Michał Michalik, *Adrianna Podbielska-Kubera
Faciocranial complications of sinusitis
Powikłania twarzoczaszkowe zapalenia zatok
Department of Otolaryngology, MML Medical Centre, Warsaw, Poland
Head of Department: Michał Michalik, MD, PhD
Zapalenie zatok to jedno z częściej występujących schorzeń. Jego etiologia nie jest do końca poznana, najczęściej dominują czynniki wirusowe i bakteryjne. Do głównych objawów należą: przekrwienie błony śluzowej nosa, obfita wydzielina z nosa, a także osłabienie węchu. Źródłem powikłań może być zapalenie w obrębie każdej zatoki. Powikłania rozwijają się najczęściej w wyniku zaostrzenia przewlekłego zapalenia zatok.
Zapalenie zatok może skutkować rozprzestrzenieniem się zapalenia do wnętrza czaszki lub w rejon oczodołów, zapaleniem kości i szpiku lub zakrzepicą zatoki strzałkowej górnej. Ze względu na anatomiczne położenie i bliskość istotnych struktur, zapalenie zatok klinowych może prowadzić do zapalenia opon mózgowych lub ropniaków podtwardówkowych, ropni płata skroniowego i zakrzepicy zatoki jamistej.
Grzybicze zapalenie zatok jest niezwykle niebezpieczne, bowiem charakteryzuje się szybko postępującym przebiegiem, często powikłanym rozsiewem wewnątrzczaszkowym i oczodołowym. Inwazyjne grzybicze zapalenie zatok przynosowych z powikłaniami oczodołowymi to stan zagrażający życiu. W przypadku obawy przed powikłaniem zapalenia zatok w obręb oczodołu lub wewnątrzczaszkowego oraz w przypadkach braku poprawy po zastosowaniu początkowej terapii empirycznej niezbędne jest wykonanie badań obrazowych, w tym tomografii komputerowej i rezonansu magnetycznego.
Wczesne diagnozowanie zapalenia zatok i multidyscyplinarne leczenie stanowiące połączenie antybiotykoterapii i leczenia operacyjnego, w tym neurochirurgii i zabiegów szczękowo-twarzowych, mogą skutecznie zapobiegać powikłaniom i znacznie zmniejszać zachorowalność i śmiertelność.
Sinusitis is one of the most common conditions. The aetiology of sinusitis has not been fully discovered; however, viruses and bacteria are usually the dominant causes. The chief symptoms include nasal congestion, profuse nasal discharge and a compromised sense of smell. Inflammation of any sinus can be the source of complications. Complications develop usually as a result of exacerbation of chronic sinusitis.
Sinusitis may result in inflammation spreading inside the cranium and to the orbital area and in the development of osteomyelitis or superior sagittal sinus thrombosis. Due to the anatomical location and proximity of important structures, sphenoid sinusitis may lead to meningitis or subdural empyemas, temporal lobe abscesses and cavernous sinus thrombosis.
Fungal sinusitis is very dangerous since it is characterised by a rapid course often complicated by intracranial and orbital spread. Invasive fungal paranasal sinusitis with orbital complications is a life-threatening emergency. If there is concern about possible orbital or intracranial complications of sinusitis or if there is no improvement after initial empirical therapy, the use of diagnostic imaging is necessary, including computed tomography and magnetic resonance imaging.
Early diagnosis of sinusitis and multidisciplinary management involving a combination of antibiotic therapy and surgical treatment, including neurosurgery and maxillofacial procedures can be effective in the prevention of complications and may significantly reduce morbidity and mortality.
Sinuses are air cavities located in the facial cranium and near the nasal cavity and closely connected with it. Sinuses are lined with epithelium with cilia (1). Not all sinuses are present at birth. Ethmoid and maxillary sinuses are present and clinically significant already at birth. Sphenoid sinuses appear at three to seven years of age. Frontal sinuses are present only in 12% of newborns and develop at puberty (2).
Sinusitis is one of the most important and common diseases (3). It affects 20% of the population at different stages of life (4). Depending on the duration of the disease process sinusitis is divided into acute (lasting less than 12 weeks) and chronic (lasting over 12 weeks) (3). Sinusitis, particularly chronic sinusitis, significantly compromises the patient’s quality of life and generates high socioeconomic costs (5).
The aetiology of sinusitis is still being researched. The most common causes include nasal polyps, facial trauma, nasal septum deviation, respiratory infections, allergies and hay fever (6, 7). Periodontal disease may also be the source of inflammation (1).
Under physiological conditions, sinuses are sterile; however, they may be temporarily colonised by upper respiratory tract flora. Inflammation is most common in the maxillary sinuses. This is where odontogenic infections predominate as a result of close proximity of the teeth and sinuses (9). Bone structures constitute a barrier against the spread of infection to areas adjacent to the sinuses. However, complications develop in the event of bone damage, congenital or acquired bone abnormalities or haematogenous infection spread (2).
