the cycle is repeated when the patient sleeps again. Clinical picture:The patient and his/her partner or relatives give the following picture:- - During sleep: Snoring In OSA ( when the pharynx is totally obstructed), snoring is interspersed with apnoeic episodes. The patient struggles for breathing with considerable movement of the chest and abdomen. Restless sleep Night mares. Nocturnal enuresis - During day time: Morning headache Impaired concentration Hypersomnlence ( excessive day-time sleepiness). Due to fragmentation of sleep by frequent arousal. Complications: - Cardiac arrhythmia - Pulmonary and systemic hypertension - Heart failure and even sudden death. Investigations Muller's maneuver: To identify the site of the collapse and the cause of obstruction. The patient inspires with closed mouth ( to simulate the state of apnea) while the upper airway is examined by the endoscope. Page | 35  Radiological examination: -Lateral plain x ray of the head and neck. -CT scan to diagnose the cause of obstruction and site of collapse. Polysomnography: To assess the overnight brain activity ( EEG), eye movement ( electro-occulography), ECG, pulse oxymetry, oral and nasal airflow, , tape recording of snoring. Treatment Conservative treatment Weight reduction Avoid sedatives and narcotics before sleep ( because they decrease the paraphryngeal muscle tone) Sleeping in lateral position CPAP ( continuous positive airway pressure) kept over night to prevent pharyngeal collapse. Surgical treatment Correction of nasal or nasopharyngeal obstruction e.g. - Reduction of hypertrophied turbinates - Septoplasty - Polypectomy - Adenoidectomy Uvulo-palao-pharyngoplasty( UPPP) better by laser ( trimming of the redundant tissue of the soft palate and lateral pharyngeal wall with excision of palatine tonsils. Anterior advancement of the mandible to pull the tongue forwards Tracheostomy to by-pass the obstruction. It is the last resort. Adenoids Definition: Hypertrophy of the pharyngeal ( nasopharyngeal ) tonsil, sufficient to produce symptoms. N.B. Adenoids is the commonest nasopharyngeal swelling. Incidence :Age Children. Etiology 1)Physiological hypertrophy Occurs at the age of 3 - 8 years. Then, the pharyngeal tonsil gradually regresses in size ➡️ to become atrophic at puberty. 2) Pathological hypertrophy Due to recurrent upper respiratory infections. Symptoms 1- Bilateral nasal obstruction Mouth breathing. Page | 36  Speech hypo-nasality. Difficult suckling in infants. Snoring and obstructive sleep apnea. 2- Bilateral nasal discharge Mucoid or muco-purulent ➡️ due to mechanical obstruction of the choanae. Nasal ➡️ excoriation of the nasal vestibule and upper lip. Post-nasal ( gummy egg white ) ➡️ nocturnal cough laryngismus stridulus and gastro-intestinal disturbances as loss of appetite and morning vomiting. Signs Posterior rhinoscopy Shows the adenoids, but is difficult. Digital palpation: condemned , as it is painfull Endoscopic examination The best. Investigation Lateral plain x-ray of the nasopharynx :A soft tissue shadow (short arrow) narrowing the airway (long arrow) ➡️ diagnostic. Complications 1- Obstructive sleep apnea It has the following secondary effects During sleep: Restless sleep ( due to fragmentation of sleep by frequent arousal ), night mares and nocturnal enuresis. During day time: Morning headache, impaired concentration and hyper-somnolence i.e. excessive daytime sleepiness ( due to fragmentation of sleep by frequent arousal ). has the following complications Cardiac arrhythmia, pulmonary hypertension, systemic hypertension, heart failure and even sudden nocturnal death. 2- Descending infections a)Ear ➡️Recurrent acute otitis media and secretory otitis media ➡️ due to eustachian tube obstruction b) Respirator ➡️Recurrent rhinitis, sinusitis, pharyngitis, laryngitis and bronchitis. 3- Adenoids facies Due to under-development of the middle 1/3 of the face. a) Nose ➡️Pinched nostrils. b) Mouth ➡️Open mouth, short upper lip, protruding upper incisors, high arched palate and receding mandible. c)face ➡️Idiot expressionless look. Page | 37 TREATMENT Adenoidectomy operation when adenoids is symptomatic or complicated. Adenoidectomy Operation Definition: Excision of the hypertrophic pharyngeal ( nasopharyngeal ) tonsil i.e. adenoids. Indcation: Hypertrophy of the pharyngeal ( nasopharyngeal ) tonsil, sufficient to produce symptoms and / or complications. Contraindication: A- Local contraindications: 1- Acute upper respiratory infection ( within 3 weeks ). Why? To avoid bleeding and infection of the wound. 2-Cleft palate. Why? To avoid aggravation of the velo-pharyngeal incompetence. Why? Because the adenoids assist in closure of the velo-pharyngeal sphincter in case of cleft palate. B- Systemic contraindications: 1- Bleeding tendency as haemophilia and purpura. Why? To avoid bleeding. 2- Uncontrolled systemic diseases as anaemia and diabetes mellitus. Why? To avoid their Complications ANAESTHESIA: General. TECHNIQUE: 1- Pass the adenoids curette behind the soft palate ➡️ into the nasopharynx. 2- Shave the adenoids mass. 3- Insert a pack into the nasopharynx to stop bleeding ➡️ remove it after 15 minutes. POST-OPERATIVE CARE: Similar to tonsillectomy. Complications: 1) Complications of general anaesthesia: Similar to tonsillectomy 2) Respiratory obstruction: Similar to tonsillectomy Page | 38 3) Haemorrhage: A- Primary haemorrhage B- Reactionary C- Secondary haemorrhage haemorrhage Excessive bleeding during the Bleeding during the first 2 Bleeding after 24 hours ; Definitio operation. hours after the operation. usually between the 5th and 10th days n Bad patient selection ( Rise of blood pressure to Wound infection ➡️ bleeding tendency or during its normal level ( during slough of vessels and acute infection ) recovery from tissues bad surgeon technique : anaesthesia) ➡️ Cause incomplete removal of the dislodgment of a blood adenoids or injury of the clot. pharyngeal muscles due to over curettage a) Remove the remnants. Vaso-constrictor nasal a) Massive antibiotics. b) Re-pack the nasopharynx drops. b) Vaso-constrictor nasal If this fails ➡️ re- drops. Treatment anaesthetize the c) If this fails ➡️ an patient ➡️ re-pack the inflatable balloon or nasopharynx. posterior nasal pack. 4) Surgical trauma: 1) Injury of the teeth. 