Adenoid

Definition : Hypertrophy of the nasopharyngeal tonsil sufficient enough to obstruct the airway.

Age incidence : Usually 3-7 years
Regress : From 10 years
Complete regress : Within 20 years


Clinical features are due to –
Hypertrophy of the adenoid causing mechanical obstruction

Fig:Enlarge adenoid

Inflammation
Generalized symptoms

Symptoms due to nasal obstruction --    Mouth breathing
     Dryness of throat
     Dribbling of saliva
     Sore throat due to associated pharyngitis
     Deafness, earache( Due to blockage of Eustachian tube)
      
 Due to inflammation :
     I.  Nasal discharge
     II. Post-nasal drip
     III. Recurrent acute suppurative otitis 
          media
      IV. Persistence of chronic suppurative
          otitis media
       V. Rhinitis/Sinusitis
 
Generalized disturbances :
Mental apathy
Mental dullness
Nocturnal enuresis
Night terror

In long standing cases patient may develop adenoid facies.

Adenoid facies :
Open mouth
Pinched nose
Retraction of upper lip
Prominent upper incisor
High arched palate
Flat chest and rounded shoulder

Sign :
Mouth breath
Digital examination
Posterior rhinoscopy

Diagnosis :
By symptoms and Xray nasopharynx lateral view


Differential diagnosis :
Deviated nasal septum
Hypertrophied posterior end of inferior turbinate
Antrochoanal polyp
Congenital chonal atresia

Complications :
Pharyngitis
Tonsillitis
Secretory otitis media
Recurrent acute suppurative otitis media
Persistance of chronic suppurative otitis media
Sleep apnoea
Mental dullness

Treatment :
When symptoms are mild-
Nasal decongestants
Antihistamine

When there is recurrent symptoms and/or complications- Adenoidectomy
In secretory otitis media, myringotomy and possibly insertion of ventilation tube(Grommet) are done together with adenoidectomy.

DIPHTHERIA

It is an acute infection caused by Gram positive bacillus, Corynebacterium Diphtheriae.
It spreads by droplet infection.
Incubation period : 2-6 days

Incidence :
The incidence has fallen markedly in the last quarter of a century.
Children are particularly affected , especially those between 2-5 years of age. But any age group can be affected.

Because of widespread and routine childhood DPT immunizations, diphtheria is now rare in many parts of the world.
Risk factors include crowded environments, poor hygiene, and lack of immunization.

Symptoms :
Sore throat
Painful swallowing
Neck swelling
Low grade fever, headache, malaise
Vomiting
Sign :
Enlarged and tender cervical lymph nodes.
Sometimes presenting a “bull-neck” appearance.
Patches of false membrane are present on the tonsils, faucial pillars, soft palate and occasionally on the posterior pharyngeal pharyngeal wall. It is usually grey in colour. It is firmly attached and when detached, leaves a bleeding surface on which it tends to re-form. It often has a strong foetor. In atypical cases no false membrane is present and picture resembles a simple streptococcal infection.
Pyrexia : The temperature is rarely above 38.30C(1010F), but the pulse rate is usually raised out of proportion.
Toxaemia is marked.( Patient is ill and toxic but fever seldom rises above 380C)

Complications :
Myocarditis
Cardiac arrythmia
Acute circulatory failure
Paralysis of soft palate, diaphragm and ocular muscles.
Laryngeal diphtheria may cause airway obstruction.

Treatment :
Antitoxin must be given  immediately, without waiting for the bacteriological results of a swab, when the disease is suspected. 20,000 – 100,000 units are injected.
Systemic penicillin : helps to control the primary and any secondary infection.

Other treatments may include:

Fluids by IV
Oxygen
Bed rest
Heart monitoring
Insertion of a breathing tube
Correction of airway blockages

STOMAS(Colostomy)

                  A colostomy is an artificial opening made in the large bowel to divert faeces and flatus to the exterior, where it can be collected in an external appliance. Depending on the purpose for which the diversion has been necessary, a colostomy may be temporary or permanent.

Figure:Colostomy bag

     SUMMRY

     Stomas

·         May be colostomy or ileostomy

·         May be temporary or permanent

·         Temporary or defunctioning stomas are usually fashioned as loop stomas

·         An ileostomy is spouted; a colostomy is flush

·         Ileostomy effluent is usually liquid whereas colostomy effluent is usually solid

·         Ileostomy patients are more likely to develop fluid and electrolyte problems

·         An ileostomy is usually sited in the right iliac fossa

·          A temporary colostomy may be transverse and sited in the right upper quadrant

·         End colostomy is usually sited in the left iliac fossa

·         All patients should be counselled by a stoma care nurse before operation

·         Complications include skin irritation, prolapse, retraction, necrosis, stenosis, parastromal hernia, bleeding and fistulation.

