Surgery C Flashcards
What structures should you identify on fundoscopy?
Macula, fovea, peripheral retina, arteries, veins, optic nerve, and optic disc
What are the key features of an ocular history?
- Past ocular history
- Nature of discomfort (itching, grittiness, pain, photophobia and pain when reading)
- Discharge (watery, purulent mucoid)
- Unilateral or bilateral
- Change in vision (reading, driving, crossing road, hobbies, daily living and any adaptations needed such as magnifying glasses)
- General medical history (allergy or atopy)
- Recent URTI?
What are the red-eye differentials?
Red-eye differentials include conjunctivitis, keratitis, allergy, trauma, subconjunctival hemorrhage, iritis, episcleritis, scleritis and acute closed angle glaucoma.
Describe bacterial conjunctivitis
Bacterial conjunctivitis presents with sticky red eye, acute onset and usually starts unilaterally but can progress to bilateral. There may be purulent discharge. Itching, burning, gritty sensation, and blurring of vision because of discharge.
On examination, there may be lid swelling, conjunctival redness, and normal pupil which is reactive. Management is with safety netting but topical chloramphenicol if needed. Fusidic acid is the second line. Referral should be made if there is a severe or persistent infection, atypical features (excessive pain or visual distortion), and signs of periorbital cellulitis.
Describe viral conjunctivitis
Viral conjunctivitis usually occurs during URTIs in children but can occur in adults. There will be a watery discharge rather than a purulent discharge and lid crustiness in the morning due to overnight discharge. It is usually unilateral moving to bilateral and can have mild grittiness.
On examination, there will be watery discharge, conjunctival redness and hemorrhages, and conjunctival follicles visible. Management is safety netting and hygiene. A referral should be made if there is a persistent infection or diagnostic uncertainty.
Describe allergic conjunctivitis
Allergic conjunctivitis has a rapid onset, presents with itching, burning, grittiness, lid swelling, conjunctival oedema (chemosis) and often associated with exposure to an allergen. On examination there will be conjunctival redness and watery discharge. Management is with systemic antihistamines, topical antihistamines (emestadine or azelastine), topical sodium cromoglycate or mast cell stabilisers.
Describe keratitis definition, causes and management
Keratitis is corneal inflammation, there are various causes classified as either infective or non-infective. Keratitis may lead to scarring and subsequent corneal opacification causing visual loss. Slit lamp examination with fluoresceine eye drops may help diagnosis visualising abrasions and ulcerations.
Viral causes include Herpes simplex (dendritic ulcers) which presents with severe pain and photophobia. There may be unilateral redness which worsens with sterioid drops. Herpes zoster ophthalmicus accounts for 10% all shingles cases and needs same day referral. Varicella zoster may also cause ulceration of the cornea.
Bacterial infection requires something weakening the corneal defences. Causes include trauma, chronic dryness, exposure (Bells or Facial nerve palsy) and immunosuppression. Protozoan infection is associated with contact lens wearers. This requires referral. Marginal keratitis can be caused by blepharitis (acne rosacea). Autoimmune keratitis is seen in Sjogren’s (dry cornea), RA, SLE, and Granulomatosis with polyangiitis.
Management is with eye lubricants. Referral is usually needed. Topical ciclosporin, systemic therapy, and corneal transplantation for refractory disease.
Describe iritis definition, causes and management
Iritis (Anterior Uveitis) presents with pain aggravated by reading, redness, photophobia, watering, haloes around lights, usually unilateral and is caused by herpes simplex or trauma. There are systemic associations with HLA-B27 (50%) and ankylosing spondylitis (40%).
On examination there is a small pupil or irregular iris and there is redness with ciliary flush around the iris. Management is with topical steroids and urgent referral because chronic disease and associated conditions may need multidisciplinary approach.
Describe episcleritis and scleritis diagnosis and management
Episcleritis and scleritis are inflammatory conditions involving the sclera. Episcleritis is common in young adults, vision is not affected, treatment self-limiting or NSAIDs and is usually not associated with systemic disease and it is unilateral in 2/3 cases.
Scleritis is rare and serious. It usually occurs between 40-60 and is painful as the full thickness of the sclera is involved. It can be uni or bilateral. 50% patients have systemic inflammatory disease. Urgent referral is needed and treatment is with topical or systemic steroids and immunosuppression.