2) Injury of the eustachian tube orifice ➡️ otitis media. 3) Injury of the soft palate ➡️ speech hyper-nasality and nasal regurgitation of fluids. 4) Injury of the pharyngeal muscles due to over-curettage ➡️ primary haemorrhage. 5) Injury of the atlas vertebra due to hyper-extension of the neck ➡️ neurological disorders. 5) Infection: 1) Wound infection. 2) Retro-pharyngeal abscess. 3) Bronchitis and broncho-pneumonia. 6) Incomplete removal ➡️ a) Primary post-operative haemorrhage. b) Persistence of symptoms. Page | 39 Chapter 5 DYSPHAGIA At the end of this chapter you should Definition: dysphagia is defined as: be able to - Difficult swallowing or, A- Describe the causes of dysphagia B- Describe the clinical picture and - Painful swallowing ( Odynophagia) or, p-Sensation of Determine the appropriate diagnostic the act of swallowing. tools to identify the cause Pathogenesis: dysphagia may be due to: C- Outline the therapeutic linest the - Mechanical factors causing narrowing of the end of this chapter you should be able lumen of the oropharynx, hypopharynx or to A- Describe the causes of dysphagia B- Describe the clinical picture and esophagus➡️ dysphagia is more to solids. Determine the appropriate diagnostic - Functional disorders: due to inadequate function tools to identify the cause of the muscles of the pharynx or esophagus ➡️ C- Outline the therapeutic lines dysphagia is more to fluids because swallowing of fluids needs highly co-ordinated act of swallowing. THE 1st STEP: differentiate between Upper & Lower dysphagia The patient often tries to localize the level of sensation: High in the neck Low in the epigastrium or retrosternal THE 2nd STEP: Age is important to identify causes of dysphagia - Congenital cause is expected in newly born - Inflammation of the pharynx in children - Tumors and neurological disorders in elderly THE 3rd STEP : The onset & Course help to identify the diagnosis - Acute Painfull onset➡️ think for acute inflammatory conditions (Pharyngitis Tonsillitis, Neck space infection) & FB - Acute Painless onset ➡️ think for Neuromascular conditions (Myasthenia gravis, multiple sclerosis, motor neurone disease) & FB - Chronic onset & progressive course➡️ think for Malignancy, Plummer Vinson syndrome , Pharyngeal pouch THE4th STEP: is to detect associated symptoms - Immediate regurgitation: in large pharyngeal tumors - Delayed regurgitation: in pharyngeal pouch - Severe pain in pharyngeal suppurations, - Hoarseness in laryngeal infiltrating tumour or in reflux esophagitis - Aspiration : in neurological disorders. - Sense of lump in the throat especially when swallowing saliva which disappears during Page | 40 swallowing food and liquids may denote Globus pharyngeus - Weight loss is seen in esophageal carcinoma Causes of dysphagia A- ORAL CAUSES They include disorders of following functions and structures: Chewing: 1- Trismus 2- fractures of mandible 3- neoplasms of the upper or lower jaw 4- temporomandibular joints disorders. Lubrication: xerostomia such as radiotherapy and Mikulicz disease. Tongue: 1- Paralysis 2- painful ulcers 3- tumors 4- total glossectomy Palate: 1- Cleft palate 2- oronasal fistula. Buccal cavity and floor of mouth: 1- Ulcers 2- Ludwig’s angina 1-Traumatic: FB The most common FB is fish bone, the most common site is the tonsil. Patient gives history of FB impaction & sensation of FB in the throat and odynophagia Caustic ingestion: The patient or relatives give a history of caustic ingestion, the patient has severe sore throat with odynophagia. Examination: burn in the tongue and oral mucosa. 2-Inflammatory: Acute Tonsillitis : - In addition to general symptoms, the patient has severe sore throat with referred otalgia. Examination: reveals fever, flushed face and marked hyperemia or the characteristic spotted appearance of the acute follicular tonsillitis, or true membrane when the spots coalesce. - Cervical lymph nodes are tender and enlarged.. Acute simple pharyngitis: In addition to general symptoms, the patient has severe sore throat with referred otalgia. Examination reveals fever, flushed face and diffusely hyperemic mucosa and tender cervical lymph nodes. Page | 41 Peritonsillar abscess: - Commonly adult patient gives a history suggesting acute tonsillitis develops - severe sore throat with referred otalgia, severe dysphagia, drooling of saliva. - Examination shows the characteristic swelling of quinsy , enlarged tender cervical lymph nodes and torticollis to the same side. Parapharyngeal abscess : Remember Boek's triad. Acute Retropharyngeal abscess: A child below 5 years, in addition to general symptoms, presents withsevere dysphagia and severe dyspnea. Examination shows swelling in the posterior pharyngeal wall limited to one side of the midline.There is foreword flexion of the neck ( Torticollis). Plain X ray shows widening of the prevertebral space with normal cervical vertebrae. NB in Pott's disease sore throat is mild. Vincent angina: In a patient with bad oral hygiene, severe sore throat with referred otalgia. Examination, false membrane on the pharyngeal and oral mucosa. A swab is needed to detect the causative organism Infectious mononucleosis: In addition to general symptoms, the patient has severe sore throat with referred otalgia. Examination shows false membrane similar to diphtheria but bilateral with enlarged tender cervical lymph nodes. There may be generalized rashes, generalized lymphadenopathy and splenomegaly. Paul Bunnel test or Monospot test confirm the diagnosis. Tuberculous pharyngitis: There is a history suggestive of pulmonary tuberculosis, and odynophagia. examination shows pallor of the pharyngeal mucosa and painful shallow ulcers with undermined edges and caseous pale yellow floor. CHRONIC PHARYNGO-ESOPHAGITIS Synonyms : Plummer-Vinson’s syndrome & Paterson-Brown-Kelly’s syndrome. Incidence: Commonly middle-aged females. Etiology: Unknown. May be iron deficiency or vitamin deficiency. Pathology: Atrophy of the pharyngeal, oesophageal and gastric mucosa. Symptom:Gradual progressive dysphagia. Signs 1- General signs a) Pallor ( due to anaemia ). b) Spoon-shaped nails ( koilonychia ). c) Splenomegaly. Page | 42 2- Pharyngeal signs 1) Angular stomatitis ➡️ fissured mouth angles. 