Temporary colostomy

                                        A transverse loop colostomy has in the past been most commonly used to de function an anaestomosis after an anterior resection. It is now less commonly employed as it is fraught with complications and is difficult to manage; a loop ileostomy is preferred.

    A loop left iliac fossa colostomy is still sometimes used to prevent faecal peritonitis developing following traumatic injury to rectum, to facilitate the operative treatment of a high fistula in ano and incontinence.

    A temporary loop colostomy is made bringing a loop of colon to the surface, where it is held in place by a plastic bridge passed through the mesentery. Once the abdomen has been closed, the colostomy is opened, and the edges of the colonic incision are sutured to the adjacent skin margin. When firm adhesion of the colostomy to the abdominal wall has taken place, the bridge can be removed after 7 days.

    Following the surgical cure or healing of the distal lesion for which the temporary stoma was constructed, the colostomy can be closed. It is usual to perform a contrast examination (distal lopogram) to check that there is no distal obstruction or continuing problem at the site of previous surgery. Colostomy closure is most easily and safely accomplished if the stoma is mature i.e. after the colostomy has been established for 2 months. Closure is usually performed by an intra peritoneal technique, which is associated fewer  closure breakdowns with faecal fistulae.

Double barrelled colostomy

                                                This colostomy was designed so that it could be closed by crushing the intervening spur by using an enterotome or a stapling device. It is rarely used now, but occasionally the colon is divided so that both ends can be brought to the surface separately, ensuring that the distal segment is completely defunctioned.

Permanent colostomy

                                      This is usually formed after excision of the rectum for a carcinoma by the abdomino-perineal technique. It is formed by bringing the distal end(end colostomy) of the divided colon to the surface in the left iliac fossa, where it is sutured in place, joining the margin to the surrounding skin. The point at which the colon is brought to the surface must be carefully selected to allow a colostomy bag to be applied without impinging on the bony prominence of the antero superior iliac spine. The best site is usually through the lateral edge of the rectus sheath, 6 cm above and medial to the bony prominence.

Complications of colostomies

                                                  The following complications can occur to any colostomy but are more common after poor technique or siting of the stoma:

• Prolapse
• Retraction;
• Necrosis of the distal end;
• Fistulae formation;
• Stenosis of the orifice
• Colostomy hernia
• Bleeding
• Colostomy diarrhoea; this is usually an infective enteritis and will respond to oral metronidazole 200 mg three times daily.

Many of these complications require revision of the colostomy.

Loop ileostomy

                           An ileostomy is now often used as an alternative to colostomy, particularly for defunctioning a low rectal anaestomosis. The advantages of a loop ileostomy over a loop colostomy are the ease with which the bowel can be brought to the surface and the absence of odour. Care is needed, when the ileostomy is closed, that the suture line obstruction does not occur.

        

Enterocutaneous Fistula

Figure:Enterocutaneous fistula

An external fistula communicating with the gut mucosa to the skin surface. It may occur following an operation for gangrenous appendicitis or the draining of the appendix abscess. A faecal fistula can occur from necrosis of a gangrenous patch of intestine after the relief of a strangulated hernia, or from a leak from an intestinal anaestomosis. The opening of an abscess connected with chronic diverticulitis or carcinoma of the colon frequently results in faecal fistila. Radiation damage is also another cause of faecal fistula. The most common cause of cutaneous fistula is however previous surgery. This happens most often in patients with adhesions following previous operations. Enterocutaneous fistula can be divided into:-

1)       Those with a high output, more than 1 L/day

2)        Those with a low output, less than 1 L/ day.

They can also be describe anatomically as simple, with a direct communication between the gut and the skin, or complex, i.e. those with one or more tracts they are tortuous and sometimes associated with an intervening abscess cavity half way along the tract.

The discharge from a fistula connected with the duodenum or jejunum is bile stained and causes severe excoriation of the skin. When the ileum or caecum is involved is involved, the discharge is fluid faecal matter; when the distal colon is the affected site, it is solid or semisolid faecal matter. The site of the leakage and the length of the fistula can be determined by small bowel enema and Ba-enema, by fistulogram and more importantly, by CT scan of the abdomen will show up any associated abscesses.

Treatment

                     This can be very challenging in patients with a high output fistula. Low output fistula can be expected to heal spontaneously, provided that there is no distal obstruction. Reasons for failure of spontaneous healing also include:

1)        epithelial continuity between the gut and the skin;

2)        the presence of active disease where, for example there is crohn’s disease or carcinoma at the site of anaestomosis or in the tract;

3)        an associated complex abscess.

