Pott’s Puffy Tumor in Teen Leads to Bilateral Blindness

Key TakeawaysPott’s puffy tumor (PPT) is a rare but life-threatening complication of sinusitis, characterized by frontal bone osteomyelitis with a subperiosteal abscess. Because intracranial and orbital extension can occur rapidly, early recognition and prompt multidisciplinary management are essential to reduce the risk for permanent neurologic and visual sequelae.The case reported a 17-year-old boy from Senegal with PPT who developed severe intracranial and orbital complications despite empirical antibiotic therapy. Although prolonged antimicrobial treatment and multiple surgical interventions controlled the infection, the patient sustained irreversible bilateral blindness, secondary to optic atrophy.PPT should be suspected in adolescents presenting with persistent frontal swelling because delayed diagnosis may result in severe intracranial complications and permanent vision loss.The Patient and His Medical HistoryThe patient was referred after a 10-day history of febrile headache and progressive right frontal and periorbital swelling. Empirical treatment with ceftriaxone, gentamicin, and metronidazole initiated previously failed to control the infection, allowing progression to facial cellulitis and necessitating referral for further evaluation and management.Findings and DiagnosisOn admission, the patient had marked right frontal swelling, periorbital cellulitis, meningeal irritation signs, and a Glasgow Coma Scale score of 11/15 because severe periorbital edema prevented eye opening rather than reflecting impaired consciousness.CT showed frontal cerebral empyema, frontal bone osteomyelitis with subperiosteal abscess, orbital cellulitis, pansinusitis, lateral venous sinus thrombosis extending into the right internal jugular vein, multiple septic pulmonary emboli, and pericardial effusion.Laboratory studies showed leukocytosis (16,400/μL), an elevated C-reactive protein (CRP) level of 107 mg/L, and a procalcitonin level of 5.1 μg/L. Cerebrospinal fluid obtained by lumbar puncture revealed neutrophilic pleocytosis with gram-positive cocci. Drainage of the frontal collection yielded purulent material containing gram-positive cocci and bacilli, and multiplex polymerase chain reaction identified Haemophilus influenzae.Because the fever and infection persisted despite antimicrobial therapy with meropenem, vancomycin, metronidazole, and fluconazole, the patient underwent endoscopic frontal sinus exclusion and bilateral ethmoidectomy. After palpebral edema improved with anti-edema treatment, examination revealed purulent chemosis and complete loss of light perception in both eyes. These findings were consistent with preexisting optic nerve involvement that could not be treated in a timely manner.On hospital day 10, the patient developed seizures accompanied by an increase in inflammatory markers, including a CRP level of 160 mg/L. MRI showed persistent cerebral empyema and ongoing venous sinus thrombosis, prompting neurosurgical drainage and debridement of frontal bone osteomyelitis. Intraoperative cultures subsequently grew Pseudomonas and Neisseria species.After 3 weeks of intravenous antimicrobial therapy, the patient became afebrile and clinically stable and was transitioned to oral fluoroquinolone therapy and amoxicillin-clavulanate, with continued clinical and laboratory monitoring.Follow-up MR venography performed 1 month later showed regression of the empyema and recanalization of the affected venous sinuses. Ophthalmologic examination confirmed bilateral optic atrophy.After 3 months, antimicrobial and anticoagulation therapy was discontinued, whereas antiepileptic therapy was continued. The patient remained blind and was scheduled for delayed cranioplasty.DiscussionFirst described by Sir Percivall Pott in the 18th century, PPT predominantly affects adolescents because of incomplete pneumatization of the frontal sinus and the presence of a highly developed diploic venous network.The condition occurs approximately three times more often in men. Additional risk factors include cocaine use, dental infections, and neurosurgical procedures. Infection spreads through septic thrombophlebitis of the valveless diploic veins via the emissary veins into the dural venous sinuses or by direct extension after open trauma.The microorganisms most commonly isolated are similar to those associated with community-acquired sinusitis and include staphylococci, streptococcal species, Haemophilus influenzae, Klebsiella species, enterococci, and oral anaerobes. Interpretation of culture results may be challenging because some organisms represent normal skin flora, and prior antibiotic therapy may result in negative cultures.Patients typically present with frontal and periorbital swelling, headache, fever, purulent rhinorrhea, and signs of meningitis. Neurologic deficits may indicate intracranial extension, which occurs in approximately 85% of cases. Reported complications included epidural abscesses (47%), subdural empyemas (25%), intracranial abscesses (12%), cavernous sinus thrombosis, and meningitis. Ocular involvement is common, but is usually reversible, and surgery is required in only approximately 5% of cases. Bilateral blindness has only been reported twice.The cavernous sinus is a major venous plexus within the middle cranial fossa that drains the orbit, face, and anterior skull base and lies in close proximity to cranial nerves III, IV, V1, V2, and VI, as well as the internal carotid artery. Visual loss associated with cavernous sinus thrombosis may result from central retinal or ophthalmic vein occlusion, carotid artery involvement, or toxic or ischemic optic neuropathy.In this patient, the combination of elevated intraorbital pressure caused by purulent chemosis, thrombosis of the cavernous and lateral venous sinuses, and possible intracranial hypertension secondary to frontal empyema most likely resulted in irreversible bilateral compressive-ischemic optic nerve injury.Diagnosis relies primarily on contrast-enhanced CT of the brain and paranasal sinuses, whereas MRI is useful when intracranial complications are suspected. Despite advances in imaging, PPT is frequently diagnosed late, increasing the risk for severe and potentially life-threatening complications.Management requires a multidisciplinary approach combining prompt surgical drainage with debridement of necrotic bone and prolonged broad-spectrum antimicrobial therapy, typically for 6-12 weeks, using agents with adequate bone penetration. Although PPT is generally considered to be a surgical emergency, some patients may be managed conservatively.This story was translated from Univadis Germany, part of the Medscape Professional Network.