2) Glossitis ➡️ smooth tongue due to loss of papillae. 3) Atrophic glazed mucosa of the hypopharynx and cervical oesophagus. Investigation 1- Blood picture ➡️Hypochromic anaemia. 2- Gastric secretion ➡️Achlorhydria due to atrophy of the gastric mucosa. Complications 1- Submucosal fibrosis ➡️ web formation and stricture at pharyngo-oesophageal junction. 2- Pre-cancerous ➡️ post-cricoid carcinoma and cancer oesophagus. Treatment 1- Iron and vitamins supply. 2- Repeated endoscopic dilatation ➡️ when stenosis occurs. 3-Regular follow up ➡️ to detect post-cricoid carcinoma and cancer esophagus. B - PHARYNGEAL CAUSES Traumatic 1-Foreign body 2- Caustic ingestion Inflammatory: 1- Acute tonsillitis, peritonsillar abscess, retropharyngeal abscess, parapharyngeal abscess, 2- acute epiglottitis, 3- Vincent angina 4- Infectious mononucleosis 5- Tuberculous pharyngitis 6- Plummer Vinson syndrome Tumors: Tonsil soft palate pharynx base of tongue supraglottic larynx Paralytic Miscellaneous : Palatal palsy, which present with nasal regurgitation bulbar palsy cerebrovascular accidents. Lesions of vagus Spasmodic: Tetanus and rabies Page | 43  3-Neoplastic: Oropharyngeal carcinoma INCIDENCE Frequency ➡️Commonest malignant tumour of the oropharynx. The 2nd commonest malignant tumour of the head & neck; after cancer larynx. Age ➡️Commonly above 50 years. Sex ➡️Commonly males. Site Commonly the tonsil. Predisposing factors: Excessive tobacco smoking and alcohol intake. Spread Local spread ➡️To the surrounding structures. Lymphatic spread ➡️To the upper deep cervical lymph nodes early and common. Blood spread ➡️To the lungs, liver, bone and brain rare and late. Symptoms Pain in the throat. It may radiate to the ipsilateral ear ( i.e. referred otalgia ). Spitting of blood. Bad mouth odour ( halitosis ). Signs Oropharyngeal examination Fungating mass or malignant ulcer. Cervical examination Unilateral enlarged upper deep cervical lymph nodes. Investigation CT scan➡️ To assess tumour extension and lymph nodes involvement. Biopsy➡️ To confirm the diagnosis. Metastatic work-up Chest x-ray, brain CT scan, bone scan & abdomen ultrasound. Treatment Surgical excision and / or radiotherapy. Radical neck dissection in the presence of palpable cervical lymph nodes Pyriform fossa carcinoma INCIDENCE Age Commonly above 50 years. Sex Commonly males. Predisposing factors: Excessive tobacco smoking and alcohol intake. Spread 1) Local spread To the surrounding structures. 2) Lymphatic spread To the upper & lower deep cervical lymph nodes ➡️ early & common/ 3) Blood spread To the lungs, liver, bone and brain ➡️ rare and late. Page | 44 Symptoms : Early cases are asymptomatic or vague throat discomfort. Later on: Gradually progressive dysphagia; first to solids then to solids and fluids. Pain in the throat. It may radiate to the ipsilateral ear ( i.e. referred otalgia ). Hoarseness of voice and stridor ➡️ due to invasion of the larynx or the recurrent laryngeal nerve. Signs: Hypopharyngeal examination ( by indirect laryngoscopy or endoscopic examination ) Shows the tumour. May be hidden by a pool of saliva. Cervical examination Unilateral enlarged upper & lower deep cervical lymph nodes. May be the earliest manifestation i.e. the pyriform fossa is a silent area. Investigation 1- Imaging a) Barium swallow Irregular filling defect. b) CT scan To assess tumour extension and lymph nodes involvement. 2- Biopsy by hypopharyngoscopy To confirm the diagnosis. 3- Metastatic work-up Chest x-ray, brain CT scan, bone scan & abdomen ultrasound. Treatment Surgical excision. The operation is pharyngo-laryngectomy. The pharynx is reconstructed by stomach pull-up, colon interposition, a free jejunal flap or a myo-cutaneous flap. Radical neck dissection in the presence of palpable cervical lymph nodes. Post-cricoid carcinoma Post-cricoid carcinoma INCIDENCE : Age Commonly middle age. Sex Commonly females. Predisposing factors Excessive tobacco smoking and alcohol intake. Plummer-Vinson’s syndrome. Spread Local spread To the surrounding structures. Lymphatic spread To the upper & lower deep cervical lymph nodes ➡️ early & common May be bilateral. Why? Because the post cricoid area is a midline structure Blood spread To the lungs, liver, bone and brain ➡️ rare and late. Symptoms 1) Rapidly progressive dysphagia; first to solids ➡️ then to solids and fluids. 2) Regurgitation of undigested acid-free food ➡️ in large tumours. Page | 45 3) Pain in the throat. It may radiate to the ipsilateral ear ( i.e. referred otalgia ). 4) Hoarseness of voice and stridor ➡️ due to invasion of the larynx or the recurrent laryngeal nerve. 5) Rapid loss of weight. Signs Hypopharyngeal examination ( by indirect laryngoscopy or endoscopic examination ) Shows the tumour. Cervical examination Enlarged upper & lower deep cervical lymph nodes. Moure’s sign i.e. absence of the normal click, which is felt when the larynx is moved from side to side over the vertebral column. Investigation 1) Imaging Lateral plain x-ray Widening of the tracheo-vertebral space with a soft tissue shadow opposite C 4, 5, 6 & 7. Barium swallow Irregular filling defect. CT scan To assess tumour extension and lymph nodes involvement. 