Primary first aid is a priority in a patient who presents with epistaxis and this includes the ABCs of resuscitation .
Assess the pt for haemodynamic stability, including pulse and respiratory rate, and look for signs of shock, such as sweating and pallor.
If the patient is actively bleeding, sit them upright. Lean the patient forward to minimise swallowing of blood and apply digital pressure at the cartilaginous part of the nose for a minimum of 10 minutes.
Consider inserting a large-bore intravenous cannula if bleeding is severe and, if appropriate, take a blood sample (for full blood evaluation and blood group determination) and hold.
If the bleeding has not resolved then the nose should be examined with a nasal speculum, topical local anaesthetic, appropriate lighting and PPE.
Cauterisation is first line treatment of an anterior bleed. This can be done using silver nitrate or electrocautery.
Care must be taken during bilateral cautery to prevent septal perforation and treatment should only be administered to a small area surrounding the bleeding point.
if cauterisation is unsuccessful in controlling the bleed, or if no bleeding point is seen on examination, anterior or posterior nasal packs are available. The Rapid Rhino has an inflatable balloon coated in a compound that acts as a platelet aggregator and is the simplest and most effective for anterior bleeds.
If bleeding continues despite anterior nasal packing then a balloon catheter (e.g. Foley Catheter) is inserted into the nose into the posterior pharynx, inflated and retracted to sit in the nasopharyngeal space (this prevented bleeding into the airway) the anterior nose should then be packed.
If bleeding has not resolved then ENT referral is appropriate for surgical management. This can be done via arterial ligation or embolisation.
EXTRA
• 90% of bleeds arise anteriorly from Little’s area (Kiesselbach’s plexus)
o Kiesselbach’s plexus:
Anterior ethmoidal artery (septal branch)
Sphenopalatine artery (lateral nasal branch)
Superior labial artery (septal branch)
Greater palatine artery (septal branch)
• 10% of bleeds arise posteriorly from Woodruff’s plexus:
o Usually the lateral wall but rarely the nasal septum
o Woodruff’s plexus:
Sphenopalatine artery
Posterior nasal artery
Ascending pharyngeal artery
Aetiology:
• Local Causes:
o Trauma
Nose picking (most common)
Fractures to the nasal septum, middle 1/3 of the face, or base of skull
o Foreign body in the nose
o Dry Nose (Rhinitis sicca)
o Vascular Malformations (e.g. nasal haemangioma, HHT)
o Nasal septal defects
o Infections
o Tumours of the nasopharynx
o Medications/ drugs (topical corticosteroids, cocaine)
• Systemic Causes:
o Bleeding disorders (e.g. Anticoagulation/ antiplatelets, VWD, severe thrombocytopaenia, haemophilia)
o HTN
Hoarseness is an alteration in the voice usually due to a laryngeal disorder.
In the history of this pt it is important to establish:
Red flags to look out for include: - history of smoking - dysphagia - odynophagia (pain on swallowing) - otalgia (ear pain) - stridor - haemoptysis AND recent fevers, night sweats and unexplained weight loss
Oral examination reveals a unilateral, left sided tonsillar swelling with a diffuse, oedematous bulge superior and lateral to the tonsil. The uvula is deviated to the right.
Quinsy triad =
Explanation of symptoms:
• Sore throat and difficulty swallowing from the acute infection
• Difficulty opening his mouth (trismus) due to involvement of the motor branch of CN V leading for spasm of the muscles of mastication
• Ipsilateral ear pain due to referred pain
• The uvula is deviated to the contralateral side due to palsy of CN X on the right side
Another cause is if the Weber glands malfunction and cannot clear the build-up of debris from the area around the tonsils, the tubes that drain the glands may become swollen. This can cause an infection to develop, which gets worse and causes an abscess to form.
Oral examination reveals a unilateral, left sided tonsillar swelling with a diffuse, oedematous bulge superior and lateral to the tonsil. The uvula is deviated to the right.
What is the diagnosis?
What is the management?
It is important to conduct a primary survey when the pt first comes in and make sure there is no airway compromise. Anxious, ill-appearing patients with drooling and posturing must be monitored continuously in a setting where emergent artificial airway can be established if necessary.
ENT referral is required for surgical intervention. The abscess can be surgically managed through needle aspiration, incision and drainage, or tonsillectomy.
Empirical antibiotic therapy is essential and therapeutic guidelines recommend benzathine penicillin IV and phenoxymethyl penicillin oral.
Supportive care includes provision of adequate hydration, analgesia and monitoring for complications.
This occurs when bacteria invades tissue of the epiglottis and/ or surrounding supraglottic structures causing inflammation and oedema that causes narrowing and obstruction of the airway.
(CAUSES:
Traditionally Haemophilus Influenzae type b (Hib) – uncommon now due to immunisation
Most cases now involve: Strep pyogenes, Strep pneumoniae, Staph aureus, non-typable H influenzae)
Clinical Features: • Most common in the 1 – 4 year age group but can occur at any age • Acute on set of high fevers (>39C) • Toxic appearance • Sore throat • Tripod position • Drooling • Dysphagia • Muffled voice • Respiratory distress and stridor • Restlessness and/ or anxiety
(Due to major vessel bleeding from ruptured clot or failure of a suture.
May involve superior thyroid or inferior thyroid or associated veins )
-Call senior + transfer to OT
-Resuscitation (ABCDE):
o A –
If non-critical perform in OT, if critical perform at bedside
Remove superficial and deep sutures and evacuate haematoma
Keep pressure on wound without occluding trachea or carotids.