The abdominal wall must be protected from erosion by the use of appliances. The patients must remain nil by mouth; intravenous nutrition is started and signs of a decrease in fistula output are sought. The higher the fistula in the intestinal tract, the more skin excoriation must be expected, and this is worst in the case of a duodenal fistula. High output fistula cause rapid dehydration and hypo-proteinaemia. Vigorous fluid replacement  and nutritional support is essential. The drainage of an intra-abdominal abscess can be life saving. This can be achieved by either CT guided drainage or occasionally laparotomy. In patients with a complex  fistula, it may be necessary to bring out a de-functioning stoma upstream of the fistula site, even if this result in a high output stoma.    

 Operative treatment  

                                        Operative repair should be attempted only after a trial of conservative management. The surgery can on occasion be extremely technically demanding and an anaestomosis should not be fashioned in the presence of continuing intra-abdominal sepsis or when the patient is hypo proteinaemic.

ABDOMINAL TUBERCULOSIS

Abdominal tuberculosis can be divided into

·         Tuberculous peritonitis and

·         Tuberculosis of the intestine.

TUBERCULOUS PERITONITIS

Acute tuberculous peritonitis

                                                  Tuberculous peritonitis sometimes has an onset that so closely resembles acute peritonitis that the abdomen is opened. Straw coloured fluid escapes and tubercles are seen scattered over the peritoneum and greater omentum. Early tubercles are greyish and translucent. They soon undergo caseation and appear white or yellow and are then less difficult to distinguish from carcinoma. On opening the abdomen and finding tuberculous peritonitis, the fluid is evacuated, some being retained for histological studies. A portion of diseased omentum is removed for histological confirmation of the diagnosis and the wound closed without drainage.

Chronic tuberculous peritonitis

                                                        The condition presents with abdominal pain (90% of cases), fever (60%),          weight loss (60%), ascites(60%), night sweats (37%) and abdominal mass (26%).

Origin of the infection

                                       Infection originate from:

·         tuberculous mesenteric lymph  nodes

·         tuberculosis of the ileocaecal region

·         a tuberculous pyosalphinx

·         blood borne infection from pulmonary tuberculosis usually the miliary.

Varieties of tuberculous peritonitis

 There are four varieties of tuberculous peritonitis:

ascitic, encysted, fibrous and purulent.

Ascitic form

                     The peritoneum is studded with tubercles and the peritoneal cavity becomes filled with pale, straw-coloured fluid. The onset is insidious. There is loss of  energy, facial pallor and some loss of weight. The patient is usually brought for advice because of the distension of the abdomen. Pain is often absent; in other cases there is considerable abdominal discomfort, which may be associated with constipation or diarrhoea. On inspection, dilated veins may be seen coursing beneath the skin of the abdominal wall. Signs of ascites can be elicited readily. Because of raised intra-abdominal pressure, an umbilical hernia commonly occurs. On abdominal palpation, a transverse solid mass can often be detected. This is rolled- up greater omentum infiltrated with tubercles.

  Diagnosis is seldom difficult except when it occurs in an acute form or when it first appears in an adult, in which case it has to be differentiated from other forms of ascites, especially malignancy. Laparoscopy is useful by allowing inspection of the peritoneal cavity, where the appearance is often diagnostic. Areas of caseation an be biopsied for histopathology. The ascitic fluid is pale yellow, usually clear and rich in lymphocytes.

  Once the diagnosis of tuberculous peritonitis has been made, it is always important to look for tuberculous disease elsewhere. A chest radiograph should always be taken before laparoscopy or laparotomy is performed.

 Encysted form

                          The encysted form is similar to the ascitic form except that one part of the abdominal cavity alone is involved. Thus a localized intra-abdominal swelling is produced, which may give rise to difficulty in diagnosis. In the women above the age of puberty when the swelling is in the pelvis an ovarian cyst will probably be diagnosed. In the case of  a child it is sometimes difficult to distinguish the swelling from a mesenteric cyst. Late intestinal obstruction is a possible complication.

Fibrous form

                      The fibrous form is characterized by the production of widespread adhesions, which cause coils of intestine, specially the ileum, to become matted together and distended. This distended coils act as a ‘blind loop’ and give rise to steatorrhoea, wasting and attacks of abdominal pain. On examination the adherent intestine with omentum attached, together with the thickened mesentery, may give rise to palpable swelling. The first intimation of the disease may be sub-acute or acute intestinal obstruction. If the adhesions are accompanied by fibrous strictures of the ileum as well, it is best to excise the affected bowel, provided that not too much of the small intestine need to be sacrificed. Anti-tubercular therapy will often rapidly cure the condition without the need for surgery.

Purulent form

                        The purulent form is rare. When it occurs, usually it is secondary to tuberculous salphingitis. Amidst a mass of adherent intestine and omentum, tuberculous pus is present. Sizeable cold abscess often form and point on the surface, commonly near the umbilicus, or burst into the bowel. In addition to prolonged general treatment, operative treatment may be necessary for the evacuation of cold abscesses and possibly for intestinal obstruction. If a faecal fistula forms, it usually persists because of distal intestinal obstruction. Closure of the fistula must therefore be combined with some form of anaestomosis between the segment of intestine above the fistula and an unobstructed area below. The prognosis of this variety of tuberculous peritonitis is relatively poor.

