11 Infection and oral and maxillofacial surgery: implications for anaesthesia

This chapter looks at the anaesthetic management of patients presenting with orofacial infection. It will examine the pathophysiology of oral and dental infection and the associated local and systemic effects. This includes a discussion on the recognition and management of sepsis syndrome and the postoperative care of these patients in a critical care environment. In addition, the anaesthetic implications of patients with transmissible bloodborne infections presenting for maxillofacial surgery will be considered.

Infection of the oral cavity, including dental caries, dental abscess, and gingivitis, is one of the commonest diseases in the world. Management of these conditions rarely involves the anaesthetist. Standard management includes improved oral hygiene, antibiotics, and drainage under local anaesthesia. However, when this fails, or when serious local or systemic infection develops, then the anaesthetist will become involved. Infection in the head and neck requiring surgical intervention represents a major part of the emergency workload in maxillofacial surgery units.

Dental caries are caused by the action of acid-producing bacteria on the dental enamel, causing it to dissolve. Once through the enamel the infection passes through the dentine and into the pulp, causing pulpitis. Infection can then track through the pulp to the root apex and into the alveolar bone of the mandible or maxilla, leading to the formation of a periapical abscess. In a recent study of odontogenic infection¹, the clinical focus of infection was found to be the maxillary dentition in 30% of cases and the mandibular dentition in 70% of cases. Having reached the medullary bone, the infection may then erode through the cortical plate and into the surrounding tissues. From this point the infection may either resolve, become localized, forming an abscess, or may spread. Spreading infection will follow the line of least resistance through the fascial planes and into adjoining structures. The direction of spread is to some extent predictable based upon knowledge of the anatomy. Pus arising from the root apices of the lower teeth, perforating the lingual surface of the mandible, may drain intraorally if the apices of the teeth lie above the bony attachment of the mylohyoid muscle (incisors, canines, and premolars), or extraorally if they lie below it (second and third molars), draining through the skin or spreading through the superficial submandibular tissues. Infection arising in the mandibular molars may spread posteriorly into the lateral pharyngeal space. From here infection may spread to regions where the consequences of local infection can be very serious. Infection spreading upwards to the base of the skull may spread intracranially, potentially resulting in cavernous sinus thrombosis. Infection spreading downwards may cause glottic inflammation and airway obstruction, or may spread into the thorax resulting in mediastinitis. Infection arising in the root apices of the maxillary teeth may spread into the maxillary sinuses, the infraorbital soft tissues, or via the venous circulation into the cranium, again risking cavernous sinus thrombosis.

Necrotizing ulcerative gingivitis, also known as Vincent’s angina or trench mouth, is a polymicrobial infection of the gums leading to inflammation and necrosis of gum tissue. It is caused by an overgrowth of normal oral bacteria as a consequence of poor oral hygiene combined with other factors such as poor diet and smoking. Management involves improved oral hygiene and antibiotics. Left untreated, the infection can spread, leading to complications such as osteomyelitis.

Dental caries are thought to be caused most commonly by serotypes of Streptococcus mutans (cricetus, rattus, ferus, sobrinus), although Lactobacilli also contribute to enamel decay by production of acid. Spreading odontogenic infection is usually polymicrobial and is caused by those organisms present as part of the normal oral flora (Table 11.1). Any combination of these organisms may be isolated in more severe odontogenic infection, although approximately 75% of isolates tend to be anaerobes (Bacteroides, Fusobacterium, Actinomyces).

Patients with an uncomplicated dental abscess who are otherwise well do not usually require antibiotics. However, the spectrum of patients presenting to the anaesthetist will have more severe local or spreading infection, which justifies early and effective antimicrobial therapy. Since a significant proportion of the isolates may be resistant to penicillin, then an intravenous cephalosporin such as cefuroxime, combined with metronidazole, would be a reasonable choice. The use of cephalosporins in patients with a history of penicillin allergy is controversial² and, if it is felt necessary to use an alternative, then clindamycin would be an appropriate choice.