Attempt intubation
If all else fails, then cricothyroidotomy
o B –
Immediate high flow O2
o C –
Establish IV access
Control haemorrhage
IN THE OT
o The wound is reopened and inspected for location of bleed and haemostasis established
o Drain is placed to remove fluid collecting in bed of haematoma
Pt is then transferred to ICU for observation
o Airway – position patient forward, encourage spitting blood into bowl, suction as required
o Breathing – O2, OBS
o Circulation – IV access, bloods (FBC, coagulation studies, Group and Hold), IV fluids
If the bleed is severe then pt should proceed to OT for surgical management such as electrocautery.
Most likely head and neck examination findings can include:
o Change in voice
o Cervical lymphadenopathy
o Signs of airway obstruction – diminished breath sounds, stridor
o Weight loss or cachexia
o Parotid or thyroid masses
What are the relevant investigations that are related to this case?
Relevant investigations include: Pathology: -Thyroid function tests (TFTs). Looking for: o Decreased TSH o Increased free T4, free T3 - Thyroid autoantibodies (positive) o Thyroid peroxidase (TPO) antibody o TSH-receptor antibody - Other: o FBC (normochromic normocytic anaemia, mild leukopenia) o LFTs (elevated ALT and AST) o Hypercalcemia
Imaging:
- Radionuclide thyroid scan (Technetium-99m)
o Normal or elevated uptake
Homogenous: graves
Heterogenous: toxic multinodular goitre
o Decreased uptake: thyroiditis, exogenous thyroid hormone
- Thyroid U/S +/- FNA
o Indicated if suspicious nodules (i.e. macrocalcification, irregular border, increased vascularity)
- ECG (document any arrhythmias or other changes)
What is the likely diagnosis and what would you do from here?
The most likely diagnosis is acute otitis media.
Clinical features include:
Management would include:
EXTRA- PATHOGENESIS
• Under normal conditions the mucociliary action and ventilatory function of the Eustachian tube clear nasopharyngeal flora that enter the middle ear
• URT viruses can infect the nasal passages, Eustachian tube, and middle ear causing inflammation and impairing these processes
• A middle ear effusion develops and is contaminated with nasopharyngeal bacteria – producing a suppurative inflammatory response
• The pressure against the tympanic membrane leads to pain and the infection leads to fever
• This inflammatory process may also include mastoid air cells
• Pathogens:
o Bacteria: Strep pneumoniae, H. influenzae, Moraxella catarrhalis, Staph aureus, Strep pyogenes
o Virus: RCV, picornaviruses (rhinovirus, enterovirus etc.), coronaviruses, influenza, adenovirus, metapneumovirus
Clinical signs:
What is the most likely diagnosis?
How would you manage this boy?
Most Likely diagnosis Acute otitis media
Management:
• Adequate and regular analgesia is essential
• For most children presenting with acute otitis media initial antibiotics are not indicated
• However children with systemic symptoms should be treated with amoxycillin
• Urgent referral to ENT is required is a suppurative complication develops (e.g. mastoiditis) or facial palsy develops.
May just need appropriate Abx and corticosteroids.
Intracranial Cx include:
Obstructive:
Neoplastic:
Infective:
Inflammatory
- Sjogrens syndrome (AI)
skin:
I would keep in mind that In adults over 40, as many as 75% of lateral neck lumps are malignant – In the absence of signs of infection, a lateral neck mass in an adult is lymphadenopathy due to metastatic carcinoma (usually SCC) until proven otherwise.
I would take a detailed history on the lump.
Nearly all thyroid cancers originate from thyroid follicular cells and form distinct pathological entities; papillary, follicular and anaplastic. Papillary and follicular are well differentiated with low metastatic potential whereas anaplastic are poorly differentiated and behave aggresively.
Papillary carcinoma constitutes about 2/3 of thryoid cancers in adults and nearly all in children. Peak incidence is between 30-45 years old. The spread is lymphatic and frequently presents with nodal metastases but distal mets are rare. It has a really good prognosis with a 5year survival rate higher than 90%.
Follicular is the 2nd most common thyroid malignancy (10-20% of all thyroid neoplasms).
Typically occurs in those between 40-60 and affects women more (3F:1M). It generally spreads haematogenously to lungs and bones.
It is essentially impossible to distinguish from benign adenomatous hyperplasia on FNAC and histology. Has a prognostic 5 year survival rate of 50-70%.
Aaplastic
• Accounts for 1 – 2% of thyroid malignancies
• Typically occurs in the elderly (6th and 7th decades)
• Presents with a rapidly enlarging diffuse hard thyroid lump, often with symptoms of tracheal or recurrent laryngeal nerve involvement
• Histologically poorly differentiated
• Spread is both lymphatic and haematogenous to lymph nodes, bones brains and lungs
• Poor Prognosis – 5 year survival 5 – 14%
Other thyroid cancers are rarer and include medullary carcinoma and thyroid lymphoma.
Medullary carcinoma:
• Accounts for 5 – 10% of thyroid malignancies
• Occurs in both sporadic (80%) and familial forms
• It sporadic cases it typically peaks in the 3rd and 4th decades
• Presents as a stony hard thyroid lump with possible secondaries in cervical lymph nodes
• Arises from parafollicular C cells of the thyroid, rather than thyrocytes
• Histologically well differentiated tumour with sheets of cells in an amyloid stroma
Has a 5 year survival rate of 70%
Thyroid Lymphoma;
• Accounts for approximately 2.5% of thyroid malignancies
• Typically presents between 50 and 70 years of age
• 3F: 1M
• The aetiology is unclear but Hashimoto’s thyroiditis is a major risk factor
• Excellent prognosis for disease limited to the thyroid- 5 year survival is 85% but this falls to 40% if local spread has occured.
Medical treatment can be achieved via:
Medical treatment aims to decrease hormone synthesis and provide symptom control.