Tuberculosis of the intestine

                                                        Tuberculosis can affect any part of the gastrointestinal tract from mouth to the anus. The sites affected most often are the ileum, proximal colon and peritoneum. There are two principal types.

 Ulcerative tuberculosis

                                          Ulcerative tuberculosis is secondary to pulmonary tuberculosis and arises as a result of swallowing tubercle bacilli. There are multiple ulcers in the terminal ileum, lying transversely and the overlying serosa is thickened, reddened and covered in tubercles

Clinical features

                             Diarrhoea and weight loss are the predominant symptoms, and the patient  will usually be receiving treatment for pulmonary tuberculosis.

Radiology

                 A barium meal and follow thorough or small bowel enema will show the absence of filling of the lower ileum, caecum and most of the ascending colon as a result of narrowing and hyper motility of the ulcerated segment.

Treatment

                  A course of chemotherapy is given. healing often occurs provided the pulmonary tuberculosis is adequately treated. An operation is only required in the rare event of a perforation or intestinal obstruction.

Hyperplastic tuberculosis

                                            This usually occurs in the ileo-caecal region, although solitary and multiple lesions in the lower ileum are sometimes seen. This is caused by ingestion of Mycobacterium tuberculosis by patients with a high resistance to the organism. The infection establishes itself in lymphoid follicles, and the resulting chronic inflamation causes thickening of the intestinal wall and narrowing of the lumen. There is early involvement of regional lymph nodes, which may caseate. Unlike CD with which it shares many similarities, abscess and fistula formation is rare.

Clinical features

                             Attacks of abdominal pain with intermittent diarrhoea are the usual symptoms. The ileum above the partial obstruction is distended, and the stasis and consequent infection lead to steatorrhoea, anaemia and loss of weight. Sometimes, the presenting picture is  of a mass in the right iliac fossa with vague ill health. The differential diagnosis is that of an appendix mass, carcinoma of the  caecum CD, tuberculosis or actinomycosis of the caecum.

Radiology

                 A barium follow thorough or small bowel enema will show a long narrow filling defect in the terminal ileum.

 

Treatment

                  When the diagnosis is certain and the patient has not yet developed obstructive symptoms, treatment with chemotherapy is advised and may cure the condition. When obstruction is present, operative treatment is required and ileocaecal resection is best.

TONSILLECTOMY

METHODS :

1. Guillotine method
2. Dissection method
3. Laser tonsillectomy
4. Electro coagulation method
5. Harmonic scalpel tonsillectomy
6. Cryosurgery
7. Electro frequency coagulation

Figure:Tonsillectomy operation

Indications of Tonsillectomy :

1. Repeated attack of acute tonsillitis more that 3 times per year for consecutive two years, every time causing 3 days or more work loss.
2. Chronic tonsillitis.
3. Hugely enlarged tonsils causing mechanical obstruction- difficulty in swallowing/ difficulty in respiration.
4. Single attack of peritonsillar abscess or Quinsy (operation is indicated  6 weeks after recovery)
5. Unilateral enlargement of tonsil when malignancy is suspected.

    6. Persistant carriers of streptococcus or diphtheria bacilli.

    7. In case of remote complications eg. Rheumatic fever or Acute Nephritis

    8. As an approach of some operations-

     - eg. Avulsion of glossophayngeal neuralgia, avulsion of elongated styloid process

    9. As a part of other operation e.g. Uvulopharyngopalatoplasty.

Contraindications :

Absolute : Some bleeding disorders

Relative contraindications :

1. Acute upper respiratory infections
2. Bleeding disorders (specially trait)
3. Epidemic of polio around the vicinity of hospitals
4. Uncontrolled Diabetes Mellitus
5. Uncontrolled Hypertension
6. Pregnancy
7. Menstruation
8. Systemic diseases
9. Debilitated conditions of patient

Complications of tonsillectomy :

Anaesthetic complications :

1. Injury to different structures :

              - Lip, teeth, gum, cheek, palate, posterior pharyngeal wall, larynx up to trachea.

2. Cardiac arrest

3. Respiratory arrest

Surgical complications :

1. Injury to different structures : Lip, teeth, angle of mouth, palate
2. Hemorrhage – primary, reactionary and secondary.
3. Laryngeal oedema
4. Parapharyngeal abscess, retropharyngeal abscess , Cellulitis of neck
5. Pulmonary complications- aspiration of blood or vomitus, lung collapse, lung abscess.

Primary haemorrhage : Bleeding during operation.