Describe subconjunctival hemorrhage
Subconjunctival haemorrhage is the leakage of blood between the sclera and conjunctiva. It looks alarming but is painless. It can be traumatic or spontaneous. Spontaneous haemorrhage is associated with high BP, clotting disorders, and use of blood thinners. It resolves in 1-2 weeks.
Describe acute closed-angle glaucoma
Acute closed-angle Glaucoma is an emergency. It presents with sudden onset severe unilateral eye pain, N+V, Haloes, and complete loss of vision within one day. There may be a history of hyperopia. It is more common in Inuit, SE Asian, and Chinese women. Usually occurs in the over 50s.
On examination, there may be unilateral red eye, cloudy cornea, and oval non-reactive pupil. Management is with same-day admission as there is a risk of permanent vision loss.
Describe retinal vein occlusion
Retinal vein occlusion can affect central vein or branch vein. It presents with sudden painless vision loss and is usually unilateral. It is most common as patient wake up. Incidence increases with age. There may be a stormy appearance on fundoscopy and it is associated with glaucoma, T2DM, hypertension, hypercholesterolaemia, arteriosclerosis and polycythaemia. Management is with emergency same day referral.
Describe retinal detachment
Retinal detachment initially causes loss of peripheral vision but as macula is reached it will cause central vision loss. Emergency referral needed for laser surgery.
What are ENT red flags?
ENT Red Flags include hoarseness, persistent odynophagia, dysphagia, weight loss, neck lump, persistent oral lesions, unilateral nasal discharge, unilateral tinnitus, stridor, or drooling.
How does laryngeal cancer present?
Laryngeal cancer presents with unexplained weight loss, hoarseness, odynophagia, dysphagia, lump, long lasting cough, persistent sore throat or earache, dyspnoea or stridor.
Investigations include CXR for potential metastases, referral, nasendoscopy, laryngoscopy and biopsy.
What key features are associated with otitis externa?
Swimming is associated with otitis externa (fungal) and pulling the pinea will cause pain
What should be suspected in a baby with red eye after birth?
A baby with red eye shortly after birth should be investigated for chlamydia and mum treated as well
Which drugs are associated with acute closed-angle glaucoma?
SSRIs and Ranitidine have increased risk of acute closed-angle glaucoma
Which condition is associated with trismus?
Quinsy
What is malignant otitis externa?
Be wary of malignant otitis externa which is where otitis externa spreads into the bones of the ear canal and base of the skull. There will be pain when moving their head.
How should double vision be assessed?
With double vision, ask to close one eye and see if it goes away. Binocular diplopia is seen in neurological pathology.
How can eye pain be distinguished into neurological and ophthalmologic?
Intermittent pain is likely neurological whereas constant is associated with the eye.
What PMH is important in ocular histories?
Hx of hypertension, diabetes and drug history is vital. (Illicit drugs are associated with sudden loss of vision, especially cocaine in young people). Cocaine is a cause of vascular pathology in young people. Travel and driving is important in the social history.
What is glaucoma?
Glaucoma is an optic neuropathy with a field defect on the disc which is comparable to the vision defect. Reducing the pressure is the treatment for glaucoma but pressure can be normal. These are normal tension glaucoma.
What is ischaemic optic neuropathy?
Ischaemic optic neuropathy presents with jaw claudication and other associated symptoms without a visual field defect. It is caused by GCS and requires urgent steroids or vision will be lost. It will spread to the other eye if not treated.
What is the significance of a hypopyon?
If a patient has a hypopyon then ask if they have had surgery in the last 72 hours. If yes, that is opthalmolitis until proven otherwise and is an emergency.
How should the red eye be assessed?
Red eye assessment: Vision affected or not, pain, location (entire eyeball or conjunctiva), cornea affected or not, and pupil size. Causes include hemorrhage, acute glaucoma, corneal abrasion, conjunctivitis, iritis, or others.
How can AOM be differentiated from AOM with effusion?
Sudden onset pain in young child is AOM and followed by discharge and pain relief is also AOM with perforation.
How will a child with cholesteatoma present?
Hours onset of worsening pain in older children with small amount of discharge and pain when moving the ear is cholesteatoma.
How will a child with adenoids present?
Adenoids can cause blockage of the nostril in young children. Spatula under the nose for condensation is important to test for this. Adenoids present with mouth breathing, nasal obstruction, runny nose and OSA.
When should a tonsillectomy be performed?
