Вінницький національний медичний університет ім. М.І. …



Anaesthesia in oral surgery

Painlessness of operations in oral and maxillofacial surgery is the same basic demand, as well as painlessness of surgical interventions in other areas. Development of surgery of this area is obliged much more to successes of a local anaesthesia. Nevertheless, it is not always possible to do without the general anaesthesia at operations in the oral cavity. The necessity of carrying out long and volumetric interventions demands carrying out general anaesthesia and thorough preoperative preparation. Therefore the dentist should know well the basic properties of narcotics, indications and contraindications to their application, to study technique of narcosis and treatment of known complications.

Analgesia is the elimination of painful sensations in the course of surgical or diagnostic manipulations.

Anaesthesia is the eliminations of all sensations (including pain) in the course of surgical or diagnostic manipulations.

Anaesthesia may be:

1. General (narcosis), which is divided into inhalation with mask or endotracheal (through the nose) and non-inhalation (intramuscular, intravenous, rectal, epidural); *

2. Local.

Patients with maxillofacial pathologies constitute a particular category with a peculiar neurotic status. This feature is combined with full-blown pain due to topographical and function peculiarities of the maxillofacial area (a lot of receptors, cranial nerves, speech, breathing and masticate functions). The knowledge of the methods and agents of local anaesthesia can make it easier to carry out surgical operations in the maxillofacial area painlessly.

The general anaesthesia

The general anaesthesia (narcosis) means the condition of the convertible inhibition of the central nervous system (cns) is achieved by pharmacological agents,

influence of physical or mental factors. It assumes suppression of perception of pain stimulations, achievement of neurovegetative blockade and muscular relaxation, deenergizing of consciousness, maintenance of an adequate gas exchange and circulation, regulation of metabolic processes.

General anaesthesia includes narcosis, nla, ataralgesia, central analgesia, audioanaesthesia and hypnosis, electronarcosis and acupuncture, electrical puncture. Neuroleptanalgesia (NLA) is the loss of pain sensitivity, which is achieved due to rational cooperation of deep analgesia and neurolepsia by the introduction of analgesic and neuroleptic drugs.

Narcosis (general anaesthetizing) is temporary, reversible, artificially caused, (for example, by medicines) change of functions of organism (mainly is braking of cns functions), that is accompanied by narcosis triad: 1) loss of consciousness (sleep, fainting fit) — is achieved by introduction of anesthetic; 2) loss of sensitiveness of different types, among them—pain (analgesia), suppression of reflex activity (areflexia)—the response to external irritants (for example, to operative interference) — is achieved by introduction of analgesics (opioids more frequent); 3) myorelaxation, or skeletal muscle relax (deep or shallow) is achieved by introduction of muscle relaxants.

Ataralgesia — sort of nla, when ataraxia and analgesia are achieved by the administration of tranquilizers and analgesics. Central analgesia is the elimination of pain sensations due to introduction of great doses of analgetics. Audioanestesia is based on stimulation of the aqflitory analyzer by the certain frequency signal, which causes inhibition in other parts of the brain cortex.

Indications for narcosis *

In the maxillofacial area it’s indicated for carrying out long-term and traumatic surgical interventions which are combined with the risk of the airways obstruction. The indications and containdications are distinguished in Table 10.1.

Potentiation is the strengthening of pharmacological action of anesthetic by other medicines, which totally has a greater effect, than the action of these preparations solely.

Premedication

Premedication is the application of medicines during the preparation of the patient. The anesthetist select 3 variants of premedication application:

Absence of premedication — more frequent in small and exigent surgical interferences.

Table 10.1.

The indications and containdications for narcosis on an outpatient basis.

|Narcosis on an outpatient basis |

|Indications |Contraindications |

|General allergic reactions on local anaesthetics |acute disease of parenchymatous organs |

|Indications |Contraindications |

|low effect or impossibility of local anaesthesia |cardiovascular collapse acute cardiac infarction and postinfarction period |

|the patient is mentally unbalanced mental deficiency traumatic |(up to 6 month) severe bronchial asthma alcoholic or drug inebriation |

|interventions surgical interventions at children Specific |epinephron disease long-term intake of hormones anemia acute respiratory |

|premorbid background anesthetic |disease pneumonia clinically apparent thyrotoxicosis pancreatic diabetes |

| |epilepsy full stomach |

Sedation without depression — more frequent in common use.

Basal anaesthesia (preinduction) — when it is impossible to make a mark between premedication and induction to narcosis.

But, in any case, the benevolent conversation with a patient is desirable before the interference.

The primary objective of carrying out preoperative medication and sedation for the patients is to provide the most favorable conditions for a patient and a doctor during the operation. Therefore premedication provides the following effects: 1) it intensifies an effect, and 2) it prolongs the action of thelocal anaesthetics, 3) it reduces the side reactions of the cns and vital systems, 4) it provides possibility to reduce the concentration and dosage of local anaesthetics, 5) it prepares the main organs and systems of the patient for the operation by increasing their compensatory mechanism, keeping their activity at the level necessary to stabilize the vital functions. 6) It prevents the possibility of complications, related to the surgical interference.

The components of preoperative medication for the patients are conditioned by the basic mechanism of stress development, before, during and after the surgery, origin of the pain feeling and its action on vital systems, especially if the patient has

concomitant diseases, for example the subcompensated forms or reacting to external irritants, which can provoke the parafunction.

Basic components of most charts of preoperative medication of patients are cho- linolitic, central analgesic, sedative drugs, antihistaminic, atonies. And also adapto- gens are useful. Atropin is administrated for the prophylaxis of hypersalivation, diminishing the bronchial secretion, prevention the reflexes of vagus (bradyarythmia and heart arrest) during the intubation of trachea. Analgesics (opioids or narcotics) block passing of pain impulse and removes feeling of pain at the level of opioid receptors in cns. Commonly morphine, fortral, tramalare used. They intensify analgesia without narcosis, have a strong action, but they don’t have anti-inflammatory activity and can provoke respiratory standstill and addiction. Antipyretics or non- steroidresolvents (aspirin, meloxicame) mostly act on the injured tissues by inhibition of prostaglandin synthesis. Prostaglandins stimulate pain receptors and take part in inflammation development. Antipyretics also reduce the body temperature by influence on the temperature control centre in cns. Their action is insufficient (the pain less but does not disappear). Due to long-time administration it can cause clotting disorders, stomach ulcer, gastritis etc. Sedatives (ataractics) and tranquilizers have the purpose to calm down the patient, and prevent agitation, keep compensatory abilities of vital systems before surgery.

At the dental office, short-time acting agents in small doses are used because the patient should go outdoors or drive a car, and it is desirable for his relatives to escort him. At hospital more active and long-term tranquilizers are used. Antihistaminic preparations must decrease the negative influence

Of antigens from the area of operation, which have absorbed into the bloodstream and can entail postoperative allergic reactions. They also have moderate sedative action and partly strengthen the action of tranquilizers. Normally the preparations with sedative and hi antagonistic action are used.

Before the urgent operation premedication is carried out by intravenous or hy- podermal injections of preparations 10-40 min. Prior.

Before the scheduled operation in somatically healthy and compensated patients premedication is conducted 1 day prior the interference (first dose — at 10 pm in the eve of operation, second -^- 2 hours prior, third — 30-40 minutes prior the interference). In somatically sub- and decompensated patients symptomatic preparation has to begin 5—10 days prior the interference with the participation of contiguous specialists (for example, internists, haematologists). It is conducted until the improvement of the patient’s state and possibility of leadthrough of operation. And after the surgery the postmedication is carried out for the sake of reducing the risk of complications and cutting down the acute postoperative period.

At out-patient’s clinic preparations of short-time activity are usually applied, taking into account the type and short time of duration of operation and necessity to dismiss the patient home, but at hospital they are more long active.

Among the complications of the known charts of premedication there are such as: orthostatic collapses, allergic reactions to the applied medicines insufficient effect or remedy overdose. Orthostatic collapse is a serious

Complication, and it arises up when a patient suddenly zooms (from the operating table, bed, transport) from the horizontal position into vertical. The cardiovascular system is being in the state of slow speed of compensatory reactions, does not have time to change (to promote) tone of the myocardium and blood vessels, promote a pulse and arterial pressure, as a result, a sudden increase of loading on these structures leads to diminishing of their function: circulation effectiveness, hypovolemia of cerebral vessels, cerebral hypoxia and as a result the loss of consciousness and severe malfunction of the nervous regulation of all organs and systems. The first aid in such a case is to put the patient into the horizontal position and carry out the intensive care, or even resuscitation.

The allergic reactions to the applied medicines can develop on any of them, within different periods after their application. In case when the several medicines are applied stage-by-stage, it is more difficult to diagnost and find out, which of them caused the allergic reaction. Treatment of such a state with the known methods requires additional attention to the clinical features and subsequent searching of causal allergen.

If the allergic reaction happened before the planned interference, then the operation will be cancelled in the condition of slow normalization of the state of the patient, if during interference — help will be given to the patient and operation will be finished as quick as possible, and if before urgent interference — the operation will be conducted after normalization of vital systems activity and removal of risk for life.

The insufficient effect of premedication can show up variously, depending on that, whatever component of the pain feeling was not diminished by the medicinal influencing. As a rule, clinically it shows up by feeling of pain, presence of psychic excitation, fear, rejection of interference, active counteraction to the doctor. In such a case it is necessary to apply proper medicines, however, it is needed to remember, that during psychic excitation action of these medications in classic doses will be disfigured, and it is easy to get undesirable clinical effects, which can be dangerous for patient’s life. Taking it into account, it is expedient to decrease a volume or to halt interference (if there is such a possibility), whether to call an anaesthetist and with his participation conduct the operation. After the surgery

a patient needs careful supervision during all the period of convalescence, especially at the presence of dangerous concomitant diseases, which can become acute as a result of the psychical and physical trauma.

Overdose of the used preparation (preparations) — clinically shows up depending on pharmacological action of this preparation manifested with unconsciousness, circulation and breathing disorders and so on. Diagnostics and treatment of such disorders need prompt assistance of anaesthetists, toxicologists, internists at the appropriate units at hospitals under the control of activity of vital systems,* application of antagonists to medicines, which have been used.

A neuroleptanalgesia (NLA) is the variety of general anaesthesia, when for achievement of medical effect neuroleptic (aminazine or haloperidol) and analgesic (strong opioid of short action 4s for example, phentanyl) are used together. Consciousness is remained, > but neuroleptic considerably increases anaesthetizing, which is caused by analgesic. Therefore, a neuroleptanalgesia (nla) is the state of neurolepsy and analgesia, which is achieved by application of two main preparations of neuroleptic droperidol and narcotic phentanyl. For the phenomenon of their combined action a new term “autonomous block” or “neurovisceraldefence” has been invented. Nla is used as an addition to the local anaesthesia, as a preoperative anesthetizing, and more frequently it is combined with an inhalation seminarcosis (nitrous oxide + oxygen) and myorelaxants. Then an anaesthesia triad (tetrade) provides: 1) sleep; 2) analgesia (or other opioid); 3) autonomous block; 4) myo- relaxation. Such anaesthesia runs smoothly, hemodynamics is stable, the patient quickly awakes after the stopping of gas supply, a wound does not hurt (due to an opioid), there is no nausea and vomits (due to neuroleptic). Droperidol and phentanyl are more frequent used in correlation 2:1, and the combined preparation with these components has the name of thalamonal (in America — innovar). Preparations should be entered intravenously and slowly.

Combined anaesthesia is supposed for the use of a few preparations, not one (monoanaesthesia).

Ataralgesia is supposed for the use of ataractics (valium, sibazonum), which in large doses remove fear and put the patient into sleep. This two-component anaesthetizing (sedation with ataractic, anaesthetizing with opioid) is used, when myorelaxation is not needed. Combination of Diazepamum+phentanylum in large doses causes the protracted sleep (well after the protracted operations). For short- time operations at a dental .office short action ataractic is used. Flumazenil is used for desedation.

Audioanaesthesia is used as an additional method of anaesthetizing by influence on an auditory analyzer by the sounds of music, “white” noises and other. It ac-

tivates the auditory focus in the brain, diminishing the level of reception of painful irritant. It diverts patient’s attention to another more pleasant irritant and, as a result, reduces the pain. The influence on a visual analyzer by a television set, special glasses for creation of “virtual reality” pictures is used lately to demonstrate emotionally positive films for patients.

Anaesthesia with acupuncture is mainly the additional method of anaesthetizing. It is used for pricking classic points and points on face, auricle.

Electro-anaesthesia is conducted with facility, which generates the weak currents of sinewave, rectangular or three-cornered form, which influences the brain of the patient through electrodes on his head. The most anaesthetic effect is had by rectangular impulses at frequency 100-200 Hz. Action of electric current causes: 1) phenomena of parabiosis (according to the studies of n. E. Vvedensky); 2) general activating of the limbic system, that causes analgesia due to diminishing of ascending nociceptive influence on the brain; 3) activating of the endogenous opioid system of the cns. Since 1952 electro-anaesthesia is applied together with the medicinal influencing. Electro-anaesthesia foresees the use of the special equipment which provides flowing of electric current through cerebral structures by skilled-up medical personnel.

Transcutaneous electric neurostimulation is carried out by the electric neurostimulation facility and electrodes which impose on a skin and skip through them the managed electric current with necessary parameters, as a result local anaesthesia is achieved.

Hypnotic influencing with the purpose of anaesthetizing — must be conducted only by doctors who have necessary qualification. It can be possible for some patients who are inclined to the hypnosis.

Indications for general anaesthesia (narcosis) in dentistry and maxillofacial surgery:

• Individual intolerance to the local anaesthetics,

• Psychoemotional agitation, unwillingness of “presence” in the operation

• Necessity of monitoring of vital functions.

• Carrying out of complex, traumatic and durative interventions.

There are such contraindications as: uncompensated heart disease, acute

Infectious diseases, acute and uncompensated diseases of parenchymatous organs, uncompensated diabetes mellitus.

Preparation of the patient includes realization of some principles: thorough examination of the patient, premedication the day before anaesthesia, the patient should not eat for 2-4 hours before narcosis (to avoid regurgitation), the bladder must be empty, dentures, glasses and jewelry should be removed. All equipment and

medications for carrying out narcosis and removing possible complications should be in enough quantity and function properly.

During the examination the possibility of typical intubation and its difficulties should be evaluated. For carrying out the typical intubation the head of the patient should throw back easily, neck should be flexible, mandible must move forward easily, tongue must be mobile, mouth opening and fauces should be wide.

Signs of the complex intubation are short and thick neck, “bird face” (brachyg- nathia) insufficient opening of the mouth, infiltration and low mobility of the root of tongue, email throat, narrowing of upper airways by a pathological process, dislocation of the tongue into gullet, side dislocation of the tissues of the mouth floor and throat and glottis, chronical inflammatory processes at nasopharynx and fauces, dislocation of the nasal septum (at nasal intubation), present chronical hypoxia, intoxication, severe condition of the patient, concomitant diseases accompanied by the reducing of compensatory abilities of the organism.

Local anaesthesia

Measures that can assist to achieve the elimination of painful sensations in the certain area without inhibition of patient’s conscience are called the local anaesthesia. It can be achieved by different ways: application to the skin or mucosa (10% lidocaine spray, 20% benzocaine, 1-2% dicaine, 4% tetracaine, etc.), Intratissue administration of anaesthetizing agents. There are the following types of the local anaesthesia in clinical dental practice, such as:

• Physical (freeze)

• Topical (applicative)

• Infiltrative

• Nerve block

• Intrapulp

• Intraligament

• Intraosseous

The topical method is carried out to anaesthetize the nasal mucosa in the maxillary sinus puncture and the site of injection. The majority of operations in the maxillofacial area and an oral cavity are carried out under injective anaesthesia. In oral surgery infiltrative anaesthesia and nerve block are used.

During infiltrative anaesthesia layered impregnation of the tissues with anesthetic occurs.

Nerve block or so called regional block is the method of local anaesthesia, when anaesthetizing agent blocks the nerve conduction at a distance from the operative area. Conductive anaesthesia is carried out at durational operations at the facial bones and soft tissues, in the operations on the mandible, when infiltration does not have effect (table 10.2).

Block (regional) anaesthesia is performed to prevent pain during tooth, root and neoplasm extraction, during major alveolar process operations, when treating for diffuse pyoinflammatoiy processes, jaw fractures, when, in the course of applying infiltration anaesthesia, there is a risk of infection spreading to the surrounding tissues and when infiltration anaesthesia proves ineffective. Applying of this kind of anaesthesia means blocking the nerve, supply to a part of the body, outlying the part being operated* Today, such method of anaesthesia is performed by specific instruments and solutions (Fig. 10.1).

Applying block anaesthesia involves using certain anatomic landmarks to deposit anaesthetics in order to block the nerve trunk. During maxillofacial operations anesthetic is deposited to the nerve where it passes or exits a bone canal. It can be done either from the mouth cavity (oral anaesthesia) or through the skin (extra oral anaesthesia).

Anaesthetization effect depends both on concentration of medication and the size of the contacting area. The target of anaesthetic action in nerve fibres is Ranvier’s

[pic]

Fig 10.1. Syringe, one-shot needle and carpule with anaesthetic solution

Table 10.2.

The methods of nerve block in maxillofacial region

|Methods of nerve block (conduction anaesthesia) |

|At maxilla |At mandible |Central anaesthesia |

|Tuberal- inffaorbital- |mandibular |At the round foramen |

|nasopalatine — palatine |torusal |subzygomaticopterigoid |

| |mental |suprazygomaticopterygoid |

| | |tuberal |

| | |orbital |

| | |pterygopalatinal At the oval foramen |

| | |subzygomaticopterigoidsuprazygomaticopterigoid |

| | |submandibular |

nodes. For the full blockage, it is necessary to form contact of at least three nodes with anaesthetic.