Dental caries is the most common chronic disease in the world. Improved public understanding of the need for good dental hygiene, combined with the widespread addition of fluoride to drinking water, led to a 39% reduction in dental caries in the UK between 1970 and 1980. With appropriate dental treatment carious teeth should not progress to the formation of dental abscess. Nevertheless, the lifetime prevalence of dental abscess has been estimated at anywhere between 5% and 46%. There is some evidence that the incidence of severe odontogenic infection requiring hospital admission may have increased in the UK in recent years³. Analysis of hospital episode statistics showed that the number of admissions in the UK for drainage of dental abscess almost doubled between 1998 and 2006. The average age of these patients was 32 years. It has been suggested that this increase may be a consequence of a reduction in access to routine dental care in the UK during this time period. A major risk factor for carious dental disease and odontogenic infection is lower socioeconomic status. Many of the patients presenting for surgery with odontogenic infection, although relatively young, will have a higher than average prevalence of other significant comorbidities, including obesity, smoking, drug and alcohol misuse, and poor nutritional status.

Undrained dental abscesses may eventually resolve, leaving a fluid-filled cyst within the bone. These can lead to recurrent infection, and patients may present for surgical excision of the cyst. Alternatively, dental abscesses may progress to cause an osteomyelitis in the surrounding bone. This can be very painful and can cause significant bony destruction and deformity, requiring surgical excision and reconstruction. Where the mandible is involved, mouth opening can be significantly compromised. These patients are at risk of haematogenous spread of infection to distant sites and may develop systemic sepsis.

Infection arising in the root apices of the maxillary teeth may spread into the maxillary sinuses or the infraorbital soft tissues. Maxillary sinusitis can cause fever, pain, and tenderness, and may require treatment with antibiotics.

Ludwig’s angina is a potentially life-threatening condition characterized by a rapidly spreading cellulitis of the tissues of the floor of the mouth. The term angina is derived from the Greek word meaning ‘strangling’, and the eponym relates to the German physician who first described the condition in 1836. The infection is odontogenic in 90% of cases and most commonly arises from the lower third molars. Other causes include trauma to the floor of the mouth, recent tooth extraction, pericoronitis (infection of the gums surrounding partially erupted lower third molars), peritonsillar abscess, and postprocedural infection after piercing of the frenulum. Impaired immunity is a major risk factor, but the condition can arise in otherwise healthy individuals. The commonest organisms involved are the Actinomyces species, although other oral pathogens are frequently involved. The patients may be severely septic, with pain and tenderness around the submandibular region. The infection can lead to boardlike swelling of the submandibular tissues and elevation of the tongue, leading to drooling, dysphonia, and ultimately to airway obstruction. The airway will not reliably improve with induction of anaesthesia, and awake fibreoptic intubation is frequently required, either for surgery or airway protection.

Periapical abscesses affecting the maxillary incisor and canine teeth can lead to spread of infection via the facial veins into the cranium. This can lead to septic thrombosis in the veins of the cavernous sinus behind the eye and at the base of the brain. It is estimated that 10% of cases of cavernous sinus thrombosis begin as a dental infection, the remainder being the result of sinusitis or superficial infection in the midface. Patients may present with headache, fever, periorbital oedema, exophthalmos, and chemosis. Staphylococcus aureus is the commonest organism, although when dental infection is the cause then other organisms are likely to be implicated. Treatment is with high dose, broad spectrum intravenous antibiotics and systemic anticoagulation. Surgical treatment of the underlying source of infection, such as dental abscess, is also required. Mortality is high at around 20% even with optimal treatment.

The fascial planes of the neck are contiguous with those of the mediastinum. In consequence, downward spread of infection arising from the head and neck into the mediastinum can occur very readily. The initial infection is frequently odontogenic and is therefore likely to be polymicrobial with a preponderance of anaerobes. The descending infection is often associated with multiple abscesses and gas formation within the tissues of the neck and mediastinum. These patients can become very unwell and may develop severe sepsis and multiorgan failure (see below).