 Due to -

1. Hurried operation
2. Extensive fibrosis
3. Acute upper respiratory infection
4. Bleeding disorder

Management :

1. Ligate/cauterize all the bleeding vessels
2. Pillar to pillar ligation if failed
3. Blood transfusion if there is bleeding disorder

Reactionary haemorrhage :

Bleeding within 24 hours after operation.

Patient is usually admitted in the hospital.

How to confirm?

1. Increase pulse rate
2. Decrease blood pressure
3. Repeated swallowing( we will suspect blood)
4. Rattling noise during respiration or noisy respiration
5. Examination of throat- Blood clot is seen

Causes : The bleeding results from :

•         Failure to ligate all bleeding vessels

•         Oozing from the vessels after relaxation of the stretched faucial tissues

•         Failure of a vessel to contract and retract after crushing or cutting

•         Postoperative rise of blood pressure. Coughing and straining dislodge a clot

•         Slipping of a ligature

Management :

1. Examine the throat under good illumination. If there is any blood clot remove it.
2. Hydrogen per oxide gargling.
3. If failed then apply wet gauge (with hydrogen per oxide) pressure over the tonsillar fossa for 10 minutes.
4. If failed then to open IV channel, start IV fluid, send blood for grouping & cross matching and arrange blood for transfusion.
5. Take the patient to operation theatre and call senior/experienced anaesthetist.
6. Under general anaesthesia, ligate all the bleeding vessels. If failed then pillar to pillar ligation.

Anaethesia for reactionary haemorrhage is always dangerous as throat is full of blood clot and blind intubation may require.

Secondary haemorrhage :

Bleeding from 24 hours after operation up to 10 day. Usually occurs after 5-6 days.

Cause : Infection.

Management :

1. Admit the patient in the hospital.
2. Pressure over the tonsils by hydrogen soaked gauge piece.
3. Send tonsil swab for culture and sensitivity and start IV antibiotics, IV fluid, Start hydrogen per oxide & antiseptic gargling, keep patient nothing by mouth.

      4.After C/S report comes, change antibiotics

      5. To relieve anxiety : Sedative

      6. If bleeding does not stop then under general anaesthesia, try for haemostasis. If      failed then pillar to pillar ligation.

Secondary haemorrahge usually stops after IV antibiotics and gargling Posoperative care :

1. Keep the patient in tonsillar position.
2. Check whether any bleeding from nose or mouth
3. Record vital signs, pulse, blood pressure and respiration
4. Diet – 2 hours after operation and when patient is fully recovered, then liquid diet and ice cream.

      Usually 1^st day – liquid diet

                    2^nd to 5^th day – Semisolid diet

                    5^th day onwards – Normal diet

        Plenty of water by mouth

5. Maintain oral hygiene : with hydrogen per oxide/ povidone Iodine mouth wash.

6. Antibiotic : Broad spectrum antibiotic for 10 days

7. Analgesic – Tab Diclofenac sodium or Paracetamol 1 tab 3 times daily after food till necessary if not contraindicated.

Patient is usually discharged 24 hours after operation.

Chronic tonsillitis

Aetiology :

1. Repeated attack of acute tonsillitis
2. Inadequate treatment
3. Repeated and persistence of infection in the nose and paranasal sinuses

Clinical features :

Symptoms :

1. Recurrent sore throat
2. Difficulty in swallowing
3. Bad smell( Halitosis)
4. Hawking

Signs : Four cardinal signs

1. Tonsils – hypertrophied or atrophied.
2. Congested anterior pillars.
3. Inspissated pus will come out from tonsils on giving pressure by tongue depressor.

Both the jugulo-digastric lymph nodes are enlarged and tender

Diagnosis :

1. From history
2. From Signs

Investigations :

For treatment purpose and for general anaesthesia. Not for diagnosis.

Treatment : Tonsillectomy under general anaesthesia.

GLAUCOMA

Figure:Glaucoma

CONGENITAL/ DEVELOPMETAL GLAUCOMA

Types:

1. Primary dev/ cong.
2. Developmental Glaucoma with associated ocular anomalies.

Primary dev/ cong. Glaucoma:

High IOP due to dev anomaly of the angle of AC.

1. True cong. Glaucoma – 40%
2. Infantile glaucoma – 50% manifests within 3 yrs
3. Juvenile glaucoma – 10%, manifests b/w 3-16yrs of life.

WHEN THE DISEASE MANIFESTS PRIOR TP AGE 3YRS, THE EYEBALL ENLARGES AND SO THE TERM ‘BUPHTHALMOS’ (HYDROPHTHALMOS)

IS USED.

Prevalence and genetic pattern: Mostly sporadic, 10% autosomal recessive,

65% boys, 75% bilateral, may be asymmetric

Affects 1 child in 10,000 live births.

Pathogenesis:

Maldevelopment of trabeculum including the irido trabecular junction (trabeculodysgenesis) is responsible for impaired aqueous outflow resulting in raised IOP.