In the presence of enough convicted hypotheses, the phenomenon of the local anaesthesia is not quite studied. It is a difficult dynamic process, which is expressed by the reverse morphologic and functional changes of the nervous fibre under the action of pharmacological preparations which repress their conductivity and excitability.

Quite often anaesthetizing is conducted without taking into account the neurotic state of the patient and concomitant somatic pathology. From statistical data 84% of the patients feel insuperable fear, fear of pain during the surgical intervention. A considerable part of parallel instances is made by persons with concomitant diseases. Thus the advantages of the combined methods of anaesthetizing are obvious.

By the acting duration local anaesthetics are divided to the long-time acting and the short time acting

By the chemical structure it is divided in two main groups:

• Etheric (cocaine, novocaine)

• Amid (lidocaine, articaine)

For the topical anaesthesia we use:

Cocaine is the anesthetic, which started the era of modern local anesthetization. But it s very toxic and now is not used in dental practice.

Dicaine — white crystal powder, well soluble in water or alcohol The solution is sterilized by boiling. It is a very active agent, which is used for the topical anaesthesia. There is applied 0.25—2% Solution. The maximum dosage for the adults is 0.09g (3% 3ml).

In dental surgery clinic novocaine, trimecaine, lidocaine, mepivacaine, artic- aine are mostly used for the injection anaesthesia.

Novocaine

For the local infiltration of the soft tissues 0.5 % Solution is used. On the alveolar process of the jaw 1-2% solution is used. There are maximum dosages: 150ml 0.5%, 75-100ml 1 % and 25-30ml 2%. Novocain is ineffective in inflammation processes.

Trimecaine

The anaesthetizing activity of trimecaine is 2.5-3 times less than novocain, and toxicity is 1.2-1.4 times less. In comparison with novocain, the acting duration of trimecaine is longer, and it is more efficient at the inflammation sites, keloid scars and granulation tissues. Unlike novocain, trimecaine is more tolerable by the patients. The anaphylactoid reactions occur rarely, but isotonic saline solution must be used for preparing the anaesthetizing solution.

Lidocaine hydrochloride (xilocaine, xicaine) is a strong anesthetizing agent. Its anesthetic activity is 2—3 times more than novocaine and toxicity is 1—2 times more as well.

Mepivacaine belongs to amid anaesthetics. It absorbs slowly but blood vessels dilatation does not occur. In overdose, there is the possibility of toxic reactions progression. The remedy is used in 2% or 3% solution for the in

Filtration or nerve blockage. The maximum dose is 4.4 mg/kg. In overdose some patients develop euphoria, depression, bradycardia, arterial hypotension or speech, swallow and vision disorders.

Articaine (ultracaine d-s, ultracaine d-s forte) — local anesthetic, that belongs to amid group and is produced in 1.7 ml cartridges and 20 ml flasks as 4% solution. It is less toxic than lidocaine and only 1.5 Times more toxic than novocaine. Anesthetizing activity of articaine is 5 times more than novocaine. Anesthetic has a high level of protein bindning and low level of fat solubility. That is basic for the choice to administer it for pregnant patients (less toxic for the fetus).

To increase the anesthetizing activity and acting duration of the local anaesthetics, it is recommended to add 0.1 % Solution of epinephrine hydrochloride (1 drop for 5 ml). It is necessary to remember, that all anaesthetics with vasoconstrictive action are contraindicated in case of:

• Hypertension

• Heart disease

• Decompensated diabetes

Local and general complications

Medical emergencies require prompt assessment and action. There may not be time for a detailed assessment but it is possible to buy time by using a basic protocol that simultaneously assesses and supports vital functions. Fortunately, serious medical emergencies in dental practice are not common, but that means that they are all the more likely to be alarming when they do occur. The ability to stay calm and manage the situation successfully depends on prior planning and rehearsal for such an event.

There are essential drugs and items of equipment that every dental practitioner should have available for use in an emergency. Some of these are based on providing simple and uncomplicated treatments while others necessitate providing early definitive treatment. Acute asthma and anaphylaxis are two examples of emergencies where simple first aid measures are inadequate and definitive treatment should be started by the dentist while waiting for the ambulance service to transfer the patient to an accident and emergency (A&E) department. This essential treatment is described as first-line treatment in the following protocols. Some drugs are available in preloaded syringes for fast preparation.

Syncope

Signs and symptoms! may be preceded by nausea and closing in of visual fields; pallor and sweating; heart rate below60 beats/min (bradycardia) during attack. First line treatment including:

• Lay flat

• Give oxygen

• Expect prompt recovery.

The main causes of faint could be pain or anxiety.

Principles of treatment:

• Need to encourage oxygenated blood flow to brain as rapidly as possible

• May need to block vagal activity with atropine and allow heart rate to in' crease.

Hyperventilation

Signs and symptoms: light-headed; tingling in the extremities; muscle spa cm may lead to characteristic finger position (carpo-pedal spasm).

First line: reassure; ask patient to rebreathe from cupped hands or reservoir bag of inhalational sedation or general anesthetic apparatus.

Causes — anxiety.

Principles of treatment: reduce anxiety; over-breathing has blown off carbon dioxide, resulting in brain blood vessel vasoconstriction. Return carbon dioxide levels in blood to normal.

Postural hypotension

Signs and symptoms: light-headed; dizzy; loss of consciousness on returning to upright or standing position from supine position.

Treatment:

• Lay the patient flat and give oxygen

• Sit the patient up very slowly.

More likely to occur if the patient is taking beta-blockers which reduce the capacity to compensate for normal cardiovascular postural changes.

Principles of treatment: encourage oxygenated blood flow to brain.

Diabetic emergencies: hypoglycaemia

Signs and symptoms: shaking and trembling; sweating; hunger; headache and confusion.

• If the patient is conscious, give three sugar lumps or glucose and a little water or glucose oral gel; repeated if necessary in 10 minutes

Cause: usually known diabetic; the patient may have taken medication as normal but not eaten before a dental visit.

The main principles of treatment is to return blood glucose level to normal by giving glucose or by converting the patient’s own glycogen to glucose by giving glucagon.

Further management

• Transfer the patient to A&E

• Give up to 50 ml 20 % glucose i.v. infusion followed by 0.9 % saline flush as the glucose damages the vein

• Expect prompt recovery.

Grand mal epileptic seizure Signs and symptoms: a sudden loss of consciousness associated with tonic phase in which there is sustained muscular contraction affecting all muscles, including respiratory and mastication; breathing may cease and the patient becomes cyanosed; the tongue may be bitten and incontinence occur; after about 30 seconds, a clonic phase supervenes, with violent jerking movements of the limbs and trunk.

First-line:

• Ensure the patient is not at risk of injury during the convulsions but do not attempt to restrain convulsive movements

• Make no attempt to put anything in the mouth or between the teeth

• After movements have subsided, place the patient in the recovery position and check the airway

• The patient may be confused after: reassure and offer sympathy

• After full recovery, send the patient home unless the seizure was atypical or prolonged or injury occurred.

Cause:

• Usually the patient is a known epileptic

• Epilepsy may not be well controlled

• Seizure may be initialed by anxiety or by flickering light tube.

• Principles of treatment:

• Maintain oxygenated blood to brain

• Protect from physical harm

• Administer anticonvulsant.

• Further management

Risk of brain damage is increased with length of attack; therefore, treatment should aim to terminate seizure as soon as possible.

If convulsive seizures continue for 15 minutes or longer or are repeated rapidly (status epileptics):

• transfer to A&E

• remove dentures, insert nasopharyngeal airway

• give oxygen

• give 10-20mg i.v. diazepam (2.5mg/30s) as Seduxen but beware of respiratory depression, or diazepam solution for rectal administration in hospital.

Acute asthma

Signs and symptoms: persistent shortness of breath poorly relieved by bron- chodilators; restlessness and exhaustion; tachycardia greater than 110 beats/min and low peak expiratory flow; respirations may be so shallow in severe cases that wheezing is absent.

First-line:

• Excluded respiratory obstruction

• Sit the patient up

• Give oxygen

• Salbutamol (Ventolin) via a nebuliser (2.5-5 mg of 1 mg/ml nebuliser solution) or via a large-volume spacer (two puffs of a metered dose inhaler 10-20 times: one put every 30 seconds up to 10 puffs for a child)

• Reassure and allow home if recovered

Cause exposure to antigen but precipitated by many factors including anxiety. Principles of treatment: oxygenation; bronchodilatation.

Further management

• If little response, transfer to A&E

• Dexamethazonei.v. : adults 200 mg; child 100 mg

• Add ipratropium 0.5 mg to nebulised salbutamol

• Euphylline slow i.v. injection of 250mg in 10ml over at least 20 minutes: monitor or keep finger on pulse during injection.

Anaphylactic shock

Signs and symptoms:

• Paresthesia, flushing and swelling of face, especially eyelids and lips

• Generalized urticaria, especially the hands and feet

• Wheezing and difficulty in breathing

• Rapid weak pulse.

These may develop over 15 to 30 minutes following the oral administration of a drug or rapidly over a few minutes or seconds following i.v. drug administration.

• Lay the patient flat and raise his feet

• Give oxygen

• Give 0.5 ml epinephrine (adrenaline) 1 mg/ml (1 in 1000) intramuscular —

0. 25ml for 6-12 years; —h 0.12ml (or 6 months to 6 years)

* Repeated every 10 min until improvement.

Principles of treatment

Requires prompt energetic treatment of

• laryngealoedema

• bronchospa cm

• hypotension.

Further management

• Transfer to A&V

• Chlorphenamine (chlorpheniramine) 10 mg in 1 ml intramuscular or slow

1. v. injection

• Hydrocortisone sodium succinate 200 mg by slow i.v. injection: valuable as action persists after that of adrenaline has worn off

• Fluids i.v. (colloids) infused rapidly if shock not responding quickly to adrenaline.

Stroke

Stroke results from either cerebral haemorrhage or cerebral ischacmia. Signs and symptoms

• Gonfusion followed by signs and symptoms of focal brain damage

• Hemiplegia or quadriplegia

• Sensory loss

• Dysphasia

• Locked-in syndrome (aware, but unable to respond).

First line: reassure; transfer to A&E.

Principles of treatment

Maintain and transfer for further investigation.

Angina pectoris and myocardial infarction Angina results from a reduced coronary artery lumen diameter because of atheromatous plaques

Myocardial infarction is usually the result of thrombosis in the coronary artery.

Signs and symptoms:

• Sudden onset of severe crushing pain across the front of the chest, which may radiate towards the shoulder and down the left arm or into the neck and jaw; pain from angina usually radiates down the left arm

• Skin pale and clammy

• Shallow respirations

• Nausea

• Weak pulse and hypotension

• If the pain is not relieved by glycery ltrinitrate (GTN), then the cause is myocardial infarction rather than angina.

First-line:

Allow the patient to rest in a position that he feels most comfortable:

• In the presence of breathlessness this is likely to do the sitting position, whereas syncopal patients will want to lie flat

• often an intermediate position will be most appropriate.

• Angina

• Angina is relieved by rest and nitrates:

• Glycery ltrinitrate spray 400 mg metered dose (sprayed on the oral mucosa or under the tongue and mouth, then closed)

• Give oxygen

Allow home if attack is mild and the patient recovers rapidly Myocardial infarction if myocardial infarction is suspected:

• give oxygen

• aspirin tablet 300 mg che\ved Principles of treatment

• Pain control

• Vasodilatation of blood vessels to reduce load on the heart.

Further management for severe angina or myocardial infarction

• Transfer to A&E

• Diamorphine 5 mg (2.5 mg in older people) by slow i.v. injection (1 mg/min)

• Early thrombolytic therapy reduces mortality.

Cardiac arrest

Most cardiac arrests result from arrhythmias associated with acute myocardial infarction or chronic ischaemic heart disease.

The heart arrests in one of three rhythms

• VF (ventricular fibrillation) or pulseless VT (ventricular tachycardia)

• asystole

• PEA (pulseless electrical activity) or EMU (declromechanical dissociation).

• Signs and symptoms: unconscious; no breathing; absent carotid pulse. Principles of treatment

• Circulation failure for 4 minutes, or less if the patient is already hypoxaemic, will lead to irreversible brain damage;

• Institute early basic life support as holding procedure until early advanced life support is available.

Early basic life support for cardiac arrest

The following instructions are based on the UK Resuscitation Council guidelines for basic life support. The essential features are remembered by ABC: airway, breathing and circulation.

Risks to the rescuer

• Before starting a resuscitation attempt, the rescuer must rapidly assess the risks: traffic, falling masonry, toxic fumes and other potential hazards relevant to the environment

• Mucous membrane exposure to hepatitis B virus (HBVJ and human immunodeficiency virus (HIV) is less of a risk than needle stick exposure, strongly suggesting that the chance of infection from mouth-to-mouth ventilation is negligible. However, the US Centers for Disease Control and Prevention advises universal precautions.

Basic life support

• Initial patient asses cment, airway maintenance, expired air ventilation and chest compression constitute basic life support (BLS) or cardiopulmonary resuscitation.

• BLS is a “holding operation” maintaining ventilation and circulation until treatment of the underlying cause can be instigated.

• BLS implies that no equipment is used. Where a simple airway or face mask is used, this is described as “basic life support with airway adjunct”.

Theory of chest compression

• The “thoracic pump” theory proposes that chest compression, an increasing intrathoracic pressure, propels blood out of the thorax, forward flow oc-

curring because veins at the thoracic

inlet collapse while the arteries remain

patent.

Even when performed optimally, chest

compressions do not achieve more than

30% of the normal cerebral perfusion.

Basic airway management

Jaw thrust rather than chin lift is meth-

od of choice for the trauma victim

(Fig. 10.2).

An oropharyngeal airway such as a

Guedel or nasopharyngeal airway,

may be used (Fig. 10.3).

• A face mask used for ventilation al-

lows oxygen enrichment (Fig. 10.4).

Sequence of actions

Ensure safety of rescuer and victim (referred to below as he, for simplicity).

Check whether casualty is responsive.

If he responds by answering or moving

• leave him in the position in which you find him (providing he is not in further danger), check his condition and get help if needed

[pic]

Fig. 10.2. The jaw thrust airway maneuver. Further management

B

[pic]

A

Fig. 10.3. The oropharyngeal (Guedal) and nasopharyngeal airway. Insertion via the mouth (A) and nose (B)

[pic]

Fig. 10.5. Head tilt and chin lift airway manoeuvre

• reassess him regularly. If he does not re-

spond

• shout for help

• open the airway by tilting the head and lift-

ing the chin (Fig. 10.5).

4. Keeping the airway open; look, listen and feel

for breathing.

5. If he is breathing

• turn him into the recovery position;

• check for continued breathing

• send someone for help.

If he is not breathing

• send someone for help or, if you are on your

own, leave the victim and go for help

• turn victim unto his back

• remove visible obstruction from the victim’s mouth

• give 2 breaths.

6. Assess the victim for signs of a circulation

• check the carotid pulse

• take no more than 10 seconds to do this.

7. If you are confident that you can detect signs of a circulation

• continue rescue breathing

• check circulation about every minute

• if the victim starts to breathe on his own but remains unconscious, turn him into the recovery position.

Fig. 10.4. Pocket face mask

If (there are no signs of a circulation or you are at all unsure

• start chest compression (Fig. 10.6)

• combine rescue breathing and compression in the ratio of 2:15.

Continue until successful, help arrives, you become exhausted.

Going for assistance

• A lone rescuer will have to decide whether to start resuscitation or go for help first. If the cause of unconsciousness is likely to be trauma, drowning, or if the victim is an infant or a child, the rescuer should perform resuscitation for about 1 minute before going for help.

• If the victim is an adult and the cause of unconsciousness is not trauma or drowning, the rescuer should assume that the victim has a heart problem and go for help immediately it has been established that the victim is not breathing.

• Transfer to A&E

• Advanced life support.

B

A

[pic]

Fig. 10.6. Chest compressions: shown from above (A) and in cross-section (B)

Advanced life support for cardiac arrest, advanced airway management techniques and specific treatment of the underlying cause of cardiac arrest constitute advanced life support (ALS).

Advanced airway management

• A self-inflating bag and mask with attached oxygen permits ventilation with around 45 % oxygen. However, it is preferable also to use a reservoir as oxygen can then be provided at around 90% (Fig. 10*7).

• The laryngeal mask airways (LMA), which seals around the larynx, is becoming popular as it provides more effective ventilation with a bag — valve system than with a face mask.

• The “gold standard” of airway management is endotracheal intubation as it protects against contamination by regurgitated gastric contents and blood, allows suctioning of the respiratory tract and drugs can be administered by this route. However, its use requires considerable training.

• A surgical airway intervention such as a needle cricothyroidotomy may be necessary if it is not possible to ventilate with bag-valve-mask or to intubate. This may be because of maxillofacial trauma or laryngeal obstruction.

[pic]

Fig. 10.7. Self-inflating bag and mask with reservoir

High-pressure oxygen is given via a can-

nula inserted into the trachea, although this

is only a temporary measure lasting about 40

minutes until a theatre is prepared for formal

tracheostomy.

Specific treatment. Specific treatment

algorithms (guidelines) are followed accord-

ing to the electrocardiogram rhythm assess-

ment and the clinical context. These are based

on best scientific evidence.

Treatment is directed toward correcting

underlying causes, use of specific drugs and

defibrillation.

Defibrillation

Defibrillation is indicated in ventricular fibrillation and pulseless ventricular tachycardia, which arc the commonest arrhythmias causing cardiac arrest and the most treatable. However, the chances of successful defibrillation decline by about 5% with each minute; therefore early management is vital (Fig. 10.8).

• Defibrillation depolarizes most or all of the cardiac muscle simultaneously, allowing the natural pacemaking tissues to resume control of the heart.

• All defibrillators have two features in common: a power source capable of providing direct current, and a capacitor, which can be charged to a predetermined level and subsequently discharged through two electrodes placed on the casualty’s chest.

• Defibrillators may be manual (the operator interprets the rhythm and decides if a shock is necessary), semi-automatic (when the tasks of recognizing the arrhythmia and preparing for defibrillation are automated) or fully automatic.