Symptoms of retrosternal or pleuritic chest pain in the presence of neck infection may suggest mediastinal spread. Chest radiograph may show pleural collections or basal consolidation but CT scan of the neck and chest should be performed early if there is clinical suspicion. This will demonstrate soft tissue swelling within the neck, particularly in the retropharyngeal and supraglottic regions, and the presence of any gas within the tissues. Fluid collections and abscesses within the mediastinum or pleural space will be identified. Corsten et al.⁴, in a case series and literature review of mediastinitis caused by descending neck infection, described a mortality rate of 31% in a group of patients with an average age of 38 years. Patients who underwent early thoracic surgery for drainage of the mediastinal collections, in addition to drainage of neck collections and intravenous antibiotics, had a significantly better outcome than those in whom mediastinal drainage was delayed or did not happen. This underlines the importance of early CT imaging of the chest in these patients.

Spreading odontogenic infection can lead to compromise of the airway by a variety of mechanisms. Patients with abscesses of the lower second or third molars may develop airway problems as a consequence of infection spreading posteriorly and inferiorly into the retropharyngeal and supraglottic tissues. Infection may also spread into the masseter muscles leading to trismus. Osteomyelitis of the mandible may lead to bone destruction and limitation of mouth opening which, whilst not compromising the airway, may make management of the airway more difficult. In Ludwig’s angina, the hardening and swelling of the tissues of the floor of the mouth and the elevation of the tongue, combined with impaired swallowing, can predispose the patient at risk of either airway obstruction or aspiration. In these patients conventional intubation is likely to be impossible, and airway management is challenging (see below). Patients with septic shock may have obtunded reflexes to the extent that they require airway protection.

The systemic inflammatory response syndrome (SIRS) is a clinical state which arises as a result of the pathophysiological response to an insult such as infection, trauma, burns, or pancreatitis. The SIRS criteria have been agreed by international consensus⁵, and SIRS is said to be present when at least two of the four SIRS criteria have been met (Table 11.2). Sepsis is defined as SIRS in the presence of suspected or documented infection. Septic shock is present when hypotension refractory to fluid resuscitation leads to evidence of inadequate organ perfusion, such as altered mental state, oliguria, and lactic acidosis. The exact process involved in this chain of events is complex and is still not fully understood. The loss of homeostasis within the vascular endothelium plays a critical role in the development of a pathologically vasodilated state, with increased capillary permeability and loss of fluid from the circulation. The role of the endothelium in the regulation of the clotting cascade is also disturbed, leading to coagulopathy and microvascular thrombosis. These processes frequently result in a patient who is shocked as a consequence of both vasodilatation and hypovolaemia. The basic principles of management in this situation are as follows:

Odontogenic infection can frequently lead to the development of sepsis. Handley et al.¹ found that amongst patients presenting to a regional maxillofacial unit with odontogenic infection, 61% met the criteria for sepsis. Patients with septic shock from odontogenic infection can present a major challenge to the anaesthetist, requiring emergency surgery in the context of unstable physiology and a difficult airway. The perioperative management of these patients is discussed below.

Many patients with dental abscess can be managed in the community with surgical drainage under local anaesthesia. However, patients with more severe odontogenic infection are likely to require management in hospital, which may well include urgent or emergency surgery under general anaesthesia.

The spectrum of patients presenting for surgery will vary widely, from those with a simple localized infection with no systemic sequelae to patients with extensive local tissue damage, airway compromise, and septic shock. The patient population is typically younger adults, but comorbidities related to drug and alcohol misuse are more common in this population and should be sought. In patients with evidence of a systemic inflammatory response, a careful assessment of fluid status needs to be made. Patients may have been unwell and unable to drink adequately due to pain and swallowing problems for some time before presenting to hospital. Increased capillary permeability and fluid loss related to sepsis can compound this problem. Intravenous fluid administration prior to surgery may well be required. Patients with septic shock may have acute renal failure and clotting abnormalities, and need a full range of blood tests prior to theatre. Careful assessment of the airway is required in patients with signs of spreading infection. Mouth opening limited by swelling or trismus related to infection cannot be reliably expected to improve following induction of anaesthesia and there needs to be a low threshold for the use of fibreoptic intubation in these patients. Patients with Ludwig’s angina develop firm, woody swelling of the tissues, including the tongue, which is likely to make conventional laryngoscopy impossible. If there is a suspicion of spread of infection to the mediastinum, then there is an indication for CT of the neck and chest to seek drainable collections. However, these patients are likely to be significantly compromised and it may be necessary to resuscitate the patient and secure the airway before going for CT.