C/F:

1. Photophobia, blepharospasm, lacrimation. And eye rubbing.
2. Corneal signs:

i.              Corneal oedema

ii.            Corneal enlargement, normal infant cornea measures 10.5 mm diameter > 13mm confirms enlargement.

iii.           Tears and breaks in Descemet’s membrane (Haab’s sinae)

3. Sclera: thin and blue.
4. AC: deep.
5. Iris: iridodonesis, atrophic patches
6. Lens: flat, may subluxate.
7. Optic disc: variable cupping and atrophy, esp. after 3^rd yr.
8. IOP: moderately high.
9. Axial myopia and anisometropic amblyopia may develop.
10. Enlargement of globe: Buphthalmos.

Examination:

-       E U A include:

1.    Measurement of IOP

2.    Measurement of corneal diameter.

3.    Ophthalmoscopy to evaluate optic disc.

4.    Gonioscopic examination of angle of AC to detect abnormality: Trabeculodysgenesis.

D/D:

1. Keratitis.
2. Megalocornea
3. Lacrimation due to cong. NLD obstruction.
4. Retinoblastoma.

Treatment:

1. Rx is primarily surgical, after lowering of IOP by use of hyperosmotic agents, Acetazolamide, beta blockers.
2. Surgical procedures:

i.              Goniotomy

ii.            Trabeculotomy

iii.           Combined Trabeculotomy and trabeculotectomy.

PRIMARY OPEN ANGLE GLAUCOMA (POAG)/ CHRONIC SIMPLE GLAUCOMA:

Definition: Slowly progressive raised IOP associated with characteristic optic disc cupping and specific field defect in eyes with open angle of AC. There is no obvious systemic or ocular cause in rise in IOP.

Etiopathogenesis: Not known exactly.

1. PDF and risk factors:
1. Heredity: polygenic inheritance
2. Age: b/e 5^th and 7^th decade.
3. Race: common and severe in blacks.
4. Myopes: common.
5. Diabetics: higher prevalence.
6. Smoking: increased risk.
7. More prevalent in Hypertensive pts.
8. Thyrotoxicosis: more prevalence.
2. Pathogenesis of rise in IOP:

Decrease in aqueous outflow facility due to increased resistance to aqueous outflow caused by age related thickening and sclerosis of the trabeculae and absence of giant vacuoles in the cells linning the canal of Schlemm.

3. Corticosteroid responsiveness:

Pt. with POAG, offspring and siblings are likely to respond to six wks topical steroid with a significant rise in IOP.

Incidence of POAG: 1 in 100 of general population of either sex above the age of 40 yrs. Forms about one third cases of all glaucoma.

C/F of POAG:

Symptoms:

1. Insidious, usually asymptomatic.
2. Mild headache and eye ache.
3. Defect in visual field.
4. Increasing difficulties in reading and close works.
5. Frequent changes in presbyopic glasses.
6. Delayed dark adaptation.

Signs:

1. Anterior segment signs: usually normal, in late stages, corneal haze and sluggish pupil.
2. IOP: raised above 21 mm of Hg.
3. Optic disc changes:
1. Vertically oval cup.
2. Asymmetry of the cup, difference more than 0.2 b/w two eyes significant.
3. Large cup: Normal cup size, 0.3
4. Splinter hrgs on near disc margin.
5. Pallor areas on the disc.
6. Atrophy of the retinal nerve fibre layer.
7. Thinning of neuro retinal rim.
8. Nasal shifting of retinal vessels.
9. Pulsation of retinal arterioles. (pathognomic sign of raised IOP)
10. Glaucomatous optic atrophy, deeply excavated white disc.
11. Lamellar dot sign.
4. Visual field defects: Visual field defects initially observed in Bjerrum’s area (10-25degree from fixation) and correlate with optic disc changes.

i.              Isopter contraction.

ii.            Baring of blind spots.

iii.           Small wing-shaped paracental scotoma.

iv.           Seidel’s scotoma.

v.            Arcuate or Bjerrum’s scotoma.

vi.           Ring or double arcuate scotoma.

vii.          Rönne’s central nasal step.

viii.        Peripheral field defects.

ix.           Advanced field defects:

1. Tubular or tunnel vision; small central island of vision.
2. Temporal island of vision.

Investigations:

1. Tonometry
2. Diurnal variation of IOP
3. Gonioscopy
4. Documentation of optic disc changes
5. Slit-lamp exam to rule out secondary causes of POAG.
6. Perimetry
7. Nerve fiber layer analyzer.
8. Provocation test: water drinking test.

à 8 mm of Hg or more rises in IOP diagnostic of POAG.

Diagnosis of POAG:

1. POAG: IOP>21 mm Hg.

àGlaucomatous optic disc cupping and or visual field defects.