[pic]

Fig. 10.8. Defibrillation technique

Inflammatory processes of maxillofacial area and neck

Inflammatory response results from interaction of exogenic (microbs, their toxins, waste and decay products) and endogenic ethiologic factors (factors and mechanisms of non-specific and immune responsiveness).

Up to now it has not been possible to determine the overall spectrum of inflammatory processes agents using microbiological diagnostic methods. Thus, clinicians and microbiologists considered aerobes to be the ethiological factor of these diseases, because only this type of bacteria has been detected in the researched material, provided by patients. With improvement of microbiological research methods it has become possible to obtain evidence that anaerobes can be agents of odontogenic infection. In the course of the researches carried out during the last few years it was ascertained that not only staphylococci, but also different representatives of gram- negative microflora: proteus, colibacillus, klebsiella and others belong to basic agents of acute odontogenic infection.

The great significance in ethiology of inflammatory diseases of the head and the neck has been attached recently to opportunistic microorganisms, asporous obligate anaerobic bacteria. Bacteroides and fusobacteria are the bacteria most frequently found among this type of bacteria. Usually these microorganisms can be found on mucous membranes of the oral cavity. When the immune responsiveness of an organism is decreased and hemodynamic in inflammatory tissue is induced, bac- teroids, fusobacteria and other opportunistic anaerobic microorganisms can cause pyoinflammatory diseases.

The role of microflora is undoubtedly great. However, microorganism — macroorganism relations have two-way connection; therefore the peculiarities of the course of the inflammation and development of complications are related not only to the peculiarities of microflora, but also to organism responsiveness, that is the property of an organism to respond to changes in the environment.

In other words, responsiveness of an organism reflects the protective and adaptive properties of an organism and is caused by inherent and acquired factors. To a great extent it depends on sex, age, and environment conditions etc.

Considering the problem of the pathogenesis of acute odontogenic inflammatory diseases, great attention is paid to sensitization of organism, producing of specific

antibodies in response to coming of the antigens into tissues. The coming of the antigens first occurs owing to their ability to penetrate deep into tissues through tissue barriers. As a result of forming and continuous existence of the chronic infection nidus the number of penetrating antigens increases and the level of sensitization rises. In response to this organism is constantly producing specific antibodies, which support antibacterial immunity.

The inflammatory process is likely to increase at the disturbance of the dynamic balance between micro- and macroorganism. It may be either the increase in the total effect, which damages from the direction of bacteria, or weakening or increase of reactivity.

One of the major factors which contribute to the beginning of inflammatory process is rise in summary effect, which damages virulence of microflora, as a result of increase in the number of microbes/microorganisms. Another significant factor is injury of the demarcation zone (connective tissue capsula or leukocytic bank), which occurs at the injury or operative treatment.

Development of acute suppurative inflammation against the background of the existing nidus of chronic infection arises as a rule after the physicalor emotional overstrain, supercooling, overheating, and also after certain diseases (especially infectious diseases).

The inflammatory processes of jaw are remarkable for a greater variety of their clinical course, that gives the basis for their various classifications. One of them was suggested by A. G. Shargorodskyi and L. M. Tsepov (1979)

Statistics:

1. Per 1 person — 10 of thousand diseases, 100 thousand symptoms and syndromes

2. Per every third patient — with odontogenic inflammatory process

• 20 % — general numbers of patients which have been sent to a polyclinic

• 8 % — surgical stomatology of patients, 13-39 % of which are hospitalized

• 60 % — pyoinflammatory

Signs for classifications of the acute odontogenic inflammatory processes

I. G. Lukomskii (1943) — 3 stages:

1. A periodontitis and osteomyelitis.

2. Perimaxillary phlegmon.

3. Spreading phlegmon and sepsis.

A. I. Evdokimov and G. A. Vassilyev (1964) developed precise differential diagnostics of a acute periodontitis, periostitis, osteophlegmon, adenophlegmon and acute lymphadenitis.

Arguments:

1. A. B.Izachik — lymphatic vessels (research — communication, anastomose between the bone, periosteum, periodontium, soft tissues).

2. Lanuk — investigated a venous grid (research — communication, anasta- moses between a bone, periosteum, a periodontium, soft tissues).

3. Inflammatory process is distributed not only per continutatem, but also on venous and lymphatic vessels, not always is osteomyelitis.

4. Current: hypoergic, hyperergic, anergic, normergic

It is possible to separate a periodontitis as a standing alone disease (G. A VassilyevA. I. Evdokimov)

1. Characteristic symptoms

2. Clinical course of disease at conservative surgical treatment

3. Modem morphological and paraclinical researches (blood from epicenter inflammatory process, infra-red radiation — thermo diagnostics) allow establishing the exact diagnosis of inflammatory process (O. M. Solntsev, A. M. Lihota)

4. Patients are not hospitalized.

Another classification of the odontogenic inflammatory processes was proposed by A.G. shargorodskiy andL. M. Tsepov:

A. Periodontitis:

1. Acute periodontitis (serous and purulent periodontitis).

2. Chronic periodontitis in the stage of exacerbation.

3. Chronic (granulating, granulomatous and fibrous periodontitis).

B. Jaw periostitis:

1. Acute periostitis (serous and purulent).

2. Chronic periostitis.

C. Jaw osteomyelitis:

1. By clinical course: a) acute; b) subacute; c) chronic; d) aggravated chronic.

2. By the character of the spread: a) limited; b) diffusion.

D. abscesses and phlegmons:

1) face; 2) perimaxillary; 3) floor of the oral cavity;

4) peripharyngeal; 5) tongue; 6) neck.

E. lymphadenitis of the face and neck

Periodontitis

Periodontitis — inflammatory process which affects the tissue of the periodontium and bones that support the teeth. The main cause of periodontitis is complicated caries.

Distinct types of periodontitis:

1. Acute periodontitis:

a) serous periodontitis (limited and generalised),

b) purulent periodontitis (limited and generalised).

2. Chronic periodontitis:

a) granulating periodontitis,

b) granulomatous periodontitis,

c) fibrous periodontitis.

3. Chronic periodontitis at the stage of exacerbation.

Clinical features of acute periodontitis. The initial symptom of acute serous periodontitis is toothache, which becomes stronger when biting. This pain doesn’t usually irradiate, so it’s easy for the patient to determine the affected tooth. Another characteristic of periodontitis is soft-tissue swelling, minor regional lymphadenopa- thy, slightly painful lymph nodes.

The affected tooth is a little loose and vertical percussion of the tooth is positive. At the same time there dental X-ray film shows no change. With the progression of the serous inflammatory process into purulent form of periodontitis the intensity of pain is growing. The pain becomes acute, throbbing and irradiates along the trigeminal nerve. There is acute pain every time one touches the tooth, which becomes loose. The patient notes that the tooth seems to be growing. The mouth of the patient is half-open, the mucous membrane of the alveolar process is hyper- emic, edematous and painful within the borders of the injured tooth. Regional lymph nodes are enlarged and painful. Edema of the soft tissue is characteristic at this stage as well. There is deterioration of the general condition of the patient. The treatment of the acute periodontitis consists of creating an exudate outflow from the periapical region. The symptomatic and physical therapy is also used.

Chronic periodontitis

Chronic periodontitis (apical) is a chronic inflammation of periodontum, characterized by transition from acute phase into chronic one or by course. Chronic periodontitis is reported to be more frequent than acute one. The morphological and

clinical pattern of chronic peridontitis is variable. It can be granulating, granulema-

tous and fibrotic.

Granulating periodontitis is marked by painful sensation, which occasionally

appears in the region of the affected tooth. There may be also no pain. It is clear

from the anamnesis that tooth disturbs the patient for a long time.

Examining the tooth, it is easy to determine whether there is any filling or cav-

ity, which can be sounded indolently. Percussion of the tooth is usually painless.

X-ray examination (Fig. 12.1) is of considerable importance in differential di-

agnostics of chronic periodontitis: fibrous periodontitis (Fig. 12.2) is marked by ir-

regular enlargement of periodontal fissure; the characteristic feature of the granu-

lomatous periodontitis (Fig. 12.3) is sharply delineated destruction zone of differ-

ent shapes and size in periapical region; the granulating periodontitis (Fig. 12.4)

is characterized by destruction of the alveolar socket and destructive changes

in spongy substance without any distinguished boundary between pathologic zone

and unaffected tissues.

Differential diagnostics. Acute periodontitis should be differentiated from pul-

pitis, periostitis, osteomyelitis, suppuration of apical cyst, odontogenic sinusitis.

In acute periodontitis a person has a pain in bite or percussion, whereas in diffuse

pulpitis it is permanent without any disturbance. In acute periodontitis there are

inflammatory changes of the gingiva around the tooth, percussion is painful. Elec-

troodontometric data may be useful for diagnosis.

In acute periodontitis a pain is located mainly in the tooth whereas in periostitis

it lessens and the soft tissues edema increases. During the evaluation, a fever, col-

lateral inflammatory edema of soft tissues and diffusive infiltration of transitional

fold, with forming of an abscess are

observed. Percussion of the casuative

tooth in periostitis is negative or slight

positive unlike acute peridontitis. Acute

osteomyelitis of jaw is differentieted

from periostitis at the same pattern

as acute purulent periostitis. For the

last it is peculiar to have bilateral infil-

tration of an alveolar process and body

of a jaw. In acute periodontitis, percus-

sion of causative tooth only is positive,

whereas in acute osteomyelitis positive

percussion and loosening of adjacent

teeth are observed. And percussion

[pic]

Fig.12.1 . X-ray examination

[pic]

Fig. 12.2. Fibrous peri- Fig. 12.3. Granulomatous Fig. 12.4. Granulating periodontitis odontitis periodontitis

of causative tooth is less painful than adjacent. Data of laboratory examination (blood test) can help in differentiating the diseases. It is necessary to differentiate acute periodontitis from suppuration of radicular cyst. For the last displacement of teeth and extrusion of the bone in the middle is peculiar. A bone lesion with robust edge is observed on X-ray.

The same clinical features are reported in acute periodontitis and odontogenous genyantritis. However in acute periodontitis, there is no stuffiness of a nose and no changes in maxillary sinus, which may be revealed with radiograph.

Odontogenic granuloma (subperiosteal, submucous, subcutaneous) can arise from spreading of granulations into submucous and subcutaneous soft tissues.

Clinical course of the process complicated with odontogenic granuloma is also quiet. There are no pain in the tooth. Inflammatory changes are accumulating in soft tissues.

In subperiostal odontogenic granuloma, bone extrusion in the middle of decayed tooth appears. The mucosa over the lesion is not changed, sometimes a few inflammatory signs can be observed.

Submucosal odontogenic granuloma is determined as local, solid formation, which is situated in submucosa of vestibular fold or cheek adjacent to the causative tooth and connected through the fistulous tract. Suppuration of submucosal granuloma is observed often. Discharging of pus through the fistula ensuing declination of process and scarring of the fistulous tract.

Round infiltration in subcutaneous fatty tissue is peculiar for hypodermic granuloma. It is solid, painless or slightly painful. A fistulous tract goes through

[pic]

[pic]

the soft tissues from responsible tooth to granuloma. Hypodermic granuloma can suppurate. Skin adheses with underlying tissues, becomes reddish, fluctuation appears. Abscess discharges outside, breaking thinned skin. Diagnosis is based upon X-ray data. In periapical granulating periodontitis, it demonstrates changes spreading of periodontal fissure around root tip as a result of bone lesion. Bone lesion has irregular edge. Contours of root tip can be irregular due to resorbtion of the cement and dentine. In the presence of odontogenous granuloma in soft tissues, lesion around apex is of a small size.

Granulematous periodontitis is charachtarized by limited growth of granulation around the root tip. As a result of compaction of the tissues adjacent to granulation fibrous capsule formed.

Depending on the structure we distinguish: 1) simple granuloma, consisting of the elements of connecting (granulation) tissue; 2) epithelial, in which epithelium remnants are located between the areas of granulation tissue; 3) cyst-like granuloma, containing cavities, covered with epithelium.

Clinical features. A flow of granulematous peridontitis may be different. Quite often granuloma does not increase or grows slowly. Thus, patients do not complain. Only by chance in roentgenologic research a granulomatous lesion can be revealed. In some patients granuloma is gradually increased. Usually it is connected with intensifying of inflammatory process and proper changes in tissue of granuloma: by hyperemia, edema, neutrophilia, suppuration. In intensifying of chronic process, capsule of granuloma gets broken, and inflammatory and dis- trophic processes occur in adjacent tissues, with prevalence of destruction. It can be manifested differently. In some cases, sensitivity and pain of the tooth in percussion are present, in others signs of an acute periodontitis appear. Then, after declination of inflammation, barrage capsule forms around lesion again. Diagnosis is also based upon X-ray data. The radiogram reveales round lesion with robust edges. In inactive flow of granulomatous periodontitis, sclerotic bone around lesion can be observed.

Differential diagnostics. It is necessary to differentiate chronic granulomatous periodontitis from an apical cyst. On X-ray in granulomatous periodontitis the area of resorbtion of bone has a diameter of 0.5-0.7 cm, in a cyst — more considerable resorbtion of bone is visible with robust clear contours.

Fibrous periodontitis. In the end of acute process in periodontium or under the influence of medical measures, scarring can happen spontaneously both in granulating or granulomatous lesion resulted in bone recovery. The local inflammatory process formes around root tip due to growth of connective tissue. However, it is reported that fibrous periodontitis can occur spontaneously.

Clinical picture. In fibrous periodontitis, there are no complaints. Some acute signs can arise in recurrence. In the oral cavity decayed tooth with disintegrated pulp can be revealed. The tooth can slightly react to percussion. Diagnostics is based upon radiographic data. There are spreading of periodontium and compaction of bone around root tip.

Treatment. Surgical treatment of chronic peridontitis consists in extraction of the tooth, replantation, allotransplantation, dental implantation, apicoectomy, rootectomy, hemisection.

Hypodermic granuloma of the face

Hypodermic granuloma of the face is an uncommon disease and has a subacute flow. It manifests by nidal inflammation in hypoderma. More frequent hypodermic granuloma has odontogenic origin as a complication of chronic peridontitis. Similar features are observed in presence of a foreing body in hypoderma. Development of non-odontogenic hypodermic granuloma is caused by insertion of organic foreing bodies, though metal or glass particles do not lead to it.

This form of odontogenous inflammatory process can be also named as: migrating granuloma, hypodermic migrating granuloma, creeping migrating granuloma, migrating abscess and most often — hypodermic granuloma of the face.

In etiology of inflammatory process a leading role belongs to microorganisms which penetrate from the nidus of chronic granulating periodontitis into the hypoderma, where granulation tissue develops as separate malformation — granulomata. Odontogenic hypodermic granuloma is connected with the causative tooth. But not all of the authors uphold such view on the mechanism of development of odontogenic hypodermic granuloma. Some of them have not seen distinctions between it and superficial chronic lymphadenitis, because of similar clinical manifestations. Development of odontogenic hypodermic granuloma is closely related to the causal tooth, and its localization depends on the location of the last one.

Hypodermic granuloma can be single or multiple. Size of granuloma can vary (from 1 to 2-4 cm), borders are regular, there can be mild pain in palpation. The affected skin is thin, cyanotic, glossy, rough, folded. Fluctuation is determined but there is no pus after incision. Fluctuation is explained by formation of granulating tissues under the skin. The tract goes from granuloma to a responsible tooth.

Hypodermic granuloma of the face can have an odontogenic and nonodontogenic origin. In first case we always find a causative tooth and tract, which

is going from tooth to granuloma, in the second — these signs are absent. In hypo- dermic granuloma the size of affection of the skin is equal to affection of underlying tissues, which is a peculiar feature of the disease.

In the development of odontogenic hypodermic granuloma, two stages are marked out: hidden, when changes of a skin are absent, and period of skin manifestations, when changes of skin are visible.

There are four clinical forms of hypodermic granuloma: initial, stationary, creeping, suppurating. In the initial form of disease changes of skin are absent, and in the area of causal tooth painless infiltration is determined, size of which does not exceed peas. In the oral cavity in this stage it is possible to reveal dense tract, which is going from the tooth to infiltration. The stationary form is characterized with the development of process on the limited area. For creeping form, involution in one area and intensificaton in another one is a peculiar feature. In the suppurative form hypodermic granuloma turns into an abscess.

The course of hypodermic granuloma is chronic and dull. Self recovery is not observed.

Treatment consists in tooth extraction, thorough curettage of the socket. The affected skin and fistulous tract must be excised. The defect of the skin, which has been formed due to excision, should be closed. Prevention of the disease consists in timely treatment of caries and its complications. Tooth-preserving treatment is presented by several types of operations:

1. Apical resection (Fig. 12.5).

2. Radectomy (Fig. 12.6).

3. Premolarization or coronary and radicular separation (Fig. 12.7).

4. Hemisection of the tooth (Fig. 12.8).

[pic]

5. Ablation (amputation).

6. Apical resection with retrograde filling.

7. Dental reimplantation

Periostitis of the jaw

Acute odontogenic periostitis is acute infection inflammation of the periosteum of the alveolar process or, that is more rarely, body of jaws. Periostitis is localized on the one side of the jaw, frequently affecting vestibular side, rarely — palatal or lingual surface. This disease is treated mainly at out-patient’s clinic.

Etiology and pathogenesis. Periostitis of the jaw develops as a complication of the acute or chronic periodontitis. It can be the result of the root or follicle cyst suppuration, or alveolitis. Periostitis sometimes develops in connection with a suppurative form of the periodontal disease. It can develop in complicated eruption of the wisdom tooth and, finally, accompanies an acute form of odontogenic osteomyelitis. Cooling, stress and inadequate nutrition are factors predisposing to the development of acute periostitis.