Tonsilectomy is performed for recurrent tonsilitis (5 per year for 2 years), OSA and a unilaterally enlarged tonsil.
How should epistaxis be managed?
Epistaxis should be managed by squeezing the nose for 5 mins, leaning forward and remaining calm. Medical treatment is naseptin, cautery, dressing and then blood loss management for shock. A Merocele is used when the bleeding cannot be stopped.
What ENT condition do children with cystic fibrosis present with?
Nasal polyps
What are the red flags for a neck lump?
Hard, irregular, immobile, larger than 2cm, involving the supraclavicular nodes or there is a thyroid mass.
What are the causes of stridor?
croup (Steeple sign on CXR), foreign bodies and epiglottitis.
What are the red flags for head and neck cancer?
red flags include 2-3 weeks, immunosuppressed, over 40, tobacco, alcohol, unexplained weight loss, previous history of malignancy, dysphonia, blood in saliva, dysphagia, odynophagia or otalgia.
How does tongue tie present?
Tongue tie affects breast feeding rather than bottle feeding in whom it presents with speech development issues.
How do wounds heal normally?
Most wounds will heal spontaneously; superficial and small wounds will heal within days to weeks whereas deep and larger wounds take weeks to months. Complex wounds, especially those with non-vascular wound beds, may never heal.
Wounds heal via a process of inflammation, proliferation, and then remodeling. Scarring may result depending on the depth and severity of the original wound, the time to healing, and the wound closure technique employed.
What is a split-thickness skin graft?
Split thickness skin grafts are epidermis and variable amounts of dermis. The donor site heals within two weeks. It can be sheet, fenestrated, meshed, or meek.
What is a full-thickness skin graft?
This is epidermis and dermis, and the donor site is closed directly to limit the size.
What are local flaps?
This involves moving adjacent tissue to fill a defect which can be advancement, transposition or rotational. The donor site is then closed. The vascular supply of the flap and the area of the flap that is in continuity with the donor site is the pedicle. This gives a better aesthetic and is often used post radiotherapy.
What are regional/pedunculated flaps?
This involves use of non-directly adjacent tissue in the same vicinity as the wound; the flap donor site is not in direct proximity or communication with the wound. This is used when there is insufficient volume for a local flap. These are still connected by a pedicle to the donor site.
What is a free flap?
Tissue is moved with its blood supply and anastomosed to another part of the body and can be used when there are no available local options, or skin grafts are not possible. Free flaps are often used to reconstructs defects secondary to trauma or cancer such as the DIEP flap.
What are the treatment options for melanoma?
Treatment options include surgical excision and reconstruction, Mohs, topical chemotherapy and radiotherapy.
How should burns be treated in an emergency?
Stop the burning process, 20 mins cool running water within 3 hours of the burn and then keep warm. ABCDE include inhalation injuries and size of the burn with TBSA. Major burns resuscitation is with the TBSA, IV fluids as per Parkland formula, consider fasciotomy or escharotomy, wound debridement and dressing and then ITU/HDU care.
How does the age of onset relate to neck lump pathology?
- Aged under 16: Likely inflammatory or congenital.
- Aged 16 – 40: Inflammatory or congenital causes are still most common, but malignancy incidence begins to increase.
- Over 40: These should be considered neoplastic and potentially malignant until proven otherwise, especially in a history of smoking or excessive alcohol use.
RED FLAGS for malignancy: Lump present for more than 2-3 weeks, patient older than 40, tobacco or alcohol use, previous malignancy, immunocompromised status, unexplained weight loss, ulcers, change in voice, blood in saliva, dysphagia, odynophagia, and otalgia.
How should a thyroid exam be conducted?
- General inspection: sweating and clothing. When palpating thyroid stand behind.
- Hands: examine for tremor, outstretched hands, sweaty palms, thyroid acropachy similar to clubbing, and palmar erythema.
- CVS: Tachycardia/AF is seen in hyperthyroidism and bradycardia is seen in hypothyroidism.
- Eyes: Loss of outer 3rd of eyebrows, exophthalmos, chemosis, red sclera, and lid lag
- Auscultation: Bruits
- Legs: Pre-tibial myxoedema (non-pitting oedema)
- Pemberton’s test: Raising both arms produces facial congestion and cyanosis due to mass in superior mediastinum which occur when retrosternal goitre obstructs the vena cava.
