Mastoiditis and otogenic complications — branching viva

Opening question

Examiner: Take me through this child. What is the diagnosis, and what is your frame for managing it? [4]

Candidate: The diagnosis is acute mastoiditis. The fever, irritability, postauricular erythema, swelling and tenderness, the lost postauricular crease, and the pinna pushed downward and outward, in a child with a bulging erythematous tympanic membrane after an upper-respiratory infection, are the hallmark postauricular signs. My frame is to recognise this as a suppurative complication of acute otitis media that threatens hearing, the facial nerve and the brain: admit, take blood cultures, start broad-spectrum intravenous antibiotics, refer urgently to ear-nose-and-throat surgery, perform a myringotomy for the intact drum, and reassess at 48 hours. [4] [5]

Examiner: How do you distinguish mastoiditis from uncomplicated acute otitis media? [4]

Candidate: The mastoid air cells are continuous with the middle ear through the aditus ad antrum, so they are inflamed to some degree in most acute otitis media — that is why simple AOM can cause mastoid tenderness. The line is the postauricular change: oedema and erythema behind the ear, a lost postauricular crease, and a pinna pushed downward and outward. Those signs mean the mastoid is obstructed and suppurating, and they are the trigger for admission and intravenous antibiotics. A child with otalgia and fever but a normal postauricular region and pinna position has acute otitis media. [4] [8]

Branch 1 — classification and pathophysiology

Examiner: Walk me through how acute otitis media becomes coalescent mastoiditis. [5]

Candidate: The progression runs from mucosal inflammation through an air-cell empyema to coalescence. Middle-ear pus reaches the mastoid through the aditus ad antrum. When mucosal swelling occludes the aditus, pus is trapped, pressure rises, and the inflamed mucosa becomes an empyema. The raised pressure and inflammatory osteitis then dissolve the thin bony trabeculae that separate the air cells — coalescence — which weakens the cortical plates and creates the routes of escape for pus. Coalescence on imaging is the point at which medical disease becomes surgical disease. [5] [9]

Examiner: What are the routes by which infection escapes the mastoid? [1]

Candidate: There are several. Erosion of the lateral cortical plate produces a subperiosteal abscess behind the ear, the commonest surgical presentation. Erosion of the mastoid tip lets pus track into the neck as a Bezold abscess. Erosion of the tegmen tympani reaches the middle cranial fossa as an extradural collection or a temporal-lobe abscess. Erosion of the sigmoid plate inoculates the lateral venous sinus, causing septic thrombus and otitic hydrocephalus. And spread through the inner-ear windows or preformed pathways causes suppurative labyrinthitis and meningitis, while tracking along the petrous apex causes petrous apicitis. The valveless venous channels also allow thrombophlebitic spread without a cortical defect. [1] [11]

Branch 2 — investigations and imaging

Examiner: What investigations will you do, and when will you image? [9]

Candidate: I would take a full blood count, C-reactive protein and blood cultures before antibiotics as a baseline against the 48-hour response, and I would always send ear discharge or middle-ear fluid from a myringotomy for Gram stain, culture and susceptibility. For imaging, contrast-enhanced CT of the temporal bone and brain is the key investigation, and I would obtain it for a suspected subperiosteal or Bezold abscess, lateral sinus thrombosis, intracranial extension, failure to improve or deterioration at 48 hours, and any neurological sign. The coalescent pattern — destruction of the trabeculae with cortical erosion — is the hallmark of surgical disease. I would reserve MRI with venography for suspected lateral sinus thrombosis, otitic hydrocephalus, brain abscess or subdural empyema. [9] [4]

Examiner: What organisms are you covering? [5]

Candidate: The dominant organisms in acute mastoiditis are Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus and non-typeable Haemophilus influenzae. When the source is chronic suppurative otitis media or cholesteatoma, Pseudomonas aeruginosa and anaerobes dominate and demand a Pseudomonas-directed regimen such as ceftazidime. I would send pus from any drained abscess for Gram stain, culture and susceptibility, and de-escalate when the results return. [5] [8]

Branch 3 — treatment and the surgical decision

Examiner: What is your intravenous antibiotic regimen, and what about the drum? [8]

Candidate: I would give intravenous ceftriaxone 50 mg per kilogram (maximum 2 g) once daily plus flucloxacillin 50 mg per kilogram (maximum 2 g) every six hours, covering the streptococci and staphylococci. Because the tympanic membrane is intact, I would perform a myringotomy to relieve the pressure and sample the organism. I would add metronidazole 7.5 mg per kilogram (maximum 500 mg) every eight hours for an intracranial collection or anaerobic concern, vancomycin if MRSA is suspected, and switch to a Pseudomonas-directed agent if chronic disease is the source. [8] [4]

Examiner: The CT shows a small postauricular subperiosteal abscess but the child has improved. When do you operate, and can you avoid surgery? [5]

Candidate: A cortical mastoidectomy with drainage is the standard for a subperiosteal abscess in most units. However, in a carefully selected young child with a small abscess and no intracranial feature, immediate needle aspiration combined with intravenous antibiotics and close observation is a validated alternative, with a low threshold to convert to surgery if there is no prompt improvement. The absolute indications for cortical mastoidectomy are failure to improve after 48 hours of intravenous antibiotics, a large or non-resolving abscess, a Bezold abscess, lateral sinus thrombosis, Gradenigo syndrome, a facial palsy, suspected cholesteatoma, and any intracranial extension. [8] [9]

Branch 4 — complications and a sick child

Examiner: What are the complications of mastoiditis? [1]

Candidate: The intratemporal complications are a subperiosteal and Bezold abscess, petrous apicitis with the Gradenigo triad of discharging ear, retro-orbital pain and a sixth-nerve palsy, facial nerve palsy, suppurative labyrinthitis with permanent sensorineural hearing loss, and lateral sinus thrombosis. The intracranial complications are meningitis, which is the commonest, extradural and subdural empyema, brain abscess, and otitic hydrocephalus from impaired venous outflow. The intracranial complications carry the highest mortality. The defence against each is prompt recognition, early intravenous antibiotics, timely imaging and surgical source control. [1] [2]

Examiner: What if the child develops spiking fevers and papilloedema? [11]

Candidate: That picture suggests lateral sinus thrombosis with otitic hydrocephalus. I would admit to intensive care, give prolonged broad-spectrum intravenous antibiotics, obtain MRI with venography to confirm the thrombus, and proceed to a cortical mastoidectomy with evacuation of the infected clot for source control. I would involve neurosurgery and haematology, and anticoagulation would be individualised. The raised intracranial pressure threatens vision, so I would monitor it closely and treat it with the surgery and the medical measures, reserving sinus decompression or thrombectomy for selected cases. [11] [8]

Wrap

Examiner: Summarise the mastoiditis stance in one sentence. [4]

Candidate: A febrile child with postauricular erythema, swelling and tenderness and a pinna pushed downward and outward has acute mastoiditis and needs admission, intravenous ceftriaxone plus flucloxacillin, a myringotomy for the intact drum, ENT review, contrast temporal-bone CT for any complication, and a cortical mastoidectomy for the abscess, lateral sinus thrombosis or intracranial spread that fails or threatens, because the one child you treat late is the one who loses hearing or dies of a brain abscess. [4] [8]