2. Ocular HTN or Glaucoma suspect:

àIOP>21mm Hg. No change in optic disc or visual field.

3. Normal tension or Low tension Glaucoma (NTG, LTG):

àTypical glaucomatous disc cupping, with or without visual field changes.

Mx of POAG:

General consideration:

Baseline evaluation and grading of severity of glaucoma.

Aim: To lower IOP to a level where further visual loss does not occur.
Therapeutic choices:

1. Medical therapy: initial choice.
2. Argon or diode laser trabeculoplasty, and
3. Filtration surgery, last resort.

A. Basic principles of medical therapy of POAG:

1. Identification of target pressure below which glaucomatous damage is not likely to progress.

     Mild to moderate damage: target pressure 12-14mm Hg,

     Severe damage: target pressure, 12-14 mm Hg, even lower in    

     NTG/ LTG.

2. Single drug therapy.
3. Combination therapy.
4. Monitoring of therapy.

Treatment regimens:

1. Single drug therapy:

i.              Topical beta blockers: these lower IOP by reducing aqueous secretion due to their effect on beta receptors in the ciliary processes.

Timolol maleate: 0.25, 0.5%: 1-2 times a day.

C/I: BA or heart block.

ii.            Pilocarpine: 1, 2, 4%- 3-4 times daily.

M/A – contracts longitudinal muscle of ciliary body and opens spaces in trabecular meshwork, thereby mechanically increasing aqueous outflow.

iii.           Latanoprost: 0.005%; once daily

A PG analogue decreases IOP by increasing uveo-scleral outflow of aqueous.

                iv.        Dorzolamide: 2%; 2-3 times a day.

                            Topical CA inhibitor lowers IOP by decreasing aqueous        

                            secretion.

2. Combination topical therapy: If one drug is not effective; Add one drug which decreases aqueous production, e.g.- Timolol, Brimonidine or dorzolamide, and other drug which increases aqueous outflow. E.g.- Latanoprost, Pilocarpine.
3. Role of oral CA inhibitor in POAG: Acetazolamide may be added for short term to control IOP; long term use is not recommended because of their side effects.

B. Argon or diod laser trabeculoplasty (ALT or DLT):

Indication:

-       Uncontrolled IOP despite maximal tolerated medical therapy.

-       As primary therapy where there is non compliance to medical therapy.

C. Surgical therapy:

Indications:

-       Uncontrolled glaucoma despite maximal medical therapy and laser trabeculoplasty.

-       Non compliance of medical therapy.

-       Eyes with advanced cupping and advanced field loss.

-       As a primary line of Rx by some workers.

Type of Surgery:

Fistulizing (Filtration) surgery makes a new channel for aqueous outflow and successfully controls IOP.

TRABECULOTECTOMY IS THE MSOT EFFECTIVE FILTRATION SURGERY FREQUENTLY PERFORMED.

PRIMARY ANGLE CLOSURE GLAUCOMA:

Definition: Type of primary glaucoma wherein there is no obvious systemic or ocular cause, in which rise in IOP occurs due to blockage of aqueous humour outflow by closure of a narrower angle of the AC.

Etiology:

1. PDF risk factors-

i.              Anatomical factors. Anatomically predisposed eyes to develop PACG:

-       Hypermetropic eyes with shallow AC

-       Anteriorly placed iris-lens diaphragm.

-       Eyes with narrow angle of AC may be due to small eyeball, smaller diameter of cornea, relatively larger lens or bigger size of ciliary body.

-       Plateau iris contiguration

ii.            General factors:

-       Age: common in 5^th decade.

-       Sex: F:M=4:1

-       Type of personality: Nervous individuals with unstable vasomotor system.

-       Family history: believed to be inherited.

-       Race: Common in Caucasians, South-East Asians, uncommon in blacks.

2. Precipitating factors:

-       Dim illumination.

-       Emotional stress.

-       Use of mydriatic drugs, atropine, cyclopentolate, Tropicamide, Phenylephrine etc.

Mechanism of rise in IOP:

-       Anatomically predisposed eye.

-       Effect of precipitating factors.

-       Mild dilatation of pupil

-       Increases amount of apposition b/w iris and lens.

-       Relative pupil block

-       Aqueous collects in PC

-       Pushes peripheral flaccid iris anteriorly, iris bombe.

-       Appositional angle closure due to iridocorneal contact,

-       -Rise in IOP begins, may be transient.

-       Appositional angle closure is converted into synechial angle closure: PAS

-       Attack of rise in IOP may last long.

Clinical presentation of PACG:

5 different clinical entities:

   -  Latent PACG (PACG suspect)

   -  Sub acute (Intermittent PACG)

   -  Acute PACG

   -  Post congestive ACG

   -  Chronic PACG

   -  Absolute glaucoma.