Clinical features. At the initial stage odontogenic periostitis can develop slowly, gradually, causing only the insignificant pain feelings. As far as expansion of inflammation area and accumulation of exudates under periostium take place subjective and objective signs of inflammation increase. However in the majority of patients periostitis develops quickly. The certain information in anamnesis is peculiar to the acute periostitis: increasing pain in a gangrenous tooth during previous days; in the beginning pain irradiates to ear, temple, eyes, but in the last days it diminished to some extend, but the facial swelling appeares or rapidly progresses. Touch to the tooth (by the tangle, tooth-antagonist, food, spoon) is painful, however not as much, as earlier, in the stage of acute suppurative periodontitis. Application of heat (rinse, hot-water bottles) does not help, and only facilitates the state to some extent (diminishes pain). Some phenomena associated with intoxication are present (languor, apathy, sometimes headache, increased temperature).

Within a few days from the beginning of the disease, the facial edema increased and pain became considerable (due to intensive tension and chemical irritation of the jaw periostium).

Objective signs depend on localization and extension of the inflammated area as well as on the microorganisms virulence and state of the immune system.

Considerable facial asymmetry is visible, if the process is localized on the vestibular side of the affected jaw. If maxilla is affected one can see the edema

expanding to the lower eyelid, upper part of the cheek, parotid and masticatory area upper lip, bottom of the nose, etc. If the mandible is affected the edema is present at the lower part of the cheek, comer of jaw, neck.

Facial asymmetry is absent, if suppuration spread on a palatal or lingual surface; in this case a subperiostal abscess will not influence the contours of the face. If the disease arises from the central incisor of the maxilla, an abscess can appear between the bottom of the nasal cavity and mucous membrane of the nose.

Examination of the oral cavity reveals edema, hyperemia and infiltration, smoothed vestibular fold, and then in 3-5 days fluctuation appears within the limits of 3-4 teeth.

If pus spreads to the comer and on the branch of the jaw, it results in trismus — inflammatory contraction of the jaws, as the refectory spasm of the inflamed masticatory and medial pterygoid muscles develops.

Especially severe clinical flow is typical to suppurative periostitis, localized on the hard palate. Formation of an abscess under palatal periostium is associated with appearance of semispherical or oval swelling with marked hyperemia. Pus accumulation under the periostium and mucous membrane, which is dense and thick in this region, causes slight aching in the beginning, and then sharp pulsating pain. The permanent contact of palatal abscess with a tangle causes increase in pain sensations.

X-ray examination of the bone in the affected area reveals only those changes, which were caused earlier by chronic inflammation around a gangrenous tooth. Usually there are typical signs of chronic periodontitis.

In accordance with clinical signs and localization of the inflammated area the following forms of acute odontogenic periostitis are distinguished: (1) serous and (2) suppurative.

It is necessary to perform differential diagnostics of acute periostitis with acute suppurative periodontitis, acute osteomielitis, facial abscesses and phlegmons.

Periodontitis (acute suppurative) differs by localization of the inflammation zone within the limits of one tooth, by the absence of edema on the face, by sharp pain in percussion of the affected tooth.

Acute osteomyelytis differs by the presence of the subperiostal reaction not from one, but from two sides of the alveolar process, and also more expressed general signs of intoxication — higher body temperature (up to 39-40 °C), pain, which arise in a few teeth during percussion, by the presence of severe bone injury resulting in necrosis and sequestration of certain areas of bone, more expressed changes in blood and urine.

A phlegmon is characterized not only by the edema of the skin but also by dense infiltration. The skin above it has signs of severe hyperemia, is glossy, the fold

could not be formed during palpation. In periostitis the color of the skin is not usually changed, the infiltration of subcutaneous fat is absent. The general state is strongly affected in quickly increasing phlegmon: the body temperature is high, there are vivid changes in haemogram, reflecting the signs of festering process in an organism.

Treatment of acute periostitis is performed in a different way depending on the phase of illness development and objective status. In an initial period, when there are no signs of suppuration and fluctuation, and there is only a small infiltrate on the transitional fold (or on the palate), it is possible (if is necessary to preserve a tooth) to make an effort to attain reverse development of process by means of endodontic treatment and application warm (physiotherapeutic procedures) in combination with antibiotics and anti-inflammatory medicines.

In those cases, when a tooth is strongly destroyed, and its preservation does not represent any value, it is essential to extract the casual tooth and prescribe common treatment without thermal procedures (bleeding from an alveola is possible).

Usually patient applies for medical help to the dental clinics when inflammation is on its marked clinical stage, infiltrate is already clear outlined and subperiostal abscess is formed. The urgent wide cut of the mucous membrane and periostium (up to the bone) in the area of the most pronounced zone of abscess or infiltrate is indicated in this period. It is necessary to perform the periostotomy within the limits of 2-3 teeth (not less) for providing good outflow of the pus. Direction of the cut in a vestibulum is along the transitional fold, and on the palate — parallel to the gum. On the palate it is better to perform not a simple linear cut, but excising the three-cornered area of the mucousa and periosteum over the abscess. Simultaneously with a cut it is necessary to extract a “causal” tooth, if it is mostly destroyed and conservative treatment is impossible. In the case, when such tooth can be preserved for cosmetic or functional reasons, it is treated.

Chronic odontogenic periostitis Chronic periostitis could be simple and ossificated. Patients complain of the deformation of the jaw and slight pain in it. Anamnesis is distinguished by pain in the affected tooth and its treatment.

Clinical features are marked by deformation of the face owing to the enlarged alveolar process of the maxilla or mandible, which is slightly painful when doctor touches it. Other distinctive characteristics are a little smoothed out transition fold

and cyanotic mucous tunic. No intoxication is observed and the general condition is almost not affected.

Treatment including: 1. Extraction or treatment of the affected tooth;

Periosteotomy in the region of the infiltration with the following draining of the wound, removing of the bone structure deformity; 3. Physical treatment modes appropriate for drained wound (phonophoresis of hydrocortisone, helium-neon exposure, electrophoresis of dimethylsulfonoxidum and iodide potassium).

Pericoronitis

Pericoronitis is the inflammation of the soft tissues surrounding the tooth crown in case of maleruption.

Eruption of wisdom teeth on à mandible, moré rarely on maxilla, can be accompanied with diffèrent complications.

After emerging of cuspids, its distal surface remains closed with periosteum and gingiva. Debris and infection are accumulatingunder operculum. During mastication the operculum is injured resulting in erosion and ulcering. The infection spreading to the operculum tissues provokes inflammation.

In some cases it is possible to discover semilunar pocket behind the tooth in addition to expansion of periodontal fissure on an X-ray. It is considered that spreading of pericoronal space distal to the tooth crown up to 2 mm is a normal feature. In case of its enlargement, pathologic process can arise. Semilunar resobtion of the bone occurs behind wisdom tooth (Vassmund’s demilune). Bone resorbtion behind wisdom tooth is caused by chronic inflammation. In that case bony pocket is a reservoir for microorganisms. Later it gets closed and periodontal cyst can appear.

Classification of complications related with impacted wisdoms (according to Magid and Steinberg, 1970):

I. Inflammatory processes, spreading into soft tissues, covering and surrounding a tooth:

1. Acute pericoronitis:

a) catarrhal (serous); b) mattery; c) ulcerous

2. Chronic pericoronitis.

II. Pathological processes, which are effecting soft tissues, surrounding a lower jaw:

1. Acute purulent periostitis.

2. Abscesses and phlegmons.

3. Ulcerous stomatitis.

HI Pathological processes of the mandible:

1. Odontogenous osteomyelitis:

a) acute; b) chronic

2. Periodontal cysts

IV Other complications (lesions of adjacent teeth, neuralgias, neuritis etc.).

In most authors opinion (A. T. Rudenko, 1961, 1971; E. A. Magid, V. M. Shteinberg. 1970, 1981, and other), wisdom teeth erupt at the age from 18 to 33. In this age, pericoronitis (acute and recurrent), lymphadenitis, abscesses and phlegmons are mostly reported. At the age of 26-30 periostitis and osteomyelitis are mainly observed.

Classification of complications related with impacted wisdoms (I. P. Gor- zov, 1975)

A. Subsequent complications related to impacted teeth

I. Pericoronitis

1. Acute:

a) acute; b) purulent; c) ulcerous.

2. Recurrent chronic.

II. Other complications

1. Complications related to adjacent teeth: a) caries; b) pulpitis; c) periodontitis.

2. Periodontal cyst.

3. Neuralgias of the III division of trigeminal nerve — symptomatic.

B. Complications of pericoronitis ' -

1. Acute purulent periostitis of the mandible.

2. Abscesses, phlegmons in surrounding soft tissues.

3. Osteomyelitis of the mandible: a) acute; b) chronic.

4. Ulcerous stomatitis.

Concerning the late (50-60 year eruption of wisdom teeth, in most cases it is related to their passive baring as a result of atrophy of toothless alveolar process.

Pericoronitis is an inflammation of soft tissues, surrounding the crown of the wisdom tooth, at its incomplete eruption or maleruption. This complication is the most frequent. Depending on a clinical course, pericoronitis can be acute or chronic, early or late recurrent.

Pericoronitis arises because of trauma of mucosa above wisdom tooth. Soft tissues above a crown during mastication are easily injured. Microorganisms and debris can get into pocket having formed and cause inflammatory process.

A disease begins with the unpleasant feelings at the site of unerupted wisdom tooth. Soon pain in swallowing, difficulty of the opening the mouth, nausea, headache, anorexia, sleep disturbance, arising of body temperature occur. There are catarrh, festering and ulcerous pericoronitis depending on the clinical form. In catarrh inflammation operculum is hyperemic, swollen and infiltrated. In general there is no exertions from operculum, but in some cases serous exudate can be. In the purulent edema, hyperemia and infiltration of soft tissues increase, a pus from operculum is reported. Pain becomes more intensive, it can irradiate through adjacent trigeminal branches, jaw stiffness appears. In ulcerous form, the ulceration of flap can be observed. This process occurs due to constant injury of the gum with occlusion of antagonists. Ulcerous pericoronitis can be complicated with ulcerous stomatitis. The general condition of the patient gets worse, the temperature of body rises, pain increases, a bad odor appears from the mouth. The main feature of ulcerous stomatitis associated with pericoronitis is a lesion of soft tissues adjacent mandible on the similar side. Ulceration spreads on cheek mucosa, which is not typical for ordinary ulcerous gingivitis.

Clinical signs of chronic pericoronitis are scanty. Local symptoms are less expressed in comparing with acute forms. Opening of the mouth is free. There are serous or mattery discharges from operculum. In acute condition, symptoms of inflammation may appear.

Maleruption is often associated with acute lymphadenitis. Lymphadenitis quite often has chronic course.

Inflammatory infiltration of soft tissues adjacent lymphatic nodes is called periadenitis, and suppuration of lyphatic node is adenoabscess. Spreading of the infection and festering of surrounding soft tissues is called adenophlegmon.

The hidden nidus of infection, which is disposed under the operculum can cause cellulitis.

In recurrent pericoronitis small portions of infection infiltrate into adjacent soft tissues causing subcutaneous odontogenous granuloma.

Spreading of inflammatory process from a bony pocket and soft tissues to the periosteum leads to acute periostitis of jaw. Pain becomes more intensive, radiates through trigeminal branches, jaw stiffness appears. As a result of localization of inflammatory process on the internal surface of body or branch of a mandible there is a pain during swallowing. There is hyperemia, swelling and infiltration of gingiva. Quite often an inflammatory process spreads to pterygomandibular fold and palatine arch provoking parapharingeal abscess.

Odontogenous osteomyelitis of the mandible has severe course as a result of wisdom impaction, and localized in the ramus, rarely in the body of the mandible.

Treatment of inflammatory complications related to the impacted teeth.

It is indicated to remove the impacted tooth, when pericoronitis arises. Decision about tooth preservation depends on tooth position and lesion in bone adjacent to the impacted tooth. Complications manifested with abscesses and cellulitis require surgery treatment to provide adequate drainage.

Osteomyelitis of the jaws

Osteomyelitis is an inflammation of bone. The inflammatory process may spread through the bone to involve the marrow, cortex, cancellous portion, and periosteum. In the jaws osteomyelitis usually is caused by pyogenic organisms that reach the bone marrow from abscessed teeth or postsurgical infection. However, in some instances no source of infection can be identified, and hematogenous spread is presumed to be the origin. In some patients no infectious organisms can be identified, possibly because of previous antibiotic therapy or inadequate methods of bacterial isolation. Bacterial colonies also may be present in small, isolated pockets of bone that may be missed during sampling.

In patients with osteomyelitis, the bacteria and their products stimulate an inflammatory reaction in bone, causing destruction of the endosteal surface of the cortical bone. This destruction may progress through the cortical bone to the outer periosteum. In young patients, in whom the periosteum is more loosely attached to the outer cortex of bone than it is in adults, the periosteum is lifted up by inflammatory exudate, and new bone is laid down. This periostal reaction is a characteristic but not pathognomonic feature of osteomyelitis. The infection becomes established in the calcified portion of bone when pus in the medullary cavity and beneath the periosteum compromises or obstructs the blood supply. Following ischemia the infected bone becomes necrotic.

Classification of the jaw ostheomyelitis by etiology:

• Odontogenous j— 12 % of patients in maxillofacial clinics.

• Hematogenous — mostly in infants, sepsis of the newborns.

• Traumatic — after jaw fractures. ,

f Specific (certain etiologic microbial factor!).-

• Contact (present not in all classifications).

By the phase of the disease:, acute (serous and purulent); subacute (identified not by all authors); chronic (destroyed and profilirative forms).

It is indicated to remove the impacted tooth, when pericoronitis arises. Decision about tooth preservation depends on tooth position and lesion in bone adjacent to the impacted tooth. Complications manifested with abscesses and cellulitis require surgery treatment to provide adequate drainage.

Osteomyelitis of the jaws

Osteomyelitis is an inflammation of bone. The inflammatory process may spread through the bone to involve the marrow, cortex, cancellous portion, and periosteum. In the jaws osteomyelitis usually is caused by pyogenic organisms that reach the bone marrow from abscessed teeth or postsurgical infection. However, in some instances no source of infection can be identified, and hematogenous spread is presumed to be the origin. In some patients no infectious organisms can be identified, possibly because of previous antibiotic therapy or inadequate methods of bacterial isolation. Bacterial colonies also may be present in small, isolated pockets of bone that may be missed during sampling.

In patients with osteomyelitis, the bacteria and their products stimulate an inflammatory reaction in bone, causing destruction of the endosteal surface of the cortical bone. This destruction may progress through the cortical bone to the outer periosteum. In young patients, in whom the periosteum is more loosely attached to the outer cortex of bone than it is in adults, the periosteum is lifted up by inflammatory exudate, and new bone is laid down. This periostal reaction is a characteristic but not pathognomonic feature of osteomyelitis. The infection becomes established in the calcified portion of bone when pus in the medullary cavity and beneath the periosteum compromises or obstructs the blood supply. Following ischemia the infected bone becomes necrotic.

Classification of the jaw ostheomyelitis by etiology:

• Odontogenous — 12 % of patients in maxillofacial clinics.

• Hematogenous — mostly in infants, sepsis of the newborns.

• Traumatic — after jaw fractures.

• Specific (certain etiologic microbial factor!).

• Contact (present not in all classifications).

By the phase of the disease:h2iCMte (serous and purulent); subacute (identified not by all authors); chronic (destroyed and profilirative forms).

By the localization and spread of the process:

1. Localized — around 2-3 teeth.

2. Regional — alveolar process, body or ramus.

3. Diffuse — total affection of the whole or half of the jaws.

Theories of pathogenesis:

1. Infection and embolic theory (Bobrov, Lexner).

2.Infection and allergenic theory (S. Derizhanov).

3. Neuro-trofic theory (G. Semenchenko).

4. Neuro-humoral theory (M. Solovjov).

5. Microcirculation theory.

6. Theory of infection with immune suppression (J. Jusubov).

7. Multifactorial theory.

Acute phase osteomyelitis The acute phase of osteomyelitis is caused by infection that has spread to the bone marrow. With this condition, the medullary spaces of the bone contain an inflammatory infiltrate consisting predominantly of neutrophils and, to a lesser extent, mononuclear cells. In the jaws the most common source of infection is a periapical lesion from a nonvital tooth. Infection also can occur as a result of trauma or hematogenous spread.

Predisposing factors:

The low incidence of osteomyelitis of the jaws is remarkable considering the high frequency and severity of odontogenic infections. This low incidence is a result of fine balance between the host resistance and the virulence of the microorganism.

The virulence of the microorganisms ip-addition to any conditions altering the host defense mechanism and alteration of] aw vascularity are important in the onset and severity of osteomyelitis

Systemic conditions that alter the host’s resistance and influence profoundly the course of the disease include:

Diabetes mellitus, autoimmune disorders, agranulocytosis, anemia, especially sickle cell, leukemia, AIDS, syphilis, malnutrition, chemotherapy for cancer, steroid drug use. *

The importance of controlling these conditions in order to achieve proper response from the treatment of osteomyelitis cannot be emphasized enough. Alchohol and tobacco use are frequently associated with osteomyelitis.

Conditions that alter the vascularity of bone predispose patients to develop osteomyelitis; those include: radiation, osteoporosis, osteopetrosis, Paget’s disease, fibrous dysplasia, bone malignancy and bone necrosis caused by mercury, bismuth and arsenic.

Etiology and pathogenesis:

In infants and children osteomyelitis occurs most commonly in long bones primarily form hematogenous spread. While long bone osteomyelitis in adults and the majority of cases of jaw osteomyelitis is initiated by a contiguous focus.

In the jaws contiguous spread of odontogenic infections that originate from pulpal or periapical tissues is the primary cause of the disease.

Trauma, especially not treated compound fractures, is the second leading cause.

Infection from periostitis after gingival ulcerations, lymph nodes, infected furuncles or lacerations and hematogenous origin account for an additional small number in jaw osteomyelitis.

The extensive blood supply of the maxilla makes it less prone to osteomyelitis when compared to the mandible. The thin cortical plates and the porosity of the medullary portion preclude infections from becoming contained in the bone and facilitate spread of edema and purulent discharge into adjacent tissues.