The majority of cases of sinusitis are secondary to upper respiratory and allergic infections. Bacterial sinusitis develops as a result of excessive bacterial growth in a closed sinus cavity. Inflammatory oedema creates an ideal environment for bacterial colonisation and growth since it hampers air exchange in narrow spaces. In addition, the activity of the mucociliary system becomes reduced, which compromises the natural protective barrier of the host and leads to discharge stasis (3).
The diagnosis of sinusitis is based on subjective symptoms, duration of symptoms and objective signs of inflammation (6). Nasal congestion, profuse nasal discharge and a compromised sense of smell are observed. The majority of sinusitis cases are viral infections, with no need for antibiotic therapy (7). However, the differentiation between a viral and bacterial infection is difficult: symptoms are similar and doctors prescribe antibiotic therapy. Sinusitis can also be caused by bacterial factors: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, coagulase-negative staphylococci and Gram-negative bacteria: Pseudomonas aeruginosa, Proteus spp., Klebsiella spp., Enterobacter spp., Escherichia coli and anaerobic bacteria (Peptostreptococcus spp., Prevotella spp., Porphyromonas spp., Bacteroides spp.) (7). Anaerobic bacteria, which are characteristic for acute disease, are usually associated with dental infection. Fungi from the families Mucoraceae and Trichocomaenae (3) may be responsible for sinusitis in patients with a compromised immune system.
The head and neck contain a number of spaces which may become infected leading to life-threatening complications, including respiratory obstruction and neurological complications and to the spread of infection. Many of the early signs are subtle and may go unnoticed by the doctor (8). Local, orbital and intracranial complications may occur as a result of sinusitis (3).
Sinusitis complication risk factors
Bacterial infections of the central nervous system require quick diagnosis and immediate treatment. The most common bacterial infections observed at intensive care units include acute bacterial meningitis, subdural empyema, intracerebral abscess and encephalitis. Infections may be acquired outside of hospital or in hospital, for example after a neurosurgical procedure or they may be associated with cerebrospinal fluid drainage. Cerebral abscesses are often the result of chronic or metastatic infection foci such as otitis, sinusitis, pneumonia or endocarditis. The development of infection may result in serious systemic and neurological complications leading to high mortality or serious disability (9).
Sinusitis is common in patients at intensive care units and is usually secondary to nasotracheal or nasogastric intubation. Sinusitis in intubated patients may manifest exclusively as unexplained fever. Proptosis and orbital pain may suggest the presence of orbital complications (8).
Inflammation of any sinus can be the source of complications. Complications occur usually as a result of exacerbation of chronic sinusitis. However, they can also develop in acute viral and bacterial sinusitis, as a result of traumatic bone loss, endoscopic nasal and sinus surgery or incorrectly performed procedures using an external approach (3).
In the era of antibiotics purulent sinusitis is rare, but it does occur. Frontal sinusitis may result in inflammation spreading inside the cranium and to the orbital area, osteomyelitis or superior sagittal sinus thrombosis. Maxillary sinusitis may result in bone inflammation and destruction; intracranial spread is rare, except for nasal and cerebral mucormycosis. Due to the anatomical location and proximity of important structures, sphenoid sinusitis sometimes leads to meningitis or subdural empyemas, temporal lobe abscesses and cavernous sinus thrombosis (8).
Approximately 0.5-2% of viral upper respiratory infections are associated with secondary acute bacterial sinusitis and may rarely transform into more serious complications such as meningitis and intracranial abscess. The symptoms are often non-specific and include fever, headache, head skin tenderness, nausea and emotional disturbances (9).
The most common bacterial complications of acute sinusitis are orbital cellulitis and abscesses. Infections are most commonly caused by the bacteria S. pneumoniae, Streptococcus pyogenes and S. aureus and anaerobic bacteria; H. influenzae strains are less common (10). Widespread use of vaccines against H. influenzae and S. pneumoniae has lead to a decrease in the prevalence of sinusitis associated with these bacteria. However, infections associated with the presence of Streptococcus (e.g. S. anginosus) and Staphylococcus (e.g. S. aureus) are more commonly observed (11). Since infections of the oral cavity, head and neck, and abdomen with an initial S. anginosus aetiology are often multibacterial, it is assumed that orbital complications of sinusitis that includes S. anginosus may also be multibacterial (12).