2) Biopsy by hypopharyngoscopy To confirm the diagnosis. 3) Metastatic work-up Chest x-ray, brain CT scan, bone scan & abdomen ultrasound. Treatment: Similar to carcinoma of the pyriform fossa. 4-Paralytic Bilateral paralysis of the pharyngeal muscles. Dysphagia is more to fluids because proper swallowing of fluids needs highly co-ordinated swallowing. Notice that ☆unilateral pharyngeal paralysis is asymptomatic due to compensation by the other side. 5- Miscellaneous Pharyngeal pouch (Zenker’s diverticulum). Definition Herniation of the pharyngeal mucosa through Killian’s dehiscence. What is Killian’s dehiscence? A potentially weak area on the posterior surface of the pharynx ➡️ between the upper oblique fibers ( i.e. thyro-pharyngeus ) and lower transverse fibers ( i.e. crico-pharyngeus ) of the inferior constrictor muscle. Incidence :Commonly elderly males. Page | 46 Physiology The crico-pharyngeal muscle acts as a sphincter ( the crico-pharyngeal sphincter ). This sphincter is normally closed, except during the oesophageal stage of swallowing. How? At the beginning of this stage ➡️ the upper thyro-pharyngeus muscle contracts to push food down through the relaxed lower crico-pharyngeal muscle. Aetiology Neuro-muscular incoordination during swallowing ➡️ failure of relaxation of the crico- pharyngeal sphincter increased intra-pharyngeal pressure ➡️ herniation of the pharyngeal mucosa through the potentially weak area of Killian’s dehiscence. Symptoms 1_Gradual progressive dysphagia more to solids. Why? As the pouch enlarges ➡️ it becomes more in line with the pharynx ➡️ food enters the pouch ➡️ exerts pressure on the oesophagus. 2- Regurgitation of undigested acid-free food. 3- Bad mouth odour ( halitosis ) ➡️ due to fermentation of the retained undigested food. 4- Mild loss of weight. Signs 1- Cervical examination Cystic swelling, partially covered by the sterno-mastoid muscle, usually on the left side. It increases in size after meals & empties on pressure ➡️ producing a gargling sensation. 2- Flexible hypopharyngoscopy Shows the mouth of the pouch. Investigation 1. Barium swallow Characteristic retort-shaped appearance. 2. Manometric studies Increased pressure in the crico-pharyngeal. Treatment 1. Repeated endoscopic dilatation of the crico-pharyngeal sphincter ➡️ temporary relief. 2. Endoscopic division of the partition between the pouch and the pharynx. 3. External excision of the pouch together with crico-pharyngeal myotomy i.e. cutting of the crico-pharyngeal sphincter to prevent recurrence. What is globus hystricus? A common disease( better called globus pharyngis ) of unknown etiology, may be due to emotional disturbances as cancer phobia. Symptoms 1- Persistent sensation of a lump in the throat, usually in the midline ➡️ frequent hawking and hemming to clear the throat. It is more marked during swallowing of saliva and is absent during swallowing of food. Page | 47 2-No dysphagia. Signs No abnormality is detected. Investigation Video-fluoroscopy & Barium swallow No abnormality is detected. Treatment :Reassurance. C- Esophageal Causes CONGENITAL:Atresia TRAUMATIC: FB Caustic ingestion Esophageal perforation NEOPLASTIC Carcinoma Rarely benign tumors NEUROMASCULAR Achalasia Esophageal atresia with trachea-esophageal fistula Definition The oesophagus consists of two segments: 1) The upper segment ends as a blind pouch. 2) The lower segment is connected to the trachea. Incidence : Commonest congenital anomaly of the oesophagus. CLINICAL PICTURE 1) Marked regurgitation and drooling ➡️ start immediately after birth. 2) Difficult suckling. Why? Because swallowing ➡️ aspiration ➡️ choking and cyanosis. Investigation 1) Failure of an oral catheter to enter the stomach. 2) Lipidol swallow Arrest of the dye with spill over in the tracheo-bronchial tree Treatment Immediate surgical repair. Foreign Body Esophageal Impaction Incidence 1. Accidental In children ( commonest ). 2. Suicidal In adults. Page | 48 Types 1- In children Coins ( commonest ) and disc batteries. 2- In adults Fish and meat bones. 3- In elderly Denture and lump of meat. 4- In suicidal cases Sharp objects as razors and pins. Site of Impaction 1- At upper end of the oesophagus, just below crico-pharyngeal sphincter ( the site of the first normal oesophageal constriction ) by far the commonest. 2- At the sites of the other normal oesophageal constriction. 3- Sharp objects ➡️ any where. Sequlae 1- All foreign bodies ➡️ mechanical obstruction. 2- Disc batteries ➡️ progressive liquefactive necrosis and even perforation. 3- Sharp foreign bodies ➡️ mucosal tears and even perforation. Symptoms 1- History of foreign body ingestion. 2- Dysphagia. The dysphagia may be so severe that the patient is unable to swallow even his own saliva ➡️ drooling of saliva from his mouth. 3- Regurgitation of undigested acid-free food. Sign Flexible oesophagoscopy Confirms the diagnosis in doubtful cases. Investigation Plain x-ray Detects radio-opaque foreign bodies. Complication Oesophagitis, ulceration or even rupture of the oesophagus. Treatment : Removal by oesophagoscopy. Caustic Ingestion Incidence 1- Accidental In children ( commonest ). 2- Suicidal In adults. Stages 1- Acute stage Corrosive oesophagitis. 3- Chronic stage Stricture oesophagus. Page | 49 i. Corrosive oesophagitis Aetiology Strong alkalis Common e.g. liquid cleaners ( as lye solution ) and disc batteries. Why? The alkali ➡️ progressive liquefactive necrosis and even perforation. Strong acids Rare. Why? The acid ➡️ self-limited coagulative necrosis. The coagulum of the damaged mucosa creates a barrier which protects the oesophagus from the acid. CLINICAL PICTURE 1- History of caustic ingestion. 