The mandible in this aspect resembles long bones with a medullary cavity, dense cortical plates and well defined periosteum. The bone marrow is composed of sinusoids rich is reticuloendothelial cells, erythrocytes, granulocytes, platelets, osteblastic precursors as well as cancellous bone, fat tissue and blood vessels.

The bone marrow is lined by the endosteum a membrane of cells containing large numbers of osteoblasts. Bone spicules radiate centrally from the cortical bone to produce a scaffold of interconnecting trabeculae.

The cortical bone has a distinctive architecture that includes longitudinally oriented haversian systems (osteons). Each osteon has a central canal and blood vessel that provide nutrients by means of canaliculi to osteocytes contained within lacunae.

Volkmann’s canals create a complex interconnecting vascular and neural network that nourishes bone and allows for repair, regeneration and function demands. These canals connect the central canals among them and with the periosteum and the marrow spaces.

An outer fibrous layer and an inner layer of osteogenic cells that constitutes the periosteum, envelopes the cortical bone.

Compromise of blood supply is critical factor in establishment of osteomyelitis.

The primary blood supply to the mandible is from the inferior alveolar artery, while the periosteal supply is a secondary source.

The venous drainage from the mandible is directed to the pharyngeal plexus and to the external jugular vein.

Acute inflammation that causes hyperemia increased capillary permeability and infiltration of granulocytes is the process that leads to osteomyelitis.

Proteolytic enzymes are released and along with destruction by bacteria and vascular thrombosis ensue cause tissue necrosis.

If this pus is not walled off by the host and an abscess is not created or if the pus does not escape to surrounding soft tissue from the medullary bone then the process of osteomyelitis is initiated.

Necrotic tissue, dead bacteria within WBCs (pus) accumulate increasing intra- medullary pressure resulting in vascular collapse, venous stasis and ischemia.

Pus travels through the Haversian system and the nutrient canals and accumulates beneath the periosteum which gets elevated from the cortex and further decreases the blood supply. The inferior alveolar neurovascular bundle is compressed further accelerating thrombosis and ischemia and results in osteomyelitis induced inferior alveolar nerve dysfunction. If the pus continues to accumulate then the periosteum is penetrated and mucosal and cutaneous abscess and fistulas may develop.

The periosteum in children is less well bound to the cortical bone thus allowing for more extensive elevation. As host defences are more effective and the therapy becomes more effective the process may become chronic. After the acute Inflammation regress, necrotized bone gets separated from the vital one forming sequestra. Small sections of bone may become completely lysed while larger ones may become isolated by a bed of granulation tissue encased in a sheath of new bone (involucrum). Sequestra may follow any of the following routes: may be revascularized, remain quiescent, resorb, or become chronically infected requiring surgical removal for complete resolution of the infection. When the involocrum is penetrated by channels, called cloacae, the pus escapes to the epithelial surface creating fistulas.

Microbiology

Appropriate collection and transportation of cultures are essential in accurate diagnosis and initiation of appropriate therapy. Repeated cultures, especially in cases of chronic osteomyelitis and chronic antibiotic therapy, are paramount for identification and isolation of the involved pathogen.

Appropriate collection and handling of specimen along with culture of all sequestra cannot be emphasized enough. Staphylococcus Aureus and epidermis were, until recently, estimated to be involved in jaw osteomyelitis 80-90% of the times. With more sophisticated methods of collection and appropriate handling of cultures

a hemolytic streptococcus is recognized as the primary organism along with oral anaerobes e.g. Peptostreptococcus, Fusobacterium and Provotela species.

Eikenella corrodens is isolated in high percentages form cultures along with Klesbsiella, Pseudomonas and Proteus species. Antibiotic treatment should therefore be directed towards Streptococcus spp and anaerobes and not towards staph. Staphylococcus spp are the most common organisms recovered from long bones in adults and are the most prominent in children and infants osteomyelitis.

Clinical Features

The acute phase of osteomyelitis can affect people of all ages, and it has a strong male predilection. It is much more common in the mandible than in the maxilla, possibly because of the poorer vascular supply to the mandible. The typical signs and symptoms of acute osteomyelitis are rapid onset, pain, swelling of the adjacent soft tissues, fever, lymphadenopathy, and leukocytosis. The associated teeth may be mobile and sensitive to percussion. Purulent drainage also may be present. Paresthesia of the lower lip in the third division of the fifth cranial nerve distribution is not uncommon. Peculiarities and differences if clinical flow of the mandible and maxillary osteomyelitis are presented in Table 12.1.

| Table 12.1.

Peculiarities and differences of clinical flow of the mandible and maxillary osteomyelitis

|In mandible |In maxilla |

|More prolonged and severe process, determined by mandible architectonics. |Process is less severe (bone is more porotic and thin. It promotes the evacuation|

|More often transformation into chronic phase. |of suppurative exudates). |

|Severe complications with infection spread into the neck spaces and |Always accompanied by sinusitis. |

|mediastinum. |Transformation into the chronic phase is rare. |

|Disorders in bone microcirculation determined by block of the, alveolaris |Sequestration of the bone is more frequent and less pronounced than in mandible. |

|inferior artery. | |

Radiographic features

Very early in the disease, no radiographic changes may be identifiable. The bone may be filled with inflammatory exudate and inflammatory cells and may show no radiographic change. The most common location is the posterior body of the mandible. The maxilla is a rare site. Acute osteomyelitis most often presents an ill-defined periphery with a gradual transition to normal trabeculae.

The first radiographic evidence of the acute form of osteomyelitis is a slight decrease in the density of the involved bone, with a loss of sharpness of the existing trabeculae. In lime the bone destruction becomes more profound, resulting in an area of radiolucency, in one focal area or in scattered regions throughout the involved bone. Later, the appearance of sclerotic regions becomes apparent. Sequestra may be formed which means the transformation to the chronic stage. In this stage they become more apparent and numerous. Acute osteomyelitis can stimulate either bone resorption or bone formation.

Portions of cortical bone may be resorbed. An inflammatory exudate can lift the periosteum and stimulate bone formation. Radiographically, this appears as a thin, faint, radiopaque line adjacent to and almost parallel or slightly convex to the surface of the bone. A radiolucent band separates this periosteal new bone from the bone surface. As the lesion develops into a more chronic phase, cyclic and periodic acute exacerbations may produce more inflammatory exudate, which again lifts the periosteum from the bone surface and stimulates the periosteum to form a second layer of bone. This is detected radiographically as a second radiopaque line almost parallel to the first and separated from it by a radiolucent band. This process may continue and may result in several lines (an onion-skin appearance), and eventually a massive amount of new bone may be formed. This is referred to as proliferative periostitis and is seen more often in children. The effects on the teeth and lamina dura may be the same as those described for periapical inflammatory lesions.

A two-phase nuclear medicine study composed of a technetium bone scan followed by a gallium citrate scan may help to confirm the diagnosis. With inflammatory lesions, a positive result on the technetium scan indicates increased bone metabolic activity, and a positive result on the gallium scan in the same location indicates an inflammatory cell infiltrate.

The differential diagnosis of the acute phase of osteomyelitis may include fibrous dysplasia, especially in children. Aside from the clinical signs of acute infection, the most useful radiographic characteristic to distinguish osteomyelitis from fibrous dysplasia is the way the enlargement of the bone occurs. The new bone that enlarges the jaws in osteomyelitis is laid down by the periosteum and therefore is on the outside of the outer cortical plate. In fibrous dysplasia the new bone is manufactured on the

inside of the mandible; thus the outer cortex, which may be thinned, is on the outside and contains the lesion. This point of differentiation is important because the histologic appearance of a biopsy of new periosteal bone in osteomyelitis may be similar to that of fibrous dysplasia, and the condition may be reported as such.

Malignant neoplasia (e.g., osteosarcoma, squamous cell carcinoma) that invades the mandible at times may be difficult to differentiate from the acute phase of osteomyelitis, especially if the malignancy has been secondarily infected via an oral ulcer; this may result in a mixture of inflammatory and malignant radio- graphic characteristics. If part of the inflammatory periosteal bone has been destroyed, the possibility of a malignant neoplasm should be considered. The differential diagnosis may include other lesions that can cause bone destruction and may stimulate a periosteal reaction that is similar to that seen in inflammatory lesions. Langerhans’ cell histiocytosis causes lylic ill-defined bone destruction and often results in the formation of periosteal reactive new bone. This lesion rarely stimulates a sclerotic bone reaction such as that seen in osteomyelitis. Leukemia and lymphoma may stimulate a similar periosteal reaction.

Management

As with all inflammatory lesions of the jaws, removal of the source of inflammation is the primary goal of therapy. Antimicrobial treatment is the mainstay of treatment of acute osteomyelitis, along with establishing drainage. This may entail removal of a tooth, root canal therapy, or surgical incision and drainage.

Acute Suppurative osteomyelitis:

The initial management usually is aided by hospitalization to administer high doses of antibiotic therapy, identify and correct host compromise factors and eliminate the cause (removal of a tooth), surgical incision and drainage, osteoperforation of the cortical plates, irrigation by antiseptics, antibiotics, enzymes, drainage and irrigation of the maxillary sinus and systemic: antibiotics, non steroid analgetics, désintoxication; immune correction, hyposensibilization, symptomatic.

Since many organisms are responsible for osteomyelitis and are resistant to penicillin, a drug effective against those should be added to the regiment.

Examples are: Penicillin + Metronidazole, Amoxicillin + Metronidazole, Amoxicillin + Clavulanate potassium and Ampicillin + Sulbactam sodium. Other effective regiments are Clindamycin, Clindamycin + metronidazole and Cephalosporines.

There are complications of the jaw osteomyelitis which could be divided into local: bone defects, resorbtive fractures, teeth and foliculi loss, affection of the jaw growth and general: sepsis, generalized infection, toxic shock.

The main factors of the chronic osteomyelitis development include: delay in medical care; inadequate treatment; insufficiency of the compensatory mechanisms.

Chronic odontogenous osteomyelitis of the jaw

The chronic phase of osteomyelitis may be a sequela of inadequately treated acute osteomyelitis, or it may arise de novo. The hallmark of osteomyelitis is the development of sequestra. A sequestrum is a segment of bone that has become necrotic because of ischemic injury caused by the inflammatory process. Numerous forms of osteomyelitis have been described. For the sake of simplicity, we group them into two major phases, acute and chronic, recognizing that these represent two ends of a continuum without a definite separating boundary in the process of bone inflammation. If not controlled within 10-14 days after onset, then subacute suppurative ostemyelitis is established. Pus travels through haversian canals and accumulates under the periosteum which penetrates to spread through to soft tissues. Deep pain, malaise fever and anorexia are present. Teeth are sensitive to percussion and become loose. Pus may be seen around the sulcus of the teeth or through skin fistulas and is associated with fetid odor. The skin overlying the effected bone is warm, erythematous, tender to touch; firm cellulites with expansion of bone from periosteal activity and paresthesia of mental nerve, regional lumphadenopathy are usually present. Mild leukocytosis with a left shift and mildly elevated ESR are present but are not valid indicators of the course or the extent of the disease. If inadequately treated the progression to subacute or chronic form is warranted. Findings are limited to fistulas, induration of soft tissues with a thickened or wooden character to the affected area with pain and tenderness.

Primary chronic form is not preceded by an episode of acute symptoms, is insidious in onset with onset of mild pain, slow increase of jaw size and gradual development of sequestra, often without fistulas. Other forms of osteomyelitis have been described as separate and distinct clinicopathologic entities with unique radiographic features. These are Garre’s osteomyelitis and diffuse sclerosing osteomyelitis. They are considered to be the part of the same continuum. Garre’s osteomyelitis is» an exuberant periosteal response to inflammation. Diffuse sclerosing osteomyelitis is a chronic form of osteomyelitis with a pronounced sclerotic response. It is important to understand that all these variations of osteomyelitis have the same underlying process of bone’s response to inflammation. The features expressed by each subtype represent only variations in the type and degree of bone reaction. Osteomyelitis may resolve spontaneously or with appropriate antibiotic

intervention. However, if the condition is not treated or is treated inadequately, the infection may persist and become chronic in about 20% of patients. Some chronic systemic diseases, immunosuppressive states, and disorders of decreased vascularity may predispose an individual to the development of osteomyelitis. For example, osteopetrosis, sickle cell anemia, and acquired immunodeficiency syndrome (AIDS) have been documented as underlying factors in the development of osteomyelitis.

Radiographic Features. As in the acute phase of osteomyelitis, the most common site is the posterior mandible. The periphery may be better defined than in the acute phase, but it is still difficult to determine the exact extent of chronic osteomyelitis. Usually a gradual transition is seen between the normal surrounding trabecular pattern and the dense granular pattern characteristic of this disease. When the disease is active and is spreading through bone, the periphery may be more radiolucent and have poorly defined borders. The internal structure comprises regions of greater and lesser radiopacity compared with surrounding normal bone. Most of the lesion usually is composed of the more radiopaque or sclerotic bone pattern. In older, more chronic lesions the internal bone density can be exceedingly radiopaque and equivalent to cortical bone. The rentgenogram shows irregular destruction of the bone tissue and sequestra. Sequestra on the upper jaw are formed during 3-4 weeks, while the sequestra on the lower jaw — during 5-6 weeks since the onset of the disease (Fig. 12.9).

In these cases no obvious regions of radiolucency may be seen. In other cases, small regions of radiolucency may be scattered throughout the radiopaque bone.

[pic]

Fig. 12.9. Irregular destruction of the bone tissue and sequestra

A close inspection of the radiolucent regions may reveal an island of bone or sequestrum within the center. Often the sequestrum appears more radiopaque than the surrounding bone (Fig. 12.10). Detection may require illumination of the radiolucent regions of the film with an intense light source.

CT is superior for revealing the internal structure and sequestra, especially in cases with very dense sclerotic bone. The bone pattern usually is very granular, obscuring individual bone trabeculae. Sequestra can be identified by closely inspecting a region of bone destruction (radiolucency) for an island of bone. This island of nonvital bone may vary from a small dot (smaller sequestra usually arc seen in young patients) to larger segments of radiopaque bone.

Computed tomography (CT) is the imaging method of choice. CT reveals more bone surface for detecting periosteal, new bone and is the best imaging method for detecting sequestra.

Chronic osteomyelitis often stimulates the formation of periosteal new bone, which is seen radiographically as a single radiopaque line or a series of radiopaque lines (similar to onion skin) parallel to the surface of the cortical bone. Over time the radiolucent strip that separates this new bone from the outer cortical bone surface may be filled in with granular sclerotic bone. When this occurs, it may not be possible to identify the original cortex, which makes it difficult to determine whether the new bone is derived from the periosteum. After a considerable amount of time the outer contour of the mandible also may be altered, assuming an abnormal shape, and the girth of the mandible may be much larger than on the unaffected side. The roots of teeth may undergo external resorption, and the lamina dura may become less apparent as it blends with the surrounding granular sclerotic bone. If a tooth is nonvital, the periodontal ligament space usually is enlarged in the apical region. In patients with extensive chronic osteomyelitis, the disease may slowly spread to the mandibular condyle and into the joint, resulting in a septic arthritis. Further spread may involve the

Fig. 12.10. Sequester formation at different areas of mandible

inner ear and mastoid air cells. Chronic lesions may develop a draining fistula, which may appear as a well-defined break in the outer cortex or in the periosteal new bone.

Differential diagnosis

Very sclerotic, radiopaque chronic lesions of osteomyelitis may be difficult to differentiate from fibrous dysplasia, Paget’s disease, and osteosarcoma. In children, osteomyelitis with a proliferative periosteal response may be misinterpreted as fibrous dysplasia. Differentiation of the chronic form of osteomyelitis may be even more difficult if considerable remodeling and loss of a distinct original cortex have occurred. In these cases, inspection of the bone surface at the periphery of the lesion may reveal subtle evidence of periosteal new bone formation. The presence of sequestra indicates osteomyelitis. Paget’s disease affects the entire mandible, which is rare in osteomyelitis. Periosteal new bone formation and sequestra are not seen in Paget’s disease. Dense, granular bone may be seen in some forms of osteosarcoma, but usually evidence of bone destruction is found. A characteristic spiculated (sunray-like) periosteal response also may be seen. As mentioned in the section on acute osteomyelitis, other entities such as Langerhans’ cell histiocytosis, leukemia, and lymphoma may stimulate a similar periosteal response, but these usually produce evidence of bone destruction.

The imaging method of choice for aiding in the differential diagnosis is CT because of its ability to reveal sequestra and periosteal new bone. Also, CT allows accurate staging of the disease * which is important for future assessment of healing. Scintigraphy using bone scans, gallium, or labeled white blood cells is not particularly useful for differential diagnosis. Bone scans indicate increased bone formation, which is nonspecific, and often gallium scans (which highlight inflammatory cells) are not supportive.

Management

Chronic osteomyelitis tends to be more difficult to eradicate than the acute fonn. In cases involving an extreme osteoblastic response (very sclerotic mandible), the subsequent lack of a good blood supply may work against healing. Hyperbaric oxygen therapy and creative modes of long-term antibiotic delivery have been used with limited success. Surgical intervention, which may include sequestrectomy, decortication, or resection, often is necessary. The probability of successful treatment, especially when using long-term antibiotic therapy with decortication, is greater in the first two decades of life.

Principles of treatment are :

1. Evaluation and correction of compromised host defenses.

2. Gram staining and culture and sensitivity testing.

3. Imaging of the region to determine the extend of the lesion and to rule out the presence of tumors.

4. Empirical administration of Gram stain-guided antibiotics.

5. Removal of loose teeth and sequestra.

6. Prescription of culture-guided antibiotic therapy.

7. Possible placement of irrigating drains / polymethylmethacrylate antibiotic beads.

8. Sequestrectomy, debridement, decortication, resection or reconstruction as indicated.

Hyperbaric oxygen therapy, it has been used to promote healing in refractory chronic osteomyelitis. In situations in which osteomyelitis is associated with decreased systemic blood flow (e.g., in diabetes, vasculitis) or segmental blood flow (eg, in trauma), hyperbaric oxygen therapy may be used as adjunctive therapy. Reduced oxygen tensions in infected bone have been shown to interfere with normal polymorphonuclear leukocyte activity. Hyperbaric oxygen therapy has been shown to increase the oxygen tensions within infected bone, thereby augmenting polymorphonuclear leukocyte and macrophage activity.