A review of literature regarding the occurrence of sinusitis complications from the beginning of the previous century until now shows that intracranial complications of sinusitis are currently observed approximately four times less commonly than in previous years. However, the rate of certain complications, orbital for example, has not changed significantly. With the introduction of new-generation antibiotics, development of diagnostic techniques, improvement of surgical techniques and the use of neuronavigation, the rate of complications caused by intracranial infections has decreased. This change is also due to an increased awareness of patients of the need for sinusitis treatment. Permanent abnormalities such as epileptic seizures, paralysis, compromised mental abilities etc. are observed in approximately 30% of patients with intracranial complications of sinusitis (3).
Acute sinusitis is very common in the paediatric population. Secondary bacterial paranasal sinusitis occurs in 6-9% of all cases of viral upper respiratory infections in children. The majority of infections are uncomplicated and some of them can be treated without antibiotics. Sometimes acute sinusitis may be associated with serious orbital and intracranial complications (13). It is estimated that in 5% of paediatric patients with acute sinusitis infection may spread beyond the sinuses directly or via the bloodstream (12).
Ethmoid sinusitis may lead to orbital complications, which are more common in younger children since ethmoid sinuses are already developed at birth. Intracranial complications are more commonly observed in older children and are secondary to frontal sinusitis (2). Children with acute bacterial sinusitis complications have an increased risk of morbidity and mortality. In addition, children from families with a lower socioeconomic status do not always enjoy a full access to primary healthcare, including vaccinations; they are also diagnosed at later stages of disease, which is associated with longer hospital stay and increased mortality (2).
Complications of paranasal sinusitis involving the orbits and the inside of the cranium occur relatively rarely, but are a serious threat to the health and life of the patient (14). The prevalence of intracranial complications is 3 to 10% (3). Clayman et al. (15) recorded a 3.7% prevalence of intracranial complications of paranasal sinusitis in children. A more recent study suggests that the prevalence of orbital and intracranial complications of sinusitis may be as high as the sinusitis patient hospitalisation rate (3-5%) (13). The proximity of the orbits and the brain makes it possible for the infection to spread in a direct manner. Quick diagnosis of the initial stages of complications and starting appropriate treatment in a short period of time remain the most important issues. This is particularly difficult in intracranial complications, since their symptoms may be non-specific at the early stages, but they do develop rapidly and may lead to serious consequences, including strong extraocular pain, high fever, meningitis, ophthalmoplegia and blindness (14). The spread of sinusitis into the orbital area usually occurs according to the pattern described by Chandler et al. in 1970 and involves the following conditions one by one: preseptal cellulitis, orbital cellulitis, subperiosteal abscess, orbital abscess and cavernous sinus thrombosis. Orbital complications represent a risk of vision loss (12).
If such symptoms as headaches, fever, neurological manifestations, seizure activity and impaired consciousness with a rapid progress occur, various possible causes should be considered and differential diagnosis should be made between viral meningitis and encephalitis, different forms of bacterial meningitis, cerebral vessel thrombosis, encephalitis and abscesses of non-cerebral origin, e.g. otogenic abscesses. Sinusitis-related bacterial meningitis is usually associated with loss of consciousness, epileptic seizures and increased intraocular pressure. If no fever is observed, differential diagnosis should mainly include primary and metastatic brain tumours, stroke and subdural haematomas (3).
In the area where the bone wall tightly adheres to the dura, extradural abscesses are observed between the internal surface of the posterior bone wall of the frontal sinus and the dura. Infection may be transferred to the dura with the development of an epidural and/or subdural empyema (3).
Subdural empyemas are characterised by a severe clinical course, which may be due to the fact that the subdural space does not contain any barriers which could stop the spread of infection. Streptococci, staphylococci and anaerobic bacteria are the most common pathogens associated with intracranial complications of sinusitis (3). Subdural empyemas are observed much more often in young men. This may be due to anatomical differences in paranasal sinuses and the frontal bone. A subdural empyema is a collection of pus which occurs usually as a result of sinusitis; it may also spread from an extradural empyema. The subdural space is large and includes few barriers that could stop the spread of infection. Cooperation between doctors from different fields, e.g. a neurologist and a neurosurgeon is very important since some complications produce non-specific symptoms. Nuchal rigidity may be an atypical sign of a peripheral empyema and brain abscesses suggesting the possible development of a subdural empyema (3).
Brain abscesses are focal infections in the brain tissue. In patients with normal immunity, a tight blood-brain barrier and good vascularisation of meninges make the brain tissue relatively highly resistant to infection. However, in bacterial invasion, brain tissue inflammation (encephalitis) develops at the first stage and, at the last stage, a closed abscess forms. Patients complain of various symptoms which evolve as the disease progresses; the symptoms usually last from a few days to a few weeks and include headache, fever, neurological manifestations, epileptic seizures, personality changes, orientation disorders, dementia and drowsiness. In the case of brain abscesses located deeper in the frontal and parietal lobes, hemiparesis on the contralateral side is observed (3).
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