2- Severe dysphagia ➡️ due to painful burns in the mouth, pharynx and oesophagus. The dysphagia is so severe that the patient is unable to swallow even his own saliva ➡️ drooling of saliva from his mouth. 3- Stridor and hoarseness ➡️ due to laryngeal oedema. COMPLICATIONS 1- Local complications a) Oesophageal perforation. b) Healing by fibrosis ➡️ stricture oesophagus. 2- Systemic complications a) Dehydration and electrolytes disturbance. b) Shock ➡️ neurogenic due to pain or hypovolaemic due to dehydration. FIRST AID MEASURES 1-Combat shock if present. 2. Buffering solution to neutralize the caustic ➡️ as vinegar or diluted lemon juice ➡️ for alkalis & ➡️ as anti-acids or magnesium oxide ➡️ for acids. 3. Demulcent solution to protect the mucosa, as milk and raw egg-white. Treatment a. Antibiotics to avoid secondary infection. b. Corticosteroids to treat laryngeal oedema and prevent fibrosis. c. Endoscopic resection of nonviable tissues. d. Naso-gastric intubation for feeding and to prevent fibrosis. e. Endotracheal intubation or tracheostomy to treat stridor; if necessary. Page | 50 ii. Stricture oesophagus Aetiology: Healing of corrosive oesophagitis by fibrous tissue formation. SYMPTOMS 1) Dysphagia re-appears after a latent period of few weeks ➡️ due to fibrosis. It is progressive; initially to solids ➡️ then also to fluids. 2) Regurgitation of undigested acid-free food. SIGN Flexible oesophagoscopy To assess site, length and degree of the stricture. INVESTIGATIONS Barium swallow To assess site, length & degree of the stricture. The stricture appears as a regular smooth narrowing of the lumen of the oesophagus. Treatment Permeable stricture Repeated dilatation, through an oesophagoscope. Impermeable stricture Colon bypass operation i.e. a segment of the colon is used to replace the stricture. Oesophageal Perforation Aetiology Accidental Foreign bodies and caustic ingestion. Iatrogenic Unskilled oesophagoscopy, foreign body removal and stricture dilatation. Sequlae Very dangerous 》 may be fatal. 1) Air in the neck ( surgical emphysema ). 2) Air in the pleura ( pneumo-thorax ) ➡️ pleural empyema. 3) Air in the mediastinum ( pneumo-mediastinum ) ➡️ mediastinitis. CLINICAL PICTURE 1- Haematemesis. 2-Dysphagia. 3- Retro-sternal chest pain. 4- Dyspnoea ➡️ due to pneumo-thorax and pneumo-mediastinum. 5- Fever and toxaemia ➡️ due to pleural empyema and mediastinitis. INVESTIGATION Plain x-ray Air in the neck, pleura and mediastinum. Gastrographin swallow To detect the site and size of the perforation. Page | 51 TREATMENT 1- Conservative treatment Nothing by mouth. Naso-gastric tube feeding ( in small perforation ) or gastrostomy ( in large perforation ). Massive antibiotics therapy. 2- Surgical treatment Cervical or trans-thoracic drainage together with repair of the perforation ➡️ if large. Cancer Oesophagus INCIDENCE Frequency Commonest malignant tumour in the oesophagus. Age Commonly above 50 years. Sex Commonly males. PREDISPOSING FACTORS Excessive tobacco smoking and alcohol intake. Reflux oesophagitis. Achalasia of the cardia. Plummer-Vinson’s syndrome. SPREAD 1) Local spread To the surrounding structures. 2) Lymphatic spread Common and early. Cervical part ➡️ lower deep cervical lymph nodes. Thoracic part ➡️ mediastinal lymph nodes. Abdominal part ➡️ coeliac lymph nodes. 3) Blood spread To the lungs, liver, bone and brain ➡️ rare and late. SYMPTOMS 1) Rapidly progressive dysphagia; first to solids ➡️ then to solids and fluids 2) Regurgitation of undigested acid-free food ➡️ in large tumours. 3) Bleeding ➡️ haematemesis and melena. 4) Pain in the chest. It may radiate to the ipsilateral ear ( i.e. referred otalgia ). 5) Hoarseness of voice ➡️ due to invasion of the recurrent laryngeal nerve. 6) Rapid loss of weight. SIGN Flexible oesophagoscopy Shows the tumour. INVESTIGATIONS 1) Imaging Barium swallow: Irregular filling defect ( rat-tail appearance ). Ct scan to assess tumour extension and lymph node Involvement Page | 52 2) Biopsy by direct oesophagoscopy To confirm the diagnosis. 3) Metastatic work-up Chest x-ray, brain CT scan bone scan & abdomen ultrasound. TREATMENT Radiotherapy and chemotherapy followed by surgical resection of the tumour and the draining lymph nodes. Achalasia of the Cardia (A neuromascular disorder) INCIDENCE Commonly middle-aged neurotic females. PHYSIOLOGY The lower oesophageal ( cardiac ) sphincter is normally closed, except during the oesophageal stage of swallowing. How? During this stage ➡️ this sphincter is relaxed. so that the oesophageal peristalsis can push food to the stomach. AETIOLOGY Neuro-muscular incoordination during swallowing ➡️ failure of relaxation of the lower oesophageal ( cardiac ) sphincter. It may be due to degeneration of the ganglion cells of Auerbach’s plexus of parasympathetic nerves in the wall of the oesophagus. SYMPTOMS 1)Dysphagia ➡️ more to fluids. Why? Because proper swallowing of fluids requires a highly coordinated act of swallowing, while solids can descend by gravity. 2) Regurgitation of undigested acid-free food. 3) No loss of weight inspite of the long standing dysphagia. Why? Because the dysphagia is intermittent with periods of remission. It usually follows a psychic trauma. SIGN Flexible oesophagoscopy Marked dilatation of the lower 2/3 of the oesophagus, with excessive stagnant food. INVESTIGATIONS Barium swallow Marked dilatation of the lower 2/3 of the oesophagus ( sigmoid- shaped oesophagus ) with smooth tapering of its lower end ( parrot-beak appearance ). Manometric studies Increased pressure in the lower oesophageal ( cardiac ) sphincter. Page | 53 COMPLICATIONS Spill of the regurgitated food and fluid over the larynx 》 aspiration pneumonia. Malignant transformation ➡️ adenocarcinoma ( rare ). TREATMENT 1- Conservative treatment 1. Muscle relaxants ( as amyl nitrite ) before meals ➡️ in order to relax the lower oesophageal ( cardiac ) sphincter ➡️ temporary relief. 