Describe parotid lumps
This is found from the zygomatic arch to ear lobe, behind the ramus of the mandible. The deep lobe extends behind the ramus of the mandible. 80% of tumours are benign.
Any patient with a parotid lump and a facial palsy has a malignant tumour.
Define a burn and how is this repaired physiologically?
Burns are defined as an injury to the skin or other organic tissue primarily caused by heat or due to radiation, radioactivity, electricity, friction or contact with chemicals. Thermal burns occur when some or all of the cells in the skin or other tissues are destroyed by hot liquids (scalds), hot solids (contact burns) or flames (flame burn).
In a burn, the Jackson burn model shows that there is a zone of coagulation (irreversible tissue loss due to coagulative necrosis), zone of stasis (decreased tissue perfusion which can deteriorate to necrosis) and a zone of hyperaemia (outermost zone with increased tissue perfusion which will recover in the absence of infection).
Burn shock occurs because of a mixture of oedema, hypovolemia, coagulability and inflammation. Fluid resuscitation is required for burns over 15% in adults and 10% in children. This is because there is rapid fluid loss through the burnt skin which can compromise the vascular stability of the patient.
How should burn surface area be measured?
When assessing burn surface area: Wallace’s rule of nines whereby each upper limb is 9%, anterior/posterior lower limb is 9%, anterior torso is 18% and head and neck 9% and genitals 1%. The palmar surface area is where each palm represents 1% TBSA. The Lund and Browder chart is a diagrammatic representation of the body which can be used. The depth of the burn is extremely important. This is described as degrees of burns or through burn depth assessment.
How are burns classified?
Superficial burns are epidermal burns. They do not have blistering and are not included in the TBSA calculations. They may be pink and painful such as sunburn.
Partial thickness burns (dermal) can be superficial dermal or deep dermal.
Superficial partial thickness burns are salmon pink, blanching with blisters and very painful.
Deep dermal injuries are mottled cherry colour that do not blanch. Blood is fixed within damaged capillaries in the deep dermal plexus. There is variable pain but less painful than superficial partial thickness burns.
Full thickness burns present as dry, leathery or waxy, hard wound that does not blanch are typically white in colour and painless.
How should a burn be treated as first aid?
Stop the burning and run the burn under lukewarm water for 20 minutes. Add cling film. Perform an ABC trauma assessment and assess weight. Inhalational injury is common and needs proactive management. Early analgesia is required. All patients should be provided tetanus prophylaxis. The burn depth and TBSA should be assessed as deep chest wall or abdomen burns can restrict ventilation. The presence or absence of vascular compromise from circumferential burns that may require urgency eschartarotomy or fasciotomy. Patient should be kept warm as they are at high risk of hypothermia.
Major burns are treated in intensive care. The age of patient plus TBSA over 100 is poor prognosis and 120-150 in likely non-survivable.
Fluid resuscitation is calculated on the TBSA and weight of the patient. Resuscitation is Parkland (crystalloid), Muir and Barclay (colloid) and hybrid. Urine output is aimed to be 0.5ml – 1ml/kg/hr and in children it should be between 1-2.
How are lacerations and stab wounds managed?
Lacerations and stab wounds are surgically debrided, and a skin graft or reconstruction may be required., Hand injuries should also be surgically debrided and vascular compromise will require microvascular repair. Amputated digits are often salvageable. Animal and human bites also require debridement, antibiotics and closure.
What is necrotizing fasciitis?
Necrotising fasciitis is a severe and rapidly progressing life threatening soft tissue infection. It is most commonly caused by Strep group A and anaerobes. There is higher incidence in diabetics, especially forneiers gangrene. It is rapidly spreading, and intensive care is needed. Multiple IV antibiotics, renal support or dialysis, inotropes and emergency debridement as every minute counts. Meningococcal sepsis can also cause extensive loss of soft tissues.
What is the Gustilo and Anderson classification
The Gustilo and Anderson classification is used for open fractures of the lower limb. The ATLS approach should be used but early and thorough surgical debridement is required in compounds fractures. Reconstruction within 72 hours is required to reduce the risk of chronic osteomyelitis. Compartment syndrome is common and should undergo fasciotomy.
What are the steps of the reconstructive ladder?
The reconstructive ladder is as follows:
1. Allow to heal
2. Primary closure
3. Skin graft (split thickness or full thickness)
4. Local flap
5. Regional flap
6. Free flap (autotransplant)
How should hand trauma be examined?