The management of the patient is clearly heavily dependent upon the clinical state at the time of surgery. Patients with an uncomplicated dental abscess could be adequately managed using conventional intravenous induction, nasal endotracheal tube, and throat pack to collect pus and debris. Intravenous antibiotics, including anaerobic cover (e.g. cefuroxime and metronidazole), should be given. Patients with spreading infection and signs of sepsis will need much more careful management. If the preoperative assessment has suggested that conventional laryngoscopy may be difficult, then awake fibreoptic intubation is probably the method of choice. If this is not possible and the airway is in peril, then awake tracheostomy under local anaesthesia is another option, although if the tissues on the anterior surface of the neck are infected this may be difficult. Patients with septic shock may need vasopressors to support the blood pressure following induction of anaesthesia. Invasive monitoring with arterial and central venous lines and urinary catheter for urine output measurements may well be required.

Patients with uncomplicated dental abscess will be extubated at the end of surgery and observed on the ward postoperatively. Those with more severe infection may need to remain intubated and ventilated either because the airway itself remains compromised by the infection or because the overall clinical state precludes extubation. These patients will clearly need to go to a critical care unit postoperatively. Patients with clear signs of systemic sepsis should ideally be observed in a critical care environment postoperatively even if they are extubated at the end of the case. The critical care management of septic shock is outside the scope of this book, but some of the principles will be outlined. The Surviving Sepsis Guidelines⁸ provide a useful appraisal of the evidence in this area. The initial management, as already outlined, includes measures aimed at optimizing tissue oxygen delivery (oxygen therapy, fluid resuscitation, and vasopressor therapy). At the same time, measures to identify and treat the infection are initiated, including blood cultures, broad spectrum antibiotics, and surgery for drainage and debridement of infected issues. Despite these measures, patients with septic shock frequently go on to develop multiorgan failure, requiring numerous modalities of organ support.

Fluid therapy to ensure an adequate circulating volume is crucial. Unfortunately, the endpoints for this therapy are not always clearly defined and will depend on the circumstances. For example, urine output is often a useful marker but ceases to be so in the context of acute renal failure related to sepsis. The response of the central venous pressure (CVP) to a fluid challenge, or the variation in the pulse pressure or volume with respiration, are reasonable endpoints but are subjective in their interpretations. Patients in the early phases of septic shock can have significant ongoing fluid requirements as a result of increased capillary permeability. There is little evidence to support the use of one particular type of fluid over another. Crystalloids are safe and cheap. Synthetic colloids are also frequently used. The pathologically vasodilated state often seen in these patients can be managed with noradrenaline (norepinephrine). However, hypotension is sometimes refractory to high doses of noradrenaline (〉0.4 μmicrograms/kg/min), and in this situation the addition of low dose vasopressin is sometimes helpful⁹. The use of corticosteroids (hydrocortisone 200 mg daily) in severe sepsis became popular following a study by Annane et al.¹⁰, but a more recent study¹¹ suggests this treatment has no effect on mortality.

This patient population frequently goes on to develop acute respiratory distress syndrome (ARDS). This condition is characterized by patchy bilateral infiltrates on chest X-ray, hypoxaemia, and reduced lung compliance. These patients often require prolonged respiratory support. The use of a lower tidal volume ventilator strategy (6 ml/kg ideal body weight) has been shown to reduce mortality compared with higher tidal volumes¹².

Acute renal failure develops in a significant proportion of patients with septic shock. Renal function usually recovers over a timescale of 1–3 weeks, but patients require renal replacement therapy during this time. The modality most commonly used in UK critical care units is continuous venovenous haemofiltration (CVVH).