2. Repeated dilatation of the sphincter ➡️ temporary relief. 2- Surgical treatment Heller’s cardio-myotomy operation i.e. division of muscle fibers of the sphincter, without injury of the mucosa. Page | 54  ANATOMY OF THE LARYNX The larynx is a funnel shaped tube about 4.5 cm in adult males and 3. cm in adult females. Lies in the midline of the neck. Lies in front of the laryngopharynx(hypopharynx) Opposite the 3rd to 6th cervical vertebrae. Extends from the tip of the epiglottis superiorly to the lower border of the cricoid cartilage inferiorly. The larynx consists of a framework of cartilages which : - articulate with each other by joints, - connected to each other by membranes and folds & moved by muscles. Lining mucosa: Lined by mucous membrane. A- Cartilages of the larynx Three unpaired paired cartilages : thyroid , epiglottis and cricoid Three paired cartilages : arytenoid, corniculate and cuneiform. 1. Thyroid cartilage The largest cartilage. Shape : Like an open book. It consists of two quadrangular laminae ( alae ). They unite anteriorly in the midline ➡️the thyroid angle. This angle is more prominent in males (called Adam’s apple). The posterior border of each lamina isprolonged superiorly and inferiorly to form ➡️ the superior and inferior horns, respectively. 2. Cricoid cartilage The only complete ring in the respiratory tract. Shape :Like a signet ring. It consists of a broad posterior part & a narrow anterior part. Site : Lies below the thyroid cartilage above the Trachea 3. Epiglottis cartilage Shape : Like a leaf. It consists of broad upper part and a narrow lower part. Site : Its broad upper part lies behind the tongue and the hyoid bone & its narrow lower part lies behind the thyroid angle. 4. Arytenoid cartilage Shape : Like a pyramid. It consists of body, anterior vocal process and lateral muscular process. Site : Lies over the broad posterior part of the cricoid cartilage. 5. Corniculate cartilage Shape : Small cartilage. Site : Lies over the arytenoid cartilage. Page | 55 6. Cuneiform cartilage Shape : Small cartilage. Site : Lies in the posterior part of the ary-epiglottic fold. B- Joints of the larynx 1. Crico-thyroid joint Between the cricoid lamina & inferior horn of the thyroid cartilage. 2. Crico-arytenoid joint Between the cricoid lamina & body of the arytenoid cartilage. C- Membranes of the larynx 1. Thyro-hyoid membrane Between the thyroid cartilage & the hyoid bone. 2. Crico-thyroid membrane Between the cricoid cartilage & the thyroid cartilage. 3. Crico-tracheal membrane Between the cricoid cartilage & the first tracheal ring. D- Folds ( sphincters ) of the larynx 1. The vocal folds ( true vocal cords ) Two; one on each side. Each vocal fold lies between the vocal process of arytenoid posteriorly &back of the thyroid angle anteriorly. The two vocal folds meet anteriorly at the anterior commissure. 2. The ventricular folds ( false vocal cords ) Two; one on each side. Each ventricular fold lies above the vocal fold. The space between the vocal fold and ventricular fold, on each side is called the ventricle 3. The ary-epiglottic folds Two; one on each side. Each ary-epiglottic fold lies at the laryngeal inlet, between the arytenoid cartilage & the lateral border of the epiglottis cartilage. Page | 56 E- Muscles of the larynx 1-Abductor muscle Pulls the vocal fold away from the midline ➡️ opens the glottis during inspiration. Posterior crico-arytenoid muscle. 2-Adductor muscles Pull the vocal fold to the midline ➡️ close the glottis during phonation, swallowing and chest fixation. Lateral crico-arytenoid muscle. Thyro-arytenoid muscle. Inter-arytenoid muscle. 3- Tensor muscles Stretch the vocal fold ➡️ increase vocal fold tension ➡️ increase voice pitch. Crico-thyroid muscle. Vocalis muscle ( internal part of thyroarytenoid muscle ). CAVITY OF THE LARYNX Openings The laryngeal cavity has two openings ➡️Upper opening Connects the arynx with the hypo-pharynx. Called the laryngeal inlet. ➡️ Lower opening Connects the larynx with the trachea at the level of the lower border of the cricoid cartilage. Page | 57 Compartments The laryngeal cavity is divided into three compartments ➡️ 1] Glottic region The space between the two vocal folds. It lies at the level of the middle part of the thyroid cartilage. 2] Supraglottic region The space above the vocal folds. 3] Subglottic region The space below the vocal folds. Lining mucous membrane 1. The vocal folds & the laryngeal inlet : Covered with non-keratinizing stratified squamous epithelium 2. The rest of the larynx: Covered with respiratory pseudo-stratified ciliated columnar epithelium. LYMPH DRAINAGE OF THE LARYNX 1. Glottic region: Has no lymphatics 2. Supraglottic region: Upper deep cervical lymph nodes. 3. Subglottic region: Pre-laryngeal and para-tracheal ➡️ lower deep cervical lymph nodes. NERVE SUPPLY OF THE LARYNX ♡ Totally derived from the vagus nerve. 1. Superior laryngeal nerve Course: Divides outside the larynx into The external laryngeal nerve & The internal laryngeal nerve Distribution ▪ Motor ➡️ to the crico-thyroid muscle, via the external laryngeal nerve. ▪ Sensory ➡️ to the laryngeal mucosa above the vocal fold, via the internal laryngeal nerve. 