The examination is with look, feel, move. Assess neurovascular function and motor function. The most common injuries are digital branches of nerves. A nerve transection is a Neurotmesis where axonotmesis is partial nerve division and neuropraxia is bruising. Damaged nerves are repaired with microsurgery.
How are grafts classified?
The transfer of tissue without a blood supply is categorised according to tissue of origin. This can be autograft (patient), allograft (same species), or Xenograft (animal).
Split thickness skin grafts are 0.008-0.012 inches involve the epithelium and thin reticular layer of elastin. Medium thickness grafts are most commonly used (0.012-0.018) whereas thick split thickness grafts (0.018-0.03) are used in face and flexor surfaces where contraction is minimal.
Full thickness skin grafts involve the epidermis, dermis and small amount of hypodermis. They are stitched on. Skin is commonly taken from the anterior thigh or buttock.
How are flaps classified?
A flap is a unit of tissue which maintains its own blood vessels whilst being transferred from a donor site to a recipient site. They can be random, pedicled or free. They are classified by circulation, contiguity (distant/local pedicled/free) and composition (singe or composite).
How do grafts heal?
These grafts heal by secondary intention over 2-3 weeks. The basal cells layers in epidermal appendages de-differentiate into basoloid morphology. They migrate into the defect by diapedesis until there is contact inhibition. Contact signal beginning re-differentiation into stratified corneal epithelium layers.
In the first 24-48 hours plasmatic inhibition occurs where nutrients and oxygen infiltrate through capillaries. Fibrin bridges are created which is why compressive dressings ar4 required.
From 36-48 hours Inosculation occurs. Capillary buds sprout through the skin graft and connect to pre-existing vascular channels and create new ones. Collagen bridges are created.
Neurotization occurs later where nerve buds from the bed grows into the graft but sensation takes many months. Sebaceous glands and sweat glands do not regenerate.
When should a skin graft be used?
Indications for a skin graft are well vascularised, non-infected beds. Contra-indications include flexion areas, constant sheer and friction, infection, cancer and non-vascularised bed. Complications include failure (non-take_, hyperpigmentation (thin) or hypopigmentation (thick), contraction, meshed appearance, dryness and scaling.
Primary contraction occurs due to elastin fibres in the dermis. It is more pronounced in FTSG and can be corrected by stretching the graft. Secondary contraction is more severe in thinner STSG, especially if meshed. May reach 40% surface. This is corrected with prolonged splinting. Contracture is where a function or joint is limited.
Meshed grafts are the most common but least cosmetically acceptable. They have more contractures but better take. They cover wider surfaces and irregularities and conform better to wound geography.
Summarise the diagnosis, causes, and treatment of otitis externa
Otitis Externa is inflammation or infection of the outer ear. This includes the pinna and ear canal. It can be non-infective such as eczema or psoriasis but is most commonly bacterial (or fungal). Bacterial causes include pseudomonas aeruginosa, Staph aureus, E.coli and fungal causes are candida or aspergillus.
Management:
Non-infective: betamethasone drops
Infective: 1st line is acetic acid, aluminium acetate drops, ciprofloxacin drops, or Gentamicin + hydrocortisone drops. There is IV ototoxicity ,but drops are ok. If there is significant debris then an aural toilet with micro-suction is required. If there is evidence of cellulitis then oral antibiotics are indicated (flucloxacillin, ciprofloxacin or metronidazole). Any anaerobic infection requires metronidazole.
What is malignant otitis externa and who is at risk?
Malignant otitis externa (Benign necrotising) is usually seen in elderly diabetic patients or immunocompromised. The infection spreads from the skin of the ear canal into the skull base and causes osteomyelitis. There will be severe pain and granulation of the floor of the ear canal and same day admission to ENT is required.
How is chronic suppurative otitis media classified?
Chronic suppurative otitis media can be split into inactive (perforated eardrum without infection) and active (with infection and/or cholesteatoma).
Active CSOM may respond to topical antibiotics (ciprofloxacin drops or Gentamicin + hydrocortisone drops) or surgery with Tympanoplasty (closing the ear drum).
What are cholesteatomas and what are the complications?
Cholesteatomas are accumulations of squamous epithelium within a retraction pocket on the ear drum. They arise in the posterosuperior part of the ear drum (pars flaccida). If they are left alone they can cause deafness (ossicular damage or inner ear damage), dizziness (semicircular canal damage), facial palsy (bony erosion of the facial canal) or meningitis.