LATENT PACG (Suspect):

Symptoms: Absent

Signs:

-       Anatomically predisposed eye.

-       Routine slit lamp examination.

-       Pt. presenting with attack of PACG in one eye.

Diagnosis:

Clinical signs:

Provocative test:

1. Prone-darkroom tests
2. Mydriatic provocative tests: IOP rises > 8 mm Hg, positive.

Treatment: Prophylactic laser iridotomy in both eyes.

ACUTE PACG (ACUTE CONGESTIVE GLAUCOMA):

-       Slight threatening emergency

-       Sudden total angle closure

-       Severe rise in IOP

-       Lasts for many days unless treated.

-       Profound loss of vision.

C/F of acute PACG:

Symptoms:

-       Pain: sudden severe pain in the eye radiates along the branches of 5^th nerve.

-       Nausea, vomiting, and prostration.

-       Rapidly progressive impairment of vision.

-       Redness, photophobia, lacrimation.

-       Past history: about 5% pt, typical previous intermittent attacks of sub acute ACG, coloured halos around light.

Signs:

-       Lids: oedematous

-       Conjunctiva: chemosed and congested. Ciliary and conjunctival congestion.

-       Cornea: Oedematous and insensitive.

-       AC: Shallow, Aqueous flare and cells may be seen.

-       Angle of AC: completely closed seen on Gonioscopy.

-       Iris: discoloured.

-       Pupil: Semi dilated, vertically oval and fixed.

-       IOP: Markedly elevated, b/w 40-70 mm Hg.

-       Optic disc: Oedematous and hyperemic

-       Fellow eye: Shallow AC with narrow angle. Features of latent ACG.

Dx of acute PACG: Obvious from clinical features.

D/D:

1. From other causes of red eye:

i.              Acute conjunctivitis

ii.            Acute iridocyclitis.

2. From secondary ACG:

i.              Phacomorphic glaucoma

ii.            Acute neovascular glaucoma

iii.           Glaucomatocyclitic crisis.

Mx of Acute PACG:

Essentially surgical

Emergency medical therapy to prepare the eye for surgery.

1. Medical therapy:
1. Systemic hyperosmotic agent: IV mannitol, 1gm/kg body wt. to lower IOP
2. Acetazolamide: 500 mg IV followed by250 mg tab 3 times a day.
3. Analgesics and anti emetics
4. Pilocarpine eye drops 2% every 30 minutes for 1-2 hrs and then 6 hrly.
5. Beta blocker: 0..5% Timolol maleate BD
6. Corticosteroid: Betamethasone or dexamethasone 4 times a day to reduce inflammation.
2. Surgical Rx:
1. Peripheral iridotomy (PI) PAS if < 50%, LASER iridotomy is a good alternative.
2. Filtration surgery: IOP not controlled with best medical therapy, PAS is >50%, Trabeculectomy, method of choice.
3. Clear lens extraction by phacoemulsification with IOL implantation has recently been recommended by some workers.

SECONDARY GLAUCOMAS:

- Group of disorders

- Rise of IOP, associated with primary ocular or systemic disease.

- C/F comprises that of primary disease and effects of raised IOP.

PHACOLYTIC GLAUCOMA (LENS PROTEIN GLAUCOMA):

Pathogenesis:

Type of secondary open angle glaucoma in which trabecular meshwork is clogged by the lens proteins and macrophages which have phagocytosed the lens proteins.

Leakage of lens proteins occurs through an intact capsule of hypermature or Morgagnian cataract.

C/F of phacolytic glaucoma:

-       Features of congestive glaucoma, acute rise of IOP, eye having a hypermature cataract.

-       Deep AC, aqueous may contain fine white protein particles.

Mx:

-       Lower IOP by medical therapy.

-       Extraction of lens with PCIOL implantation.

STEROID INDUCED GLAUCOMA:

Secondary open angle glaucoma.

Develops following topical and rarely systemic steroid therapy.

Etiopathogenesis:

-       Steroid responsiveness genetically determined.

-       Rise of IOP after 6wks topical steroid.

-       5% general population, high responders.

Precise mechanism for rise in IOP not known.

Theories are:

1. Glycosaminoglycans (GAG): Accumulation of GAG in trabecular meshwork decreases aqueous outflow.
2. Endothelial cell theory: Suppression of phagocytic activity of living endothelial cells of Schlemm’s cana;.
3. Prostaglandin theory: Steroid inhibits synthesis of PGE and PGF thereby decreases aqueous outflow.

C/F: Resembles POAG, Develops following wks of topical steroid..

Mx:

Treatment:

-       Discontinuation of steroid.

-       Medical therapy: 0.5% Timolol maleate.

-       Trabeculectomy, in intractable cases.

Prevention:

-       Judicious use of steroids.

-       Regular monitoring of IOP when on steroids.