Early nutrition, preferably via the enteral route, is accepted as the standard for all critically ill patients. Hyperglycaemia is common in these patients and there is much interest in the benefit of maintaining tight glycaemic control with the use of insulin infusion. The major benefit seen in some of the earlier studies has not been replicated in subsequent clinical trials^13,14.

There is some evidence to support the use of recombinant activated protein C in patients with severe sepsis¹⁵. However, this agent carries an increased risk of bleeding and would need to be used with caution in patients following maxillofacial surgery. Oversedation should be avoided in these patients. Nursing the patients with 30° head-up tilt helps to reduce secondary ventilator-associated pneumonia¹⁶. Frequent positioning of patient which avoid pressure sores, stress ulcer prophylaxis, and deep vein thrombosis prophylaxis are all important. Evidence of ongoing sepsis requires prompt action, including further imaging, removal or change of intravascular catheters and further surgery if necessary.

Septic shock remains a condition which is frequently associated with a poor outcome. International studies frequently demonstrate 28-day mortality rates in the range of 30–40% in these patients. Those patients that do survive may be left with physical or psychological needs requiring long-term support.

The subgroup of patients presenting for surgery for odontogenic infection has a much higher risk for the presence of transmissible infections, including human immunodeficiency virus (HIV), hepatitis B and C, and tuberculosis. It is a fundamental responsibility of every practising anaesthetist to minimize the risk of these infections being transmitted either between patient and anaesthetist, patient and other members of the theatre team, or between patients. Every hospital has a statutory requirement to enforce effective infection control procedures. The Association of Anaesthetists of Great Britain and Ireland has published guidelines on infection control in anaesthesia¹⁷.

Patients with a history of intravenous drug use present a particular set of challenges. They are at high risk of infection with transmissible bloodborne viruses. Many will have been tested, but previous negative serology does not rule out recently acquired infection and these patients should always be treated as high risk irrespective of their serological status. Venous access may be very difficult to obtain. The patients themselves can sometimes advise of the best sites, but it is sometimes necessary to use a central vein to secure good access. Patients who have been heavy users of opiates will exhibit tolerance to therapeutic opiates and may need significantly higher doses to achieve adequate analgesia. These patients should not be denied adequate opiate medication during the perioperative period. Patients on regular methadone should generally have this continued if possible whilst in hospital.

It is generally accepted (previous concept) that certain groups of patients with cardiac conditions are at increased risk of developing infective endocarditis. This includes patients with the following conditions:

Since the mid 1950s it has been standard practice to offer antibiotic prophylaxis to patients with these conditions undergoing dental procedures. This practice has been based on a number of assumptions. These include an assumption that the dental procedure may cause a bacteraemia, that the bacteraemia may lead to infective endocarditis, and that antibiotic prophylaxis will prevent endocarditis from developing. The evidence underlying these assumptions was studied in detail by the UK National Institute for Health and Clinical Excellence, leading to the publication of a guideline in 2008¹⁸. Although studies suggest that dental treatment may well lead to a transient bacteraemia, there is some evidence that normal toothbrushing and many other daily activities can cause similar bacteraemias. The evidence for a causal link between dental treatment and the subsequent development of endocarditis is weak, and there is even less evidence that antibiotic prophylaxis is of any benefit. The authors felt that, given the available evidence, the routine use of antibiotic prophylaxis had the potential to do greater harm through anaphylaxis and increasing microbial resistance. The guideline recommends that antibiotic prophylaxis should not be used in routine dental treatment. The risk of infective endocarditis from an odontogenic source can best be minimized by maintaining good oral hygiene, regular check ups and prompt dental treatment when required. Patients with severe or spreading odontogenic infection are likely to be on antibiotics anyway. In patients at risk of infective endocarditis, it is important to choose antibiotics which will effectively cover the likely pathogens in infective endocarditis, including Streptococci, Staphylococcus aureus, and Enterococci.

Patients requiring surgery for maxillofacial infection can present a number of challenges to the anaesthetist. The problems of managing a potentially difficult airway can be compounded by the requirement for emergency anaesthesia in patients with significant systemic disturbance and a high prevalence of major comorbidities.