How should a dizziness history be taken?
Patient needs to be asked what dizziness means: light headed, ‘detached from reality’ or vertigo. Vertigo is a hallucination or movement, often rotary but can be linear or the feeling that you are on a boat. The duration of the vertigo and the associated symptoms often gives the diagnosis.
Describe BPPV
Benign Paroxysmal Positional Vertigo: This is diagnosed by the history of vertigo induced by rolling over in bed with a few seconds delay and around 30 seconds of vertigo. Diagnosis can be confirmed by the Dix-Hallpike manoeuvre where torsional nystagmus can be observed. Treated with the Epley Manoeuvre or Brandt-Daroff exercises.
Describe Meniere’s disease
Meniere’s disease has an unknown aetiology and is episodic. There is often a preceding aura (tinnitus or aural fullness) and the rotary vertigo will last for hours. It is associated with sensorineural deafness during the attack with partial recovery afterwards. There will be gradual sensorineural loss over time with repeated attacks.
Management is with prochlorperazine, betahistine hydrochloride, low salt diet, thiazide diuretics, transtympanic steroids or chemical labyrinthectomy (gentamicin ablation). Hearing aids may be eventually required. Tinnitus treatment is with sound enrichment or CBT. Vestibular rehabilitation exercises (Cooksey-cawthorne exercises) can be used to treat the dizziness.
Describe vestibular neuronitis
Vestibular neuronitis is inflammation or infection (usually viral) of the vestibular nerve. Therefore, vertigo is the only ontological symptom but it is usually accompanied by nausea and vomiting.
Describe labyrinthitis
Labyrinthitis is inflammation or infection, usually viral, of the labyrinth structures (semi-circular canal, saccule or utricle). This is associated with other ontological symptoms including deafness and tinnitus.
How should labyrinthitis and vestibular neuronitis be managed?
Both vestibular neuronitis and Labyrinthitis have spontaneous onset, may follow a URTI, present with severe rotary vertigo for over a week and the patient is initially bed bound. This will gradually subside over 6 weeks or so as central compression occurs. They will benefit with prochlorperazine in the first week but this should not be continued as it prevents the brain from compensation and thus stops spontaneous recovery. Cooksey-Cawthorne exercises for dizziness will also be helpful.
Describe vestibular migraine
Vestibular migraine is episodic and most will have a headache. Headache may precede, occur during or after the vertigo. There is often a personal history of classic migraine and it is associated with photo and phono phobia. There may be visual aura as well.
Management is to identify the triggers with a food diary and bedtime routine. Tryptans can be used to treat acute attacks but are contraindicated in CVD, HTX, and liver disease. Preventatives such as betablockers, Calcium channel blockers, antiepileptics (Gabapentin) and tricyclic antidepressants (nortriptyline) can be considered.
How does adenocystic carcinoma present?
Adenocystic carcinoma breaks the rule of UMN sparing of the forehead because it can invade the nerves of the lower face, presenting with UMN symptoms but in reality a LMN palsy.
Describe the anatomy of the LMN of the facial nerve?
Bell’s palsy is the most common cause of LMN facial palsy and is idiopathic. The LMN runs from the geniculate ganglion, through the middle ear and mastoid, out through the stylomastoid foramen and into the parotid where it branches before supplying the muscles of facial expression. Pathology along this path can damage the nerve.
How is facial palsy graded?
Facial palsy can be graded by the House-Brackmann 1-6 score:
1. Normal
2. A bit weak
3. Eye closure
4. Unable to close eye
5. A bit of movement
6. Complete palsy
How should a facial palsy be assessed?
When assessing a VII palsy always check for vesicles (Ramsey-Hunt syndrome), look in the ear for infection/tumour/cholesteatoma, feel parotid for masses, document eye ability and remember parasympathetic involvement causing fewer tears and drying of the eyeball.
Management is with prednisolone (1mg/kg) daily for a week and taper 10mg every 3 days thereafter. PPI cover as needed. Viscotears or similar may be needed and lacrilube for nighttime. If Ramsey-Hunt then valacyclovir is required.
What are the three types of deafness?
Conductive, sensorineural, or cortical
Conduction (lesion in the ear canal, drum, or ossicles)
Sensorineural (lesion in cochlea or nerve)
Cortical (lesion in brainstem/auditory cortex)
What is conductive hearing loss?