Wound healing is a dynamic process that requires an adequate oxygen tension to proceed. In the ischemic or infected wound, hyperbaric oxygen therapy provides oxygen to promote collagen production, angiogenesis, and ultimately wound healing. Referral for hyperbaric oxygen is made whenever refractory osteomyelitis occurs or a soft tissue infection develops that is not amenable to a local or microvas- cular flap.

Surgical therapy: Surgical management of contiguous focus osteomyelitis can be very challenging. The principles of treating any infection are equally applicable to the treatment of infection in bone. These include adequate drainage, extensive debridement of all necrotic tissue and obliteration of dead spaces, stabilization, adequate soft tissue coverage and restoration of an effective blood supply.

The number and nature of the required surgical procedures increases with thé severity of the infection, which can be divided into 4 categories, as follows:

• Category 1 — Removal of necrotic tissue by extensive debridement

• Category 2 — Dead space obliteration with flaps, antibiotic beads, and bone grafts

• Category 3 — Provision of soft tissue coverage of the bone

• Category 4 — Stabilization of bone by external or open reduction and internal fixation

Category 1

Debridement surgery is the foundation of osteomyelitis treatment. It is the most commonly performed procedure and may need to be repeated multiple times. The goal of debridement is to reach healthy, viable tissue, but even when all necrotic tissue has been adequately debrided, the remaining bed of tissue must be considered contaminated with the responsible organism. Debridement should be direct, atraumatic and executed with reconstruction in mind. All dead or ischemic hard and soft tissue is excised unless a noncurative procedure has been chosen. Surgical excision of bone is carried down to uniform haversian or cancellous bleeding, known as the paprika sign.

Sequestrectomy: sequestra which can be cortical or cortico-cancelous are usually seen after 2 weeks from the onset of the infection and once fully formed can persist for several months. Sequastra are avascular therefore poorly penetrated by antibiotics. Sequastra can be removed with minimaltrauma, but the risk of subjecting the patient to a chronic infection and prolong antibiotic treatment should be bared in mind.

Sequestectomy and Saucerization: saucerization is the unroofing of the bone to expose the medullary cavity. This is usefull in chronic osteomyelitis, since it permits excision of sequestra either formed or forming ones. It should be performed as soon as the acure stage has resolved, so to decompress the bone allow for extrusion of pus, debris and avascular bone.

Procedure

A full thickness mucoperiosteal flap is reflected usually buccaly, to exposed infected bone. Reflection should not comprise blood supply.

Loose teeth and bony sequestra are removed.

The lateral cortex of the mandible is reduced, until bleeding bone is encountered, producing a saucerlike defect.

All granulation tissue and loose bony fragments are removed, irrigation follows and hemostasis is achieved.

The wound is packed lightly with gauze covered with triple antibiotic ointment and the flap is loosely sutured over. The packing is removed 3-6 days and is replaced several times until the surface of the bone is epithelialized.

There is minimal or no risk of fracture in the jaws with this type of procedure unlike long bones. In long bones primary closure and immediate bone graft may be required.

Saucerization is rarely required for the maxilla.

Decortication

First introduced in 1917 and further described by Mowlem, decortication involves removal of the chronically infected cortex, usually the buccal and the inferior border are removed 1-2 cm beyond the affected area. It can be used as initial treatment of primary or secondary chronic osteomyelitis or more commonly when initial conservative treatment has failed.

Procedure

Full thickness mucoperiosteal flap is reflected buccaly and extends to the inferior border.

Involved teeth are removed.

The buccal cortex and the inferior borders are removed until bleeding bone is encountered.

Primary closure is achieved and pressure dressing is applied to maintain close contact of the bone bed to the vascular soft tissue. Irrigation tubes and or antibiotic beads may be placed.

If extensive debridement is required and the remaining bone is suspected to be prone to fracture, appropriate stabilization and reconstruction should be performed.

Resection and reconstruction

May be required for low-grade persistent or chronic osteomyelitis. It is especially used in cases of persisted infection after decortication, marked disease involving both buccal and lingual cortices and in cases of pathologic fractures.

Category 2

Adequate debridement may leave a large bony defect (dead space). Appropriate management of dead space created by debridement surgery is mandatory in order to arrest the disease and to maintain the integrity of the skeletal part. The goal of dead space management is to replace dead bone and scar tissue with durable vascularized tissue. Local tissue flaps or free flaps may be used to fill dead space. An alternative technique is to place cancellous bone grafts beneath local or transferred tissues where structural augmentation is necessary. Careful preoperative planning is critical for conservation of the patient’s limited cancellous bone reserves. Open cancellous grafts without soft tissue coverage are useful when a free tissue transfer is not a treatment option and local tissue flaps are inadequate.

Complete primary or delayed primary wound closure should be performed whenever possible. Suction irrigation systems are not recommended because of the high incidence of associated nosocomial infections and the unreliability of the ap-

paratus. Healing by secondary intent is also discouraged since the scar tissue that fills the defect may later become avascular. Antibiotic-impregnated acrylic beads can be used to sterilize and temporarily maintain dead space. The beads are usually removed within 2-4 weeks and replaced with a cancellous bone graft. The most commonly used antibiotics in beads are vancomycin, tobramycin and genta- micin. Local delivery of antibiotics (amikacin, clindamycin) into dead space also can be achieved with an implantable pump.

Category 3

Adequate coverage of the bone by soft tissue is necessary to arrest osteomyelitis. Most soft tissue defects are closed primarily, but small soft tissue defects may be covered with a split thickness skin graft. In the presence of a large soft tissue defect or an inadequate soft tissue envelope, local muscle flaps and free vascularized muscle flaps may be placed in a 1- or 2-stage procedure.

Local and free muscle flaps, when combined with antibiotics and surgical debridement of all nonviable osseous and soft tissue for chronic osteomyelitis, have a success rate ranging from 65% to 100%. Local muscle flaps and free vascularized muscle transfers improve the local environment by supplying blood vessels, which are critical for host defense, antibiotic delivery, and osseous and soft tissue healing.

Category 4

If movement is present at the site of infection, measures must be taken to achieve permanent stability of the skeletal unit. Stability can be achieved with plates, screws, rods, and/or an external fixator. One type of external fixation allows bone reconstruction of segmental defects and difficult infected nonunions. The II- izarov external fixation method uses the theory of distraction histogenesis, in which bone is fractured in the metaphyseal region and slowly lengthened. The growth of new bone in the metaphyseal region pushes a segment of healthy bone into the defect left by surgery. The Ilizarov technique is used for difficult cases of osteomyelitis when stabilization and bone lengthening are necessary. It also can be used to compress nonunions and correct malunions, and in a small group of patients for reconstruction of difficult deformities that result from osteomyelitis.

However, this technique is labor intensive and requires an extended period of treatment, averaging 9 months in the device. The Ilizarov pins usually become infected, and the device is painful. Infected pseudoarthrosis with segmental osseous defects can be treated by debridement and microvascular bone transfers. Vascularized bone transfer is also useful for the treatment of infected segmental osseous

defects of long bones that are more than 3 cm in length. Vascularized bone transfers can be placed after 1 month without clinical evidence of infection.

Loss of bone stability, bone necrosis, and soft tissue damage frequently occur in contiguous focus osteomyelitis. Surgical debridement of infected bone and soft tissue provides specimens for culture and hastens eradication of the infection. Other steps in the surgical management of contiguous focus osteomyelitis should be tailored to the specific anatomy of the bone infection. When osteomyelitis is characterized by a full thickness, cortical sequestration, patients usually can be treated with removal of the dead infected bone (bone saucerization). Bone grafting may be necessary to augment structural support. These patients may require external fixation for structural support while the bone graft incorporates. Complex reconstruction of both bone and soft tissue is frequently necessary.

In some cases, osteomyelitis progresses to an infection involving the entire diameter of the bone. These patients often require an intercalary resection of the bone in order to arrest the disease process. Since this advanced stage of osteomyelitis involves an entire through-and-through section of bone, a loss of bony stability occurs either before or after debridement surgery. As a result, treatment often must be directed toward establishing structural stability and obliterating debridement gaps by means of cancellous bone grafts or the Ilizarov technique. Vascularized bone grafting is the other possible treatment modality.

Abscesses and phlegmons of the maxillofacial region

Phlegmon — (Greek inflammation) — diffuse purulent inflammation of hypo- dermal, submocousal, intermuscle and interfascial cellular tissue.

Abscess — localized purulent inflammation which occurs as a result of purulent desintigration of hypodermal, submocousal, intermuscle and interfascial cellular tissue or lymphatic nodes.

Microorganisms are the main etiology factor in beginnings of purulent inflammation, which are distinguished by aerobes (78.8%), anaerobes — 21.2%. Monoculture — 67.5% (aerobes — 56.7%, anaerobes — 8.8%). Aerobes — staphylococcus aureus, staphylococcus epidermidis, E. coli, St. haemoliticus, enterococcus, proteus, diplococci. Anaerobes Gr(-) — bacteroides, streptococci — 19% (floor of the oral cavity) Gr(+) — peptostreptococci, eubacteria — 10%. In monoculture St. epidermidis, veilonellae, peptostreptococci was inoculated.

Sources of infection include odontognic (84%), stomatogenic (gingival, mucosal), endosseous, salivary, tonsillar, rhinogenic, otogenic.

For optimal planning of approach to inflammation nidus against anatomic location in soft tissue, there is clinical anatomic classification of abscesses and phlegmons.

I. Abscesses and phlegmons at maxilla:

• Infraorbital region;

• Zygomatic region;

• Orbital area (upper and lower eyelids);

• Temporal region;

• Infratemporal and pterygopalatine fossa;

• Hard and soft palate.

II. Abscesses and phlegmons at the mandible:

• Submental space;

• . • Buccal area;

• Submandibular area;

• Pterygomandibular space;

Parapharingeal space;

• . Submasseteric (masseteric) space, parotid region;

• Retromandibular fossa.

III. Abscesses and phlegmons of the flooi; of the mouth:

• Upper division of oral cavity floor;

• Sublingual space;

• Lower division of oral cavity floor.

IV. Abscesses and phlegmons of the tongue:

• The tongue;

• The tongue root.

V. Abscesses and phlegmons of the neck:

Superficial, deep, space of neurovascular bundle, paratracheal and paraesophageal space, paravertebral space.

Classification of abscesses and phlegmons (M. V, Far bicant, 1935) Paramaxillar:

• subcutaneous.

• phlegmons of intercelular space are always diffuse.,

, • Adenophlegmons

• Osteophlegmons

Classification of abscesses and phlegmons (A.i. Evdokimov, 1964):

• Phlegmons and abscesses in anatomic regions (cheeks, orbits, zygomatic and temporal regions)

• Paramaxillar and paramandibular phlegmons

• Phlegmon of the mouth floor

• Parapharingeal

• Phlegmon of the tongue

• Phlegmon of the neck (lower than upper neck fold)

Spreading of phlegmons realize per continuitatem; through lymphatic vessels; through venous vessels; trough arterial vessels.

Clinical signs

General signs of severe intoxication are marked by nausea, anorexia, general sweating, increasing of pulse and breathing rate. Sometimes — thrombosis of face and neck veins. Significant leucocitosis in periferial blood, leukocyte shift, increasing of neutrophils, decreasing of eosinophils, ESR — up to 70 mm per hour. In more severe conditions of the patient lymphopenia develops (amount of leukocytes decreases to 10%), against the background of which eosinophiles deplete, and amount of neutrophiles increases up to 80% and more. It can be sign of toxic nephritis. Necrotic and gas phlegmons have the severest course. Thermoregulation disorders — body temperature arises to 39.5—40 °C. If general intoxication increases dramatically, and local inflammation is low it can evident about infiltration of infection through local reticuloendothelial barrier and regional lymphatic nodes, which indicates to decreasing of resistance and could be the basis for unfavorable prognosis.

Local signs rely on location:

1. Superficial phlegmons — presence of diffuse swelling is peculiar, swelling is tight and painful, skin hyperemia; skin cannot be folded, tensed and glossy; the face is asymmetric. There is a clinical case with typical signs of superficial phlegmon (Fig. 12.11).

2. Deep phlegmons (in pterygomandibular and parapharingeal space, in the depth of the tongue and so forth) skin changes and face asymmetry are absent or insignificant. Keep in mind the signs of inflammation by Halenus and Celsus: tumor, rubor, color, dolor, functio lease.

More or less significant disorder of mandible movement up to stiffness (trismus) .Impairment and severe pain in mastication and swallowing, especially in pter

ygomandibular and submasseteric phlegmons,

and in other cases, when masticatory muscles

involved in inflammation.Impairment of ar-

ticulation, speaking and breathing (as a result

of swelling of oral cavity, trachea, vocal cords).

Saliva becomes tough, viscous and it spits out

with difficulties.

By clinical course phlegmons are divided to :

1. group — mild — phlegmons located in 1

anatomic region.

2. group1— moderate — phlegmons located

in 2-3 anatomic regions.

3. group — severe — phlegmons of the mouth floor, half of the face, and two different anatomic regions.

Course severity depends on microbiotic virulence and condition of the immune system.

In case of the anaerobic phlegmon of the mouth floor (Ludwig’s angina), the clinical course is of major importance. Anaerobic infection is marked by crepitation symptom (gases are accumulated in the subcutaneous fat and are cracking during palpation, resembling the creak of snow); necrotic mass is determined during draining of the nidus; muscles achieve the colour of the boiled meat; foul, grey substance is exuded, there is no pus.

Treatment consists of such principles: 1. Drain of abscesses and phlegmons via incision (under general anaesthetic) taking into consideration their localization, spreading of the n.facialis bacillus, natural folds of face, neck and creating of the favorable conditions for exudate outflow. 2. Draining of the inflammatory nidus.

3. In case of odontogenic origin of the disease — extraction of the affected tooth.

4. Bacterial examination for determining of the microflora antibiotic susceptibility.

5. General medical treatment (anti-inflammatory, antibiotic, detox, hyposensitive, fibrinolytic, immune therapy, desagregants — aspirin, trental, ticlid).

In case of the Ludwig’s angina:

Drain of the abscesses, phlegmons, infiltrates by means of section in the sub- maxillary, retromandibular, submental regions, joined by means of the perforated tube drainage.

[pic]

Fig. 12.11. Clinical case with signs of superficial phlegmon

Creating of the highest possible conditions for aeration of the wound, its dialysis with antiseptic liquid and oxidizing substances.

Prevention of the joining of the commonplace microflora.

Anti-inflammatory, antibiotic, detox, hyposensitive, fibrinolytic, immune therapy, desagregants — aspirin, trental, ticlid.

Antigangrenous serum (preventive dose, or therapeutic dose if necessary).

Wound draining to be carried out with drains, draining sorbents, dialysis.

Sorbents: uvesorb, carbovit, carbolong, enterosgel — per os, sorbilact, rheo- sorbilact (i/v).

There are some forms of dialysis: fractional, continuous, circulating, aspirating. Detoxication includes hemosorbtion — arteriovenous shunt, plasmasorption, lym- phosorbtion. Blood processing by UV, helium — neon laser, infrared rays (for improvement of rheologic properties).

Wound management in postoperative period is distinguished by wound processing with pulsing current, vacuum processing of the wound, laser processing + photosensitive agents based on hematoporphirines — discharged oxigen amplifies antimi- crobic effect, ultrasound wound processing, cryoprocessing, hyperbaric oxigenation.

Accelaration of wound healing is reached by preparations, which stimulate wound healing, physiotherapy, diet, primary delayed sutures (2-5 day), secondary delayed — on granulating wound — 7-10-12, days. Contraindications — fever, hematogenous osteomyelitis and immune disorders (diabetes mellitus, rheumatism, poliarthritis, nephritis, chronic radial disease.), hemo-, plasma-, lymphosorbtion.

Complications

Complications of the abcesses. and phlegmons could be general: phlegmon of retrobulbal cellulae. Thrombophlebitis of facial veins, sepsis, mediastinitis, thrombosis of cavernous sinus (7.1%), purulent basal meningitis (2.6%), arachnoiditis etc.:

• in favorable course — in 13 % of patients;

• in unfavorable course — in 80 % of patients.

Pneumonia, pleuritis (metastatic — 14%, kidney abscess — 7.1%). DIC — syndrome of disseminating intravascular clotting.

Furuncle and carbuncle

Furuncle — acute purulo-necrotic inflammation of a hair follicle and surrounding tissues caused by pathogenic microorganisms, more often by staphylococcal infection.

Carbuncle — acute purulo-necrotic inflammation of several hair follicles which

are close to each other, and sebaceous glands, and also extend to surrounding tissues

(skin, hypoderm). ; ,

Predisposing factors to development of furuncles or carbuncles are skin

pollution, microtraumas, especially after squeezing out of abscesses on a skin,

increased perspire and increased fat production. Very often these processes

arise in people suffering from hypovitaminoses, with carbohydrate metabo-

lism disorders (diabetes), with parallel conditions (overheat, supercooling,

etc.).

The most dangerous in the prognostic plan are furuncles and carbuncles which

are situated in a site of the upper lip, mouth angles and infraorbital site. It is asso-

ciated with the mesh structure of piogenic membrane, which surrounds furuncles

and carbuncles, instead of formation of a solid “bank” as it is in the abscesses.

Therefore squeezing of abscesses can lead to development of dangerous to pa-

tient’s life complications. There is clinical case of furuncle of the buccal region

(Fig. 12.12).

Complication of furuncles and carbuncles can be divided on local and gen-

eral.