2. Recurrent laryngeal nerve Course: The right nerve descends to the root of the neck ➡️ then turns around the subclavian artery ➡️ then ascends between the trachea and oesophagus ➡️ enters the larynx opposite the crico-thyroid joint. The left nerve descends to the chest ➡️ then turns around the aortic arch Page | 58 ➡️then ascends between the trachea and oesophagus ➡️ enters the larynx opposite the crico-thyroid joint. Distribution ▪ Motor ➡️ to all laryngeal muscles, except the crico-thyroid muscle. ▪ Sensory ➡️ to the laryngeal mucosa at and below the vocal fold. PHYSIOLOGY OF THE LARYNX 1- RESPIRATORY FUNCTION The larynx acts as a respiratory airway. How? It transfers air from the pharynx ➡️ to the trachea. ▪ During quiet respiration ➡️ the vocal folds lie in the resting position the distance between the two vocal folds ( i.e the glottic chink ) is about 8 mm. ▪ During deep inspiration ➡️ the vocal folds lie in the full abduction position the distance between the two vocal folds ( i.e the glottic chink ) is about 18 mm. 2- PHONATORY FUNCTION The larynx is responsible for voice production i.e. phonation. How? ▪ The expiratory air current causes vibration of the tense adducted vocal folds. How? The vocal folds are adducted to the midline and become tense. ▪ The expiratory air current passes forcibly under pressure between the tense adducted vocal folds ➡️ setting them into vibration. Vibration of the vocal folds ➡️ voice production i.e. phonation. 3- PROTECTIVE FUNCTION The larynx prevents inhalation of fluids, food & foreign bodies into the lungs. How? a) Cessation of respiration during the pharyngeal phase of swallowing. b) Closure of the laryngeal sphincters i.e. the ary-epiglottic ( mainly ), ventricular and vocal folds during the pharyngeal phase of swallowing. c) Elevation of the larynx the laryngeal inlet is hidden by the base of the tongue ➡️ during the pharyngeal phase of swallowing. d) Backward tilt of the epiglottis to cover the laryngeal inlet. e) Reflex coughing when a foreign body enters the larynx. Page | 59 N.B. The protective function is the most important function of the larynx. 4- FIXATIVE FUNCTION The laryngeal sphincters are closed to fix the thoracic cage a) during rise of the intra-thoracic pressure as coughing. b) during rise of the intra-abdominal pressure as defecation & labour. c) during muscular exertion of the upper limbs as climbing & lifting heavy weights. Page | 60  EXAMINATION OF THE LARYNX INDIRECT LARYNGOSCOPY DEFINITION: Examination of the larynx by a laryngeal mirror. At the end of this chapter TECHNIQUE: you should be able to: )1Warm a laryngeal mirror to the body temperature. Perform adequate clinical Why? examination of the larynx, To avoid fogging of the mirror by the respiratory water vapour. identify diversions from normal and use equipment 2)Ask the patient to protrude his tonguHold the patient’s tongue available to the primary 3)in a piece of gauze by the left hand ➡️ pull it forwards. care practitioner. 4) Hold the mirror by the right hand and place it against the base of the uvula. 5) To assess mobility of the vocal folds ➡️ ask the patient to say “eee”: a) to assess adduction of the vocal folds b) to take deep inspiration ➡️ to assess abduction of the vocal folds. VISIBLE STRUCTURES: The larynx. The laryngopharynx (hypopharynx ). The base of the tongue. OTOLARYNGOLOGY ENDOSCOPIC EXAMINATION DEFINITION: Direct visualization of the ear, nose or throat by a rigid or flexible endoscope. VALUE: It has the following advantages : 1. It is carried out in the out patientclinic under surface local anaesthesia. 2. It provides brilliant illumination and perfect visualization of the field. 3. It allows examination of areas which are difficult-to-examine by clinical examination as ➡️ the nasopharynx, the hypopharynx and larynx. 4. It allows examination of uncooperative patients during clinical examination as ➡️ children and patients with uncontrollable gag reflex. Page | 61  INVESTIGATIONS OF THE LARYNX 1- Imaging Of The Larynx CT SCAN: Accurately demonstrates the larynx and its surrounding structures together with the cervical lymph nodes. PLAIN X–RAY ( LATERAL VIEW ): Of limited value ➡️ used mainly to demonstrate the lumen of the larynx. MRI (Magnetic resonance imaging) Direct Laryngoscopy DEFINITION: Direct visualization of the larynx by an open rigid laryngoscope. INDICATIONS: Diagnostic: The use of the operating microscope ( called micro-laryngoscopy ) ➡️ is very helpful. Why? It provides magnification and brilliant illumination ➡️ lesions are better seen. To examine the larynx ➡️ when the patient is unable to co-operate during indirect and endoscopic laryngoscopy To take a biopsy Therapeutic: o The use of the operating microscope ( called micro-laryngeal surgery ) o The therapeutic procedures are performed by ➡️ surgical instruments or laser surgery. for :- Page | 62  Excision of benign lesions as inflammatory masses and benign tumours. Excision of small malignant tumours. Treatment of vocal fold paralysis as teflon injection and arytenoidectomy. Removal of an impacted laryngeal foreign body. CONTRA-INDICATIONS: Cervical spine deformities as severe kyphosis. Page | 63  Chapter 2 STRIDOR Definition: Stridor is a harsh, high-pitched musical sound that results from turbulent airflow through the upper airway. Stridor is not a diagnosis but merely a symptom of underlying pathology. Stertor is a low pitched inspiratory sound that is produced by nasal or nasopharyngeal obstruction. Stridor may be : 1- Inspiratory: when obstruction is at the level of the glottis or supraglottic region. 2- Expiratory: when the obstruction affects the distal (intra-thoracic ) trachea and bronchi. 