Conductive hearing loss is impairment of sound reaching the cochlea and can be caused by wax, otitis externa, perforated tympanic membrane, otitis media with effusion and otosclerosis. These are generally reversible or treatable.
What is sensorineural hearing loss?
Sensorineural hearing loss can be congenital but is acquired through presbyacusis, Meniere’s disease, Barotrauma, ototoxicity, meningitis and autoimmune conditions. It is not always reversible.
What is cortical hearing loss?
Cortical hearing loss are often following intracranial pathology such as stroke, brain tumour or surgery. Auditory processing disorder is the hearing equivalent of dyslexia where there is a normal pure tone audiogram but struggles to understand conversational speech.
What is Weber’s and Rhinne’s test?
Weber’s test is normal when both ears hear the same. In conductive loss it will be heard loudest in the affected ear and in sensorineural loss the opposite ear.
Rinne’s test states that air conduction is greater than bone in normal ears and conductive hearing loss is when bone conduction is greater than air. (can also occur in sensorineural loss but rarely).
How should a pure tone audiogram be interpreted?
Pure tone audiogram is the gold standard test but it is subjective. Patients are asked to push a button when they hear a noise. Each ear is tested individually and there is bone vibrator attached to the headphones. The standard audio presented is adjusted to take into account the average thresholds at different frequencies. 20dB or better is normal hearing. The pure tone audiogram is then plotted.
Whenever you see an abnormal response look at the BC and AC and ignore gaps of 10dB or less. If AC worse than BC by more than 10dB then conductive hearing loss at that frequency. If BC greater than 20bD there is sensorineural hearing loss. If BC >20dB and AC worse than BC by 10bD there is mixed hearing loss at that frequency.
Pure tone average is the average threshold of hearing at 500Hz, 1KHx, 2 and 4 in each ear. This is a quick assessment for comparison between two ears. When fairly flat it is useful but asymmetrical is less useful. In presbycusis the graph will slope down as there is progressive worsening.
How do nasal polyps appear
These will be a slightly different colour than the nasal septum, they are glistening and often pale/translucent yellow.
Describe rhinosinusitis symptoms, acute and chronic
Rhinosinusitis is inflammation of the nose and paranasal sinuses characterised by two or more symptoms, one of which should be either nasal blockage/obstruction/congestion or nasal discharge. Other symptoms include facial pain/pressure and reduction or loss of smell. Endoscopic findings include polyp/middle meatal oedema or pus. CT evidence of mucosal disease affecting the osteo-meatal complex or inflammation of the paranasal sinus.
Acute sinusitis lasts less than 12 weeks, is usually viral and will completely resolve. Recurrent acute rhinosinusitis is the same but more than 3 episodes in one year. Chronic rhinosinusitis is longer than 12 weeks (+/- nasal polyps) and will never completely resolve.
Chronic rhinosinusitis affects 11% and is very strongly linked with respiratory problems. Asthmatics have an 80% chance of CRS, COPD 88% and patients with poorly controlled CRS have a 50% chance of developing asthma.
How can sinusitis be managed?
Initial management of CRS is saline nasal douching and intranasal corticosteroid spray such as fluticasone or mometasone because there is likely other steroid medications for respiratory illness. If this does not resolve in 4 weeks then there should be maximum medical therapy with a saline nasal douching, fluticasone propionate nasals 400mcg, and clarithromycin 250mg for three months (or doxycycline). If the patient has nasal polyps then they should have prednisolone, fluticasone propionate, saline douching and doxycycline 100mg for three months.
Consider a different diagnosis if there is unilateral symptoms (malignancy), excessive crusting/bleeding (Vasculitis such as GwP) and immediately refer to hospital if there are orbital abscesses, evidence of cellulitis or intracranial infection (meningitis or intracerebral abscess).
Surgery for CRS should be done if there was failure of maximal medical therapy. The surgical management aims to unblock normal sinus drainage pathways to facilitate future medical management. It is frequently required to manage orbital or intracranial manifestations. It is also useful in unilateral disease for obtaining a biopsy or removing a lesion.
How should epistaxis be managed in an emergency?