Local complications:

1. Cheilitis (catarral, glandularis, impetiginous).

2. Phlebitis, thrombophlebitis.

3. Lymphangitis, serous and purulent lymphadenitis, periadenitis, adeno-

phlegmons.

4. Inflammatory infiltrates,

abscesses, phlegmons.

5. Osteomyelitis.

6. Different forms of an

erysipelas.

General complications: sinus

thrombosis; meningitis; different

forms of a sepsis.

The main tasks of a doctor dur-

ing the treatment of patients with fu-

runcles and carbuncles are reduction

of the terms and prevention of the

development of local and general

complications.

[pic]

Fig. 12.12. Clinical case of furuncle of the buccal region

Erysipelas

Erysipelas (Greek spuamsAa — red skin) (also known as “Ignis sacer,” and “St

Anthony’s fire” is an acute streptococcus bacterial infection of the dermis, resulting

in inflammation and characteristically extending into underlying fat tissue.

Most cases of erysipelas are due to Streptococcus pyogenes (also known

as beta-hemolytic group A streptococci), although non-group A streptococci can

also be the causative agent. Historically, the face was most affected; today the legs

are affected most often.

Erysipelas infections can enter the skin through minor trauma, eczema, surgical

incisions and ulcers, and often originate from strep bacteria in the subject’s own

nasal passages.

Clinical forms distinguish: erythematous; erythematous bullous; erythematous

hemorrhagic; bullous hemorrhagic.

Patients typically develop symptoms including high fevers, shaking, chills, fa-

tigue, headaches, vomiting, and general illness within 48 hours of the initial infec-

tion. The erythematous skin lesion enlarges rapidly and has a sharply demarcated

raised edge (Fig. 12.13). It appears as a red, swollen, warm, hardened and painful

rash, similar in consistency to an orange peel. More severe infections can result

in vesicles, bullae, and petechiae, with possible skin necrosis. Lymph nodes may

be swollen, and lymphedema may occur. Occasionally, a red streak extending to the

lymph node can be seen.

The infection may occur on any part of the skin including the face, arms, fingers,

legs and toes, but it tends to favor the extremities. Fat tissue is most susceptible to infec-

tion, and facial areas typically around

the eyes, ears, and cheeks. Repeated

infection of the extremities can lead

to chronic swelling (lymphangoitis).

This disease is mainly diagnosed

by the appearance of well-demar-

cated rash and inflammation. Blood

cultures are unreliable for diagno-

sis of the disease, but may be used

to test for sepsis. Erysipelas must

be differentiated from herpes zos-

ter, angioedema, contact dermatitis,

and diffuse inflammatory carcinoma

Fig. 12.13. The erythematous skin lesion ofthe breast. Erysipelas can be distin-

[pic]

guished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titre occurs after around 10 days of illness.

There are some severe complications: spread of infection to other areas of body through the bloodstream (bacteremia), including septic arthritis and infective endocarditis (heart valves); septic shock; recurrence of infection — Erysipelas can recur in 18-30% of cases even after antibiotic treatment; lymphatic damage; necrotizing fasciitis; treatment.

Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.

Because of the risk of reinfection, prophylactic antibiotics are sometimes used after resolution of the initial condition.

The maxillary sinusitis

The infectious-inflammatory disease characterized by involving in the inflammatory process of the sinus mucousa.

Distinguish rhinogenic, odontogenic, allergic or an extent maxillary sinusitis.

Odontogenic maxillary sinusitis according to different authors makes from 3 to 4.2% of number of the admitted patients. Given statistical data concerning patients of the maxillofacial department as patients of the given group also can undergo treatment in ENT-department.

As a result of acute and chronic odontogenic inflammatory processes in the maxillary region there can be inflammation of maxillary sinus.

Comparatively frequent origin of odontogenic antritis is explained by the near location of apexes of the roots of the second premolar, first and second molar, more rarely — the third molar to the sinus (Fig. 12.14).

Sometimes apexes of the roots of these teeth are dissociated from the sinus by a thin bone plate, and on occasion — only by one mucus membrane (to 40% cases). These anatomic features facilitate the breach of pus in the sinus cavity at acute purulent processes in the area of the second premolar and molars and explain possibility of connection of sinus with the cavity of the mouth during extraction of tooth with its next infecting by a mouth liquid.

A chronic process near the apexes of teeth, spreading toward the sinus, can entail thinning, up to complete disappearance of bone lay er between the apex of tooth and sinus cavity and transition of inflammation to the mucous membrane of the sinus (Fig. 12.15).

Fig. 12.14. The location of apexes

1. Saggital position;

2. Horizontal position.

Fig. 12.15. Complete disappear-

ance of the teeth roots bone

layer between the apex of tooth

and sinus cavity

Also inflammatory process can extend to ossteomyelitic process or as a result of a suppuration of new growths of the upper jaw. An immediate cause of development of an inflammation is the microbie microflora. In odontogenic maxillary sinu- itis staphylococcus is more often sown -— both in a monoculture, and in microbic associations.

Odontogenic maxillary sinusitises divide into the acute, chronic, becoming aggravated chronic one. Among them is subacute, an initially-chronic sinusitis. And also they divide in opened (after perforation) and closed ones. Classification by pathologoanatomic signs: catarrhal; purulent; polypous; purulent-polypous.

Acute odontogenic maxillary sinusitis is difficult enough for differentiating from an aggravated chronic one. This proceeds and can come to an end with the treatment or transition into a chronic process. Often enough unique acknowledgement of the diagnosis is the absence of similar aggravations in the anamnesis. For a clinical picture odontogenic maxillary sinusitis are characterized by tearing pain, sense of weight in the infraorbital area, a pain can simulate that in a pulpitis, the body temperature is raises, depending on a type of reactivity. In the oral cavity causal tooth can be found, painful on percussion, an X-ray examination reveals destructive inflammatory process or cyst. On roentgenograms of the maxillary sinus opacity is observed. The maxillary sinus puncture makes it possible to finalise the diagnosis.

Local treatment consists of the creation of conditions for outflow of exudates from the maxillary sinus that is provided either by vasoconstrictive therapy or max-

[pic]

Шагу sinus puncture, and also in sanitation of odontogenic source by removal of a tooth or its endodontic treatment. It is also prescribed local and general antibacterial, hyposinsebilizating and anti-inflammatory therapy.

The chronic maxillary sinusitis often enough proceeds as initially-chronic inflammatory process.

The clinical picture of chronic odontogenic maxillary sinusitis is characterized by: a headache, heavy feeling in the maxilla with prevailing localization in the infraorbital area, passage of air or passage of a liquid from the oral cavity into the nasal one (at the closed forms), discharges from the fistula, discharges from the nose, presence of a causal tooth. It is typical to reveal the sinus opacity on the X-ray with primary localisation process in the bottom part of the sinus..

For making diagnosis we could use:

• X-ray examination including panoramic films

• Electoodontodiagnostics

• Endoskopic research of sinus

• Spiral or cone-beam computer tomography

It is necessary to differentiate odontogenic maxillary sinusitis follows with radix and other cyst, grown into the sinus (presence of a shadow, like a dome on the roentgenogram), malignant tumours. Maxillary sinusitis also can be accompanied with an odontogenic osteomyelitis, acting thus as its symptom. The treatment of chronic odontogenic maxillary sinusitis is similar. In inefficiency of conservative treatment, we have to provide the surgical one.

Surgical treatment is performed by the following operative approaches:

• Caldwell — Luc (Fig. 12.16).

• Wasmund — Neumann — Zaslavsky (a Figured incision with access to an alveolar shoot with possibility of plastic elimination of fistula).

• Evdokimov — apertures in an anterior wall maxillary sinus.

• Parch — bow-shaped.

• Trapezoid Novak — Peteru.

Thus formation offollowing flaps is possible:

• Muco-periostal flaps.

• Muco-periostal-bone flaps (V O. Malanchuk).

• Muco-periostal-bone-adiposal flaps (V. A. Sukachyov).

• Muco-periostal flaps from the pallet.

Fig. 12.16. Opening of the maxillary sinus:

A — incision of mucus; B — forming of the trepanation opening; C — scheme of location of the maxillary sinus and trepanation opening (1 — foramen infraorbital; 2 — a lower naso- turbinal; 3 — lower nasal path; 4 — alveolar process of the maxilla; 6 — trepanation opening; 6 — maxillary sinus); D — connection of the sinus with a lower nasal path; E — scheme of this connection (7 — opening which connects a sinus with lower nasal path); F — incision in the area of lower nasal path (8 — incision of mucus of the nose; 9 — the area of nasoturbi- nal is remote).

• The overturning muco-periostal flaps.

• Bridge flaps.

• Multilayered flaps with use of GTR technique.

In the case of perforation of the maxillary sinus, the area of connection of the sine through the oral cavity passes in development of a stage of the connection, a fistula (at the presence of granulations) and anatomizes (at the presence of epithelium).

Approaches to treatment can he the following:

I. Oneself closing: in the case of absence an artificial body in the maxillary sinus; after ending over of acute inflammatory process; in a case of absence of an

[pic]

aggravation of chronic inflammatory process, without presence of polyps and the pathologically changed mucosa.

II. Plastic elimination of communication without sinusotomia:

In the presence of a punched aperture or fistula in a course without an maxillary sinusitis; in chronic, but not polyp inflammatory process; in presence of fibrous changed mucous membrane that probably can be assessed by endoscopic devices.

III. Plastic closing with sinusotomia, without formation of unnatural communication: after conservative treatment in removal of only changed mucous membrane; in endoscopical revision for estimation of a sinus — in the presence of single polyps

IV. Radical sinusotomia with formation of unnatural communication.

• At polypous changed mucousa in the maxillary sinus;

• Along with punching or presence of an foriegn body in a sinus (a root in maxillary sinus).

Sialadenitis

Sialadenitis means inflammatory processes involving the salivary glands. The process may be acute and may result in an abscess formation particularly as a result of bacterial infection. The involvement can be unilateral or bilateral as in viral infections.

Chronic sialadenitis may be nonspecific resulting from ductal obstruction due to sialolithiasis or external radiation or may be specific, caused by various infectious agents and immunologic disorders. The ductal obstruction or decreased salivary flow, allowing retrograde spread of bacteria throughout the ductal system. Blockage of the duct can be caused by sialolithiasis, congenital strictures, or compression by an adjacent tumor.

Etiology

Inflamation of the salivary glands (sialadenitis) can arise from various infectious and noninfectious causes. One of the more common causes of sialadenitis is recent surgery (especially abdominal surgery), after which an acute parotitis (surgical mumps) may arise because the patient has been kept without food or fluids and has received atropine during the surgical procedure. Other medications that produce xerostomia as a side effect also can predispose patients to such an infection. Most cases of acute bacterial sialadenitis are due to Stapfylococcus aureus, but they also may arise from streptococci or other organisms. Noninfectious causes of salivary

inflammation include Sjogren syndrome, sarcoidosis, radiation therapy and various allergens.

The most common viral infection is mumps, although a number of other viruses also can involve the salivary glands, including Coxsackie A. ECHO, choriomeningitis, parainfluenza, and cyiomegalovirus (in neonates).

It may be subdivided temporally into acute, chronic and recurrent forms.

Clinical and radiographic features mumps (epidemic parotitis)

Mumps is a paramyxovirus infection that primarily affects the salivary glands. As with measles and rubella, the epidemiology has been affected dramatically by the MMR vaccine (measles-mumps-rubella vaccine). Before the advent of widespread vaccination, epidemics were seen every 2 to 5 years. Although most authorities assume that natural infection is associated with lifelong immunity, rare cases of recurrent mumps have been well documented in patients with a confirmed history of prior natural infection.

The mumps virus can be transmitted through urine, saliva, or respiratory droplets. The Incubation period usually is 16 to 18 days, with a range of about 2 to 4 weeks. Patients are contagious from 1 day before the clinical appearance of infection to 14 days after its clinical resolution.

Approximately 30% of mumps infections are subclinical. In symptomatic cases, prodromal symptoms of low-grade fever, headache, malaise, anorexia, and myalgia arrive first. Most frequently, these nonspecific findings are followed within 1 day by significant salivary gland changes. The parotid gland is involved most frequently, but the sublingual and submandibular glands also can be affected. Discomfort and swelling develop in the tissues surrounding the lower half of the external ear and extending down along the posterior inferior border of the adjacent mandible. The enlargement typically peaks within 2 to 3 days, and the pain is most intense during this period of maximal enlargement. Chewing movements of the jaw or eating saliva-stimulating foods tends to increase the pain. Enlargement of the glands usually begins on one side and is followed by contralateral glandular changes within a few days. Unilateral involvement is seen in about 25 % of patients.

The second most common finding is epididymoorchitis, which occurs in about 25 % of postpubertal males, in those affected, the testicle exhibits rapid swelling with significant pain and tenderness. The enlargement can range from a minimal swelling to a fourfold increase In size. Unilateral involvement is most common. On resolution of the swelling, atrophy occurs in the affected testicle. Permanent

sterility from testicular changes is rare. Less commonly, oophoritis and mastitis can

be seen in postpubertal females. In addition, spontaneous abortion occurs In ap-

proximately 25 % of females who contract mumps during the first trimester of preg-

nancy.

Less commonly, meningoencephalitis, cerebellar ataxia, hearing loss, pancre-

atitis, arthritis, carditis, and decreased renal function may occur. Isolated changes

such as orchllis or meningitis, may occur in the absence of salivary gland Involve-

ment, thereby making diagnosis difficult in nonepidemic settings. Mumps-related

mortality is exceedingly rare and most frequently associated with mumps encepha-

litis.

The most frequently reported oral manifestation is redness and enlargement

of Wharton’s and Stenson’s salivary gland duct openings. In addition, involvement

of the sublingual gland may produce bilateral enlargements of the floor of the mouth.

The diagnosis of mumps can be made easily from the clinical presentation

when the infection is occurring in an epidemic fashion; however. Isolated cases

must be differentiated from other causes. Saliva, urine, or cerebrospinal fluid speci-

mens can be obtained for culture.

The most frequently used confirmatory measures are demonstration of mumps-

specific IgM or a fourfold rise of mumps-specific IgG titers when measured during

the acute phase and about 2 weeks later.

Acute bacterial sialadenitis is most common in the parotid gland and is bilateral

in 10% to 25 % of cases. The affected gland is swollen and painful, and the over-

lying skin may be erythematous (Fig. 12.17). An associated low-grade fever may

be present, as well as trismus.

A purulent discharge of-

ten is observed from the duct

orifice when the gland is mas-

saged (Fig. 12.18).

Recurrent or persistent

ductal obstruction (most com-

monly caused by sialoliths)

can lead to a chronic sialad-

enitis. Periodic swelling and

pain occur within the affected

gland, usually developing

at mealtime when salivary

flow is stimulated, unilateral,

duct orifice is reddened and

[pic]

Fig. 12.17. Sialadenitis. Tender swelling of the submandibular gland

Fig. 12.18. Sialadenitis. A purulent exudate arising from Stensen’s duct

flow decreases, may or may

not have visible/palpable

stone. Depends on ethiology

and pathogenesis, sialogra-

phy demonstrates various

types of changes either ductal

or parenchyma gland’s tissue

(Fig. 12.19; 12.20; 12.21).

Parotid sialogram dem-

onstrating ductal dilatation

proximal to an area of ob-

struction

In the submandibular

gland, persistent enlargement

may occur (Kuttner tumor), which is difficult to distinguish from a true neoplasm.

Chronic sialadenitis also can occur in the minor glands, possibly as a result of block-

age of ductal flow or local trauma. Subacute necrotizing sialadenitis is a recently

recognized form of salivary inflammation that occurs most commonly in teenagers

and young adults. The lesion usually involves the minor salivary glands of the hard

or soil palate, presenting *as a painful nodule that is covered by intact, erythematous

mucosa. Unlike necrotizing sialometaplasia, the lesion does not ulcerate or slough

necrotic tissue. An infectious or allergic cause has been hypothesized.

Histopathologic features in patients with acute sialadenitis, accumulation

of neutrophils is observed within the ductal system and acini. Chronic sialadenitis

is characterized by scattered or patchy infiltration of the salivary parenchyma

by lymphocytes and plasma

cells. Atrophy of the acini

is common, as is ductal dila-

tation. If associated fibrosis

is present, the term chronic

sclerosing sialadenitis is used

(Fig. 12.22).

Subacute necrotizing sial-

adenitis is characterized by a

heavy mixed inflammatory

infiltrate consisting of neu-

1 trophils, lymphocytes, histio-

Fig. 12.19. Chronic sialadenitis

[pic]

[pic]

[pic]

Fig. 12.20. Chronic sialadenitis (interstitial form)

Fig. 12.21. Chronic sialadenitis (parenchymatous form)

cytes, and eosinophils. There is loss of most of the acinar cells, and many of the

remaining ones exhibit necrosis. The ducts tend to be atrophic and do not show

hyperplasia or squamous metaplasia. Chronic sialadenitis has been misinterpreted

as other non-neoplastic entities and also overcalled as several different types of neo-

plasms, both benign and malignant (Table 12.2).

Treatment and Prognosis

The treatment of acute sialadenitis includes appropriate antibiotic ther-

apy against S. aureus (eg, oxacillin, 250mg, a lst-generation cephalosporin,

or clindamycin), modified according to culture results. With the increasing preva-

lence of methicillin-resistant

S. aureus, especially among the

elderly living in extended-care

nursing facilities, vancomycin

is often required and hydration,

sialagogues (eg, lemon juice,

hard candy, or some other sub-

stance that triggers saliva flow),

warm compresses, compress with

10% Dimeksid, gland massage,

and good oral hygiene are also

important. Surgical drainage may

be needed if there is abscess for-

mation. Although this regimen

[pic]

Fig. 12.22. Chronic sclerosing sialadenitis. Chronic inflammatory infiltrate with associated acinar atrophy, ductal dilatation, and fibrosis

[pic]

Table 12.2.