3- Biphasic: when the obstruction affects the subglottic region and proximal ( extrathoracic) trachea. Stage of respiratory obstruction Stage of respiratory failure ( Hypoxia) - Dyspnea - Irritability and mental confusion. - Face: open mouth and flaring of the - Tachycardia nostrils - Tachypnea - Neck: congested neck veins (due to - Later: increased positivity of intrathoracic - Physical fatigue pressure during expiration). - Cyanosis - Chest: retraction of the suprasternal notch and intercostals spaces. ( due to increases negativity of the intrathoracic pressure during inspiration). ❖ Diagnosis History History suggesting foreign body aspiration, birth injury may suggest vocal fold paralysis, while a history of intubation suggests subglottic stenosis. Age of onset: -In laryngomlacia stridor starts soon after birth. -Multiple papillomatosis is seen in children. Duration: Course progression: it is rapidly progressive in inflammatory conditions ( acute laryngitis in children) and slowly progressive in neoplastic conditions. Relation to feeding and position: In laryngomalacia stridor improves in prone position. Page | 64 Other symptoms Inflammatory conditions are associated with fever. ✓ In cute laryngitis in children stridor is accompanied by Hoarseness of voice. ✓ In acute epiglottitis, inspiratory stridor is accompanied by dysphagia, drooling and muffled voice. ✓ In multiple papillomatosis stridor is associated with hoarseness ❖ Examination: □ Assess the severity of stridor: - Flaring of the nasal alae and the use of accessory neck and chest muscles are clues to increased respiratory effort.: - Assess for signs of impending respiratory failure : ▪ Irritability and mental confusion. ▪ Tachycardia ▪ Tachypnea Later: ▪ Physical fatigue ▪ Cyanosis □ Level of consciousness, □ Fever □ Toxaemia □ Position: - Supraglottic obstruction with air hunger will often cause the patient to sit with the neck hyperextended to improve airflow. - Positional stridor most frequently results from laryngomalacia, micrognathia, macroglossia, or vascular compression. In all of these cases, improved airflow occurs when the baby is prone with the neck extended. □ Auscultation over the nose, mouth, neck, and chest can localize the site of obstruction and correlate the stridor with the respiratory phase. Glottic and supraglottic obstruction prolongs inspiration, while bronchial obstruction prolongs expiration. □ Oro Pharyngeal examination Passage of a nasal catheter can determine the patency of the nasopharyngeal airway. The placement of an oral airway will bypass the obstruction in choanal atresia. In Pierre-Robin sequence, the placement of a nasopharyngeal airway will maintain the airway until a long-term decision is made, e.g., tracheostomy, mandibular distraction, etc. One must ALWAYS maintain a high index of suspicion for an aspirated foreign body Page | 65 □Neck examination: - Ludwig's angina : stridor may occur due to laryngeal edema, swelling in the submandibular region with edema in the floor of the mouth, trismus dysphagia and salivation. ❖ ETIOLOGY OF STRIDOR In the larynx Croup is the most common cause of acute stridor. Laryngomalacia represents the most common cause of congenital chronic stridor. Congenital - Laryngomalacia - Laryngeal web if large - Subglottic stenosis. Inflammatory Acute Chronic - Acute laryngitis in children, -Laryngeal scleroma -Laryngotracheobronchitis, - Epiglottitis 1-Traumatic: Accidental: FB, Penetration trauma, compression trauma, burns. Iatrogenic: after direct laryngoscopy, endotracheal intubation, radiotherapy. 2. Neoplastic Benign: Juvenile multiple papillomatosis. Malignant: laryngeal carcinoma. The 3. Paralytic: underlined Bilateral abductor paralysis causes 4. Miscellaneous represent Laryngismus stridulus stridor in Laryngocele children. Outside the larynx ✓ Retropharyngeal abscess. ✓ Ludwig's angina ✓ Tumors of the trachea, hypopharynx, esophagus and thyroid gland. ✓ Enlarged mediastinal lymph nodes. ❖ TREATMENT Treatment of the cause (Medical treatment): Page | 66 In inflammatory conditions: 1. Hospitalization & close observation , be ready for the possibility of endotracheal intubation or tracheostomy if indicated. 2. Oxygen inhalation via a face mask. 3. Steroids, to reduce laryngeal edema, 4. Nebulized racemic adrenaline to reduce laryngeal edema. 5. Antibiotics,( the drug of choice is amoxicilline/clavulnate), 6. antipyretics, and ample fluids. 7. Room humidification with steam or atomizer to liquefy secretions. ❖ CONGENITAL ANOMALIES 1- congenital Laryngomalacia INCIDENCE Commonest congenital anomaly of the larynx. PATHOLOGY 1. Anatomical defect a) The epiglottis is folded backwards on itself i.e. it is omega-shaped. b) The ary-epiglottic folds are short and approximated → narrow laryngeal inlet. 2. structural defect Softening of the laryngeal cartilages→ the supraglottis collapses inwards during inspiration. SYMPTOMS 1. Inspiratory stridor; starts soon after birth. It improves on lying in the prone position. 2. Normal cry i.e. no hoarseness of voice. SIGNS The supraglottis collapses inwards during inspiration & becomes normal during expiration. Page | 67 TREATMENT No treatment is required. The condition improves spontaneously at the age of two years. 2-Congenital Subglottic Stenosis PATHOLOGY ( TYPES ) Mucosal or cartilaginous narrowing of the subglottic region. SYMPTOMS 1- Bi-phasic stridor. 2- Normal cry i.e. no hoarseness of voice. SIGNS Narrowing of the subglottic region. TREATMENT 1- Tracheostomy when necessary. 2- Surgical widening of the subglottic region. How? ▪ Micro-laryngoscopic by laser surgery in case of mucosa stenosis. ▪ Through external laryngoplasty operation → in case of A large laryngeal web present with hoarseness and stridor TRAUMATIC LARYNX 1-Laryngeal foreign body Impaction of a foreign body in the larynx is rare but potentially fatal. TYPES 1. Sharp foreign body as pin or glass. 2. Large foreign body as food bolus. SEQULAE: Sudden severe respiratory obstruction. CLINICAL PICTURE a. History of foreign body inhalation → may be present. Page | 68 b. Sudden violent attack of coughing stridor and choking→followed by asphyxia and cyanosis. TREATMENT 1- First aid measures To dislodge the foreign body. Infants Back blows: How? Sit down → put the infant on your knees in the prone position with his head below the level of his chest → slap his back ( between the scapulae ) sharply with the heel of the hand. Children & adults ▪ Back blows: How? The patient leans forwards so that his head becomes below the level of his chest → slap his back ( between the scapulae ) sharply with the heel of the hand. ▪ Heimlich’s manoeuvre: How? Stand behind the patient → place clasped hands jus