Epistaxis can be life-threatening. Patient should sit upright with their head forward to facilitate spitting out of bleed. Pinch the nose at the bottom for 10 minutes. If this doesn’t work then examine nose, spray with topical anaesthesia or decongestant, if there is a visable vessel then it can be cauterised with silver nitrate, if posterior bleed then nasal packing can be done. Cannulate if not already done and get an FBC, U%E, clotting, G+S and LFTs. Consider tranexamic acid.
Rapid Rhino packing create an internal balloon for pressure and an outer haemostatic gel coat. If nasal packing fails, then radiological embolization can be used for branches of the external carotid. Otherwise, surgery is needed such a ligation/cautery of sphenopalatine artery, anterior or posterior ethmoid arteries.
How should nasal trauma be assessed?
Nasal trauma should be assessed for other facial injuries such as orbital/zygoma fractures and hand fractures. Check for a septal haematoma (between perichondrium and cartilage of nasal septum). If septal haematoma is present then refer to ENT. Manage any epistaxis.
How does ENT anatomy differ in children?
Ear: soft cartilage, narrow cartilaginous external ear canal and the length/width/direction of the estuation tube. The soft cartilage allows for easily manipulation of deformed pinna. The direction of the tube in children is upward and backwards whereas in adults it is downward and inferior. The shorter and narrower tube increases the risk of infection and glue ear.
Nose: Children are obligate nasal breathers. There is also the presence of adenoids which enlarge infancy which can become problematic. The adenoid produce B-cells (IgG and IgA). Adenoidectomy might reduce serum IgG and IgA but does not reduce overall immunity. Adenoid enlargement can affect the estuation tube and cause stagnation of air.
Enlarged adenoids can reduce the nasal airway and cause sleep disordered breathing or OSA. OSA is more likely if the tonsils are also enlarged. There is a peak incidence of 306 years and there is no difference with gender.
Throat: Babies have a smaller jaw, no teeth, and a relatively larger tongue. The larynx is higher relative to other anatomical structures. Babies are not able to drink and breathe at the same time, but they have a high efficiency. Tonsils are graded in size. They drain into the jugulodigastric nodes and mi cervical nodes. Therefore, there is enlarged neck nodes with tonsillitis. The larynx is also funnel shaped in children with the narrowest part at the cricoid ring. Inflammation at the cricoid gives rise to croup. The cricothyroid space is poorly developed until roughly 12 years old so tracheotomy cannot be done.
The larynx of children is much softer than in adults and thus there is increased likelihood of movement of walls with significant breathing efforts. This can be seen in Laryngomalacia and tracheomalacia which produces stridor with an URTI.
Define and describe acute otitis media?
Acute otitis media is acute inflammation in the middle ear cleft and associated effusion. It presents with red bulging tympanic membrane, otalgia and pyrexia. The infection is usually self limiting but can be life-threatening (mastoiditis or intracranial sepsis). 40% are caused by viruses which need analgesia alone. If there is pain for more than 48 hours then it is likely bacterial and antibiotics can be considered. Common bacterial causes are H Influenzas, S pneumoniae and M catarrhalis.
Recurrent AOM is more than 3 episodes in 6 months or 4 in 12. Treatment if not self-limiting is with prophylactic antibiotics or grommet insertion. Grommet insertion is not a cure but very effective.
Define and describe otitis media with effusion (glue ear) and how is it treated?
Otitis media with effusion (glue ear) is very common with 5% of 5-year-olds. It is more common in winter and in those with allergic rhinitis and can follow AOM. Risks include artificial feeding, reflux, parental smoking, day care and genetics. It always happens in Down’s syndrome and common in those with cleft palate. Presents as painless hearing reduction with a retracted, opaque TM with fluid or bubbles. The glue is mucous.
Investigations include a pure tone audiogram (bone air gap of 30dB) and tympanogram (flat trace because fluid under the TM is not compressible so will be flat reading).
Treatment with grommet insertion works because the grommet acts as a ventilation tube. The risks include perforation, infections, discharge and damage. The alternative is hearing aids which is especially common in Down’s syndrome and Cleft palate. Otherwise grommet insertion can be considered if BC>AC by 25-30dB. Grommets allow drainage so there is increased discharge but less infections.
What are the causes for tympanic membrane perforation?
Tympanic membrane perforation commonly occurs following AOM. The child’s pain will suddenly improve alongside discharge. It can also occur as a complication of grommet insertion. Traumatic perforation (Barotrauma or cotton buds) usually occurs in the posterior tympanic membrane whereas AOM is anterior.