Differential Diagnosis of Chronic Sialadenitis

|A. Non-neoplastic |B. Neoplastic |

|Mucocele, mucus retention cyst Benign lymphoepithelial cyst Benign |Warthin’s tumor Pleomorphic adenoma Low-grade adenocarcinoma, NOS Adenoid |

|lymphoepithelial lesion Intraparotid lymph node Amylodosis |cystic carcinoma Mucoepidermoid carcinoma Acinic cell carcinoma |

is usually sufficient, a 20% to 50% mortality rate has been reported in debilitated patients because of the spread of the infection and sepsis.

The management of chronic sialadenitis depends on the severity and duration of the condition. Early cases that develop secondary to ductal blockage may respond to removal of the sialolith or other obstruction. If sialectasia is present, the dilated ducts can lead to stasis of secretions and predispose the gland to further sialolith formation, if sufficient inflammatory destruction of the salivary tissue has occurred, surgical removal of the affected gland may be necessary.

Subacute necrotizing sialadenitis is a self-limiting condition that usually resolves within 2 weeks of diagnosis without treatment.

The treatment of mumps is palliative in nature. Frequently, nonaspirin analgesics and antipyretics are administered. In an attempt to minimize orchitis, bed rest is recommended for males until the fever breaks. Avoidance of sour foods and drinks helps to decrease the salivary gland discomfort. As with measles and rubella, the best results come from prior vaccination, thereby preventing the infection.

Physiotherapeutic procedures for treatment chronic forms of the sialadenitis consists of: magnet-therapy, UHF (ultrahigh frequencies), ultrasound, electrophoresis (hydrocortisone 0.25%, trypsin 0.01). Gland massage — 2-3 times a day, everyday. 4

Arthtritis

Arthritis can occur in a chronic, low-grade form or an acute inflammatory form. In addition, it can occur as a degenerative condition, associated with either overuse or aging, or it can occur as an auto-immune disease, such as juvenile rheumatoid arthritis. Most cases are chronic degenerative joint disease and are successfully

treated with non-surgical management. The cartilage of the jaw is specifically designed to absorb and cushion the stress associated with movement and chewing. In some patients, the cartilage may lose its elasticity and become stiff. This can occur due to premature aging of the joint or as a result of overuse, such as a patient who grinds their teeth.

Infectious arthritis: Infection of the TMJ may result from direct extension of adjacent infection or hematogenous spread of bloodbome organisms. The area is inflamed, and jaw movement is limited. Local signs of infection associated with evidence of a systemic disease or with an adjacent infection suggest the diagnosis. X-ray results are negative in the early stages but may show bone destruction later. If suppurative arthritis is suspected, the joint is aspirated to confirm the diagnosis and to identify the causative organism. Diagnosis must be made rapidly to prevent permanent joint damage.

Treatment includes antibiotics, proper hydration, pain control, and motion restriction. Parenteral penicillin, ampicillin, ceftriakson are the drugs of choice until a specific bacteriologic diagnosis can be made on the basis of culture and sensitivity testing. Suppurative infections are aspirated or incised. Once the infection is controlled, jaw-opening exercises help prevent scarring and limitation of motion.

Traumatic arthritis. Rarely, acute injury (e.g., due to difficult tooth extraction or endotracheal intubation) may lead to arthritis of the TMJ. Pain, tenderness, and limitation of motion occur. Diagnosis is based primarily on history. X-ray results are negative except when intra-articular edema or hemorrhage widens the joint space. Treatment includes NSAIDs, application of heat, a soft diet, and restriction oijaw movement.

Osteoarthritis. The TMJ may be affected, usually in people > 50 yr. Occasionally, patients complain of stiffness, grating, or mild pain. Crepitus results from a hole worn through the disk, causing bone to grate on bone. Joint involvement is generally bilateral. X-rays or CT may show flattening and lipping of the condyle, suggestive of dysfunctional change. Treatment is symptomatic.

Rheumatoid arthritis. The TMJ is affected in > 17 % of adults and children with RA, but it is usually among the last joints involved. Pain, swelling, and limited movement are the most common findings . ’In children, destruction of the condyle results in mandibular growth disturbance and facial deformity. Ankylosis may follow. X-rays of the TMJ are usually negative in early stages but later show bone destruction, which may result in an anterior open-bite deformity. The diagnosis is suggested by TMJ inflammation associated with polyarthritis and is confirmed by other findings typical of the disease.

Treatment is similar to that of RA in other joints. In the acute stage, NSAIDs may be given, and jaw function should be restricted. A night guard or splint is often

helpful. When symptoms subside, mild jaw exercises help prevent excessive loss of motion. Surgery is necessary if ankylosis, develops but should not be done until the condition is quiescent.

For children who suffer from chronic arthritis, there are challenges of daily living that are associated with decreased range of motion, pain and inflammation. For many children, the complications of arthritis extend well beyond that of the arms, legs, feet, and hands, and even include the joints in the face, including the temporomandibular joint, TMJ. Children who suffer from complications associated with juvenile rheumatoid arthritis often develop complications involving pain when feeding. This pain is associated with arthritic complications in the TMJ. While some TMJ pain can be associated with infection in and around the mouth, most children experience the complication of feeding in direct response to the arthritic and associated arthritic effusions.

If child is complaining of pain in and around the j aw, or TMJ, and complications associated with feeding are becoming apparent, ask your child’s physician to run the diagnostic studies to determine if the complication is related to the development of arthritis in the temporomandibular joint. MRI is often the diagnostic tool used to confirm the development of arthritic conditions in children. With MRI of the head, your child’s complications of pain in the temporomandibular joint can also be confirmed.

Degenerative arthritis Degenerative arthritis can be either primary or secondary. Primary disease is seen in old people and is a disease of wear and tear. Patients are usually asymptomatic, and when symptomatic, the complaints are usually mild. Secondary degenerative arthritis: This type of arthritis usually develops in people aged 20 to 40 after trauma or in people with persistent myofascial pain syndrome. When degenerative arthritis occurs, the cartilage may then splinter and fracture. Once this occurs, the joint will gradually become stiff and painful. The patient will often hear noise or grinding in the joint and may feel roughness or grating. Joint noise indicates that the cartilage and the disk are beginning to lose their normal smooth contour. Pain in the joint often indicates progression of the disease leading to destruction of the joint components. It is characterized by limited opening of the mouth, unilateral pain during jaw movement, joint tenderness, and crepitus. When it is associated with the myofascial pain syndrome, symptoms wax and wane. Diagnosis is based on X-rays, which generally show condylar flattening, lipping of the joint with osteophyte formation, spurring, or erosion of the articular surface of the condyle. Uni

lateral joint involvement helps distinguish secondary degenerative arthritis from

osteoarthritis.

Treatment of degenerative arthritis is similar to that of myofascial disorders and early internal derangements. NSAIDs, such as ibuprofen, and muscle relaxers with a soft diet are the primary treatment. Bite appliances are added as necessary. When conservative medical management fails to improve symptoms after a 3-6 month trial, surgery is considered. Surgical intervation includes removal of any surgical capsular abnormality, including osteophytes, until the joint space is smooth. A condylar shave is when the entire cortical plate is removed. It should be avoided if possible, as resorption of the condyle is a known complication.

Physical findings which support an initial diagnosis of temporomandibular arthralgia include:

Complete absence of molar teeth in any one quadrant.

Deviation of the jaw to the painful side on wide opening.

Reproducibility of the pain by pressure below the ear forward in the direction of the mandibular condyle.

Reproducibility of the pain by pressure from within the membraneous ear canal forward in the direction of the mandibular condyle, typically by reversing a laryngeal mirror and pressing with the round end of the handle in the ear canal.

Reproducibility of the patient’s complaint of “ear pain” by inserting two tongue blades between the opposite molars and instructing the patient to bite down hard on the tongue blades.

Diagnosis

There are two elements to diagnosis. The first is a comprehensive history and clinical examination. The second is a series of diagnostic studies. In general, the diagnostic studies available for TM Joint diagnosis and evaluation are:

• X-rays of the TM Joints & Skull

• MRI (Magnetic Resonance Imaging)

• Computed tomography

• Electromyography (studies of muscle function)

• Motion Performance Studies

• Joint Vibration Analysis (a form of ultra-sound sonography)

• Diagnostic Study Casts of the Mandible & Maxilla

• X-rays of the Dentition

Lymphadenites of maxillofacial area and a neck

Lymphadenitis is an inflammation of lymph nodes (Fig. 12.23), often combined

with inflammation of lymph vessels.

Lympadenites in submaxillary and mental areas as well as in the area of a neck

can be characterized as odontogenic or non-odontogenic inflammatory processes.

Odontogenic inflammatory processes in a periodontium, bones of a face, maxillaiy

sinus, soft tissue of a face and an oral cavity inevitably result in penetration of infec-

tion to respective regional lymph nodes: submaxillary, mental, cheek, parotid, neck.

As a result symptomatic lymphadenites develop in the aboved mentioned nodes and

both nonspecific and specific lymphadenites can occur.

Acute attack of chronic periodontitis, periostitis and acute pericoronitis were

considered to be the most frequent reasons of lymphadenitis. Serous inflammation^

of a lymph node usually developed on 1-3 day of primary disease while purulent

fusion more often was observed on 3-6 day. It is noted that pathological process

in primary odontogenic lesion can be curable while the inflammatory occurrences

in regional lymph node continue to increase.

Acute odontogenic lymphadenites have been connected with pathological

changes in the region of molar teeth and premolar teeth of lower jaw, less often —

molar teeth and lateral cutters of the upper jaw. It caused more frequent affect

of submandibular ganglion, submental, cheek and parotid lymph nodes, having

been major collectors of lymph out-

flow from mentioned sites of lesion.

Usually one lymph node was in-

volved in inflammatory process, the

increase in two region nodes areas

wasn’t often observed.

Group of non-odontogenic

lymphadenites comprises those which

have no pathogenetic relation with

the dental-maxillary system. They

are so-called stomatogenic, rhinoge-

nous, otogenous and other symptom-

atic lymphadenites, developing due

to stomatites, gingivites, glossites,

rhinites, inflammatory diseases of an

ear. Regional lymphadenites quite

often arise in connection with more

[pic]

Fig. 12.23. The lymph nodes of the maxillofacial area and neck

or less expressed damage of skin or the mucous membrane of the mouth: at a site trauma an entrance gate for an infection are created.

Classification of the lymphadenitis including such forms: acute; serous; purulent; chronic; exudative; productive; traumatic; odontogenic; nonodontogenic; Infectious — Non-specific (acute, chronic); Specific (tuberculous; syphilitic; actinomycotic; viral; vaccinal)

Acute lymphadenitis

Acute inflammation begins with feeling of some awkwardness at head motion, pain in the area of the injured node or groups of nodes.

Both in serous and hyperplastic forms increased lymph nodes are well determined by palpation and under such conditions they are a little bit painful and have dense-elastic consistency. General disorders at the beginning of an inflammation can be absent or be of low-grade. The serous inflammation seldom turns into purulent process; it gradually calms down in compliance with the efficacy of the treatment of the underlying disease which has caused an inflammation of lymphatic vessels and regional nodes. The nodes gradually decrease in sizes, become less painful in some weeks, have usual form and a consistency. At adverse course of serous inflammation it can turn into purulent: in the field of the node infiltration appears (perilymphadenitis), the node becomes not mobile, commissures with other nodes forming with them a package, suppurates. The body temperature raises up to 37.2-37.8 °C. As for blood, there are changes characteristic for abscesses. The general state of health and of the patient is quite often abnormal: indisposition, weakness, loss of appetite, etc. Inflamed lymph node gradually fuses and causes formation of the sinus tract (with transition of disease into the chronic form) or adenophlegmon (see below). In acute purulent lymphadenitis its general parameters (changes in blood, urine, temperature reaction) can be shaded and can be explained as changes due to underlying odontogenic or nonodontogenic inflammation caused lymphadenitis.

Process of purulent fusion of the node can develop quickly — within several days, but sometimes slowly even after elimination of the underlying process on the face, the jaw and in the oral cavity. In the maxillofacial area the most often lymph- adenites are those in submandibular nodes as they are the major nodes of the first stage on the way of lymphatic outflow from the given area. The second by frequency of occurrence are inflammatory processes in mental as well as in parotid and supramaxillar (buccal) nodes. Odontogenic lymphadenites developing on the background of acute or chronic leucosis usually have plural character, locating simultaneously on the face, in the submaxillary areas and the neck. In odontogenic source

of infection localized on one side, lymphadenitis can be bilateral as in leucosis all protective immunologic mechanisms are significantly lowered.

Chronic lymphadenitis

Chronic nonspecific lymphadenitis develops as a result of attenuation of the acute process or it is caused by poorly virulent microorganisms. It is characterized by enlargement of lymph nodes to various sizes and restriction of their motion. Separate, clearly determined nodes, painless, but dense enough are palpated. The general state of health of a patient usually is not disordered. The purulence of lymph nodes in chronic nonspecific inflammation occurs seldom; it is a feature of transition of chronic process to the acute due to the flare-up of a dormant infection. If odontogenic or other source of infection “bombards” node during a long period of time, it is gradually decaying during a chronic inflammation and is replaced by granulation tissue; from time to time there are aggravations; the latter finally lead to skin perforation and formation of a fistula which is closed and cicatrizes with time. Then beside a fistula appears., r

Chronic specific lymphadenitis has, as a rule, tubercular or actinomycotic ethi- ology and affects mandibular, submandibular, retromandibular and cervical nodes. Sometimes it is combined with injury of other lymph nodes of a body, including bronchial both retroperitoneal. Tubercular and actinomycotic chronic lymphad- enites initially have similar courses, creating a picture of so-called hypodermic migrating granuloma of a face or mandibular area. Later actinomycotic lymphadenitis differs by greater tendency to suppuration and formation of fistulas. Course of tubercular lymphadenitis is variable and depends on a stage of disease, amount of injured lymph nodes, reactions of tissues surrounding a node, etc.

It is important to determine first of all, whether lymphadenitis is banal or specific.

In this connection it should be taken into account, that tubercular lymphadenitis is characterized by the absence of the inflammatory features in the oral cavity, jaws, face; rather slow and quite often bilateral increase of inflammatory process in lymph nodes, prolonged mild pyrexia, positive Mantoux test, sterility of pus obtained during a puncture. If chronic lymphadenitis has syphilitic ethiol- ogy, thus in the anamnesis or the objective status there are proofs of this disease (Wassermann test, availability of specific destructions of the nose, palate, soft tissue in the area of the pharynx, etc.).

The diagnosis actinomycosis of lymph nodes is determined on the basis of the characteristic anamnesis, infiltrate density, immunoreactions, findings ofpathologo- histological or cytological examinations.

Differences between adenophlegmon and lymphadenitis include more extensive area of injury, skin tension and more expressed general disorders (see below).

Sialoadenitis (inflammation of parotid or submandibular salivary gland) is characterized by purulent or serous-purulent discharge from the efferent duct of the gland. If in chronic lymphadenitis there is infiltrate tuberosity, it is necessary to exclude a neoplasm. In such cases biopsy is indicated.

Syphilitic injury of a node is characterized by its significant induration and availability of corresponding findings and the objective status in anamnesis (see above).

Brill-symmers disease or giant follicular lymphoma is one of benign variants of lymphosarcomas. For many years it can represent asymptomatic increase of parotid, submandibular, mental lymph nodes, dense by touch and by that supposing chronic nonspecific lymphadenitis or reactive follicular hyperplasia.

Giant follicular lymphoma (known also as medullar lymphosarcoma by WHO classification 1976) is diagnosed only by histologic study. As in this disease occurs generalization (injury of the nearby and remote lymph nodes with involving of the skin, a hypodermic layer, tonsils, internal organs, bone marrow), it is necessary to not hesitate with radical removal of palpated nodes and their careful histological examination.

Differential diagnostics of LAP (lymphoadenopaties)

Local (regional) LAP:

• Local infections bacterial (pharyngitis, mild otitis, ethmoiditis, frontitis, an antritis, an abscess and caries of teeth).

• Viral (disease of “the cat’s scratch”, a tuberculosis, children’s infections, etc.).

• Fungous (actyinomycaosis, candidiasis) lymphogranulematosis (Hodgkin’s disease).

• Non-Hodgkin’s lymphomas (lymphoma of tonsiles, LN).

• Carcinoma (secondary).

Generalized (systemic) LAP:

• Infections bacterial (sepsis, tuberculosis, brucellosis, tularemia, syphilis, etc.); viral (measles, adenoviral infection, flu, AIDS, infectious mononucleosis etc.) fungoid (histoplasmosis, actinomycosis) protozoan (toxoplasmosis, listeriosis, leishmanioisis).

• Autoimmune diseases (rheumatoid arthritis, systemic red erythematosus, dermatomyositis, sclerodermia, nodular periarteritis, granulematous arterites, etc.).

• Benign tumor diseases (sinus histiocytosis with massive LAP, associated with infections, hemophagocytic syndrome, sarcoidosis).

• Malignant tumor diseases primary: LGM (Hodgkin’s disease). Non-Hodgkin’s disease (lymphoma of peripheral LN, skin lymphoma, malignant histiocytoses; metastatic: leukemia, neuroblastoma, rhabdomyosarcoma. Kaposi’s sarcoma, cancers of the lungs, bronchus and thyroid gland.

• Storage diseases (Gaucher’s disease, Niemann — Pick disease).

• Reactions to medicinal and chemical substances (serum sickness, medica- mentous allergy, pollinosis).

• Other diseases.

Treatment

Treatment of acute serous and chronic lymphadenites should be conservative only when it is impossible to define a source (an entrance gate) of infection in the oral cavity, teeth, jaws, face, ENT-organs, etc. In such cases there are applied: dry heat, UHF-therapy, short-term novocaine-antibitics blockade. For the treatment of acute serous lymphadenitis inflammatory infiltrates A. A. Timofeev (1989) recommends daily novocaine nerve-blockade for 5 days of superior cervical and stellate sympathetic ganglions on a side of injury and after dissection of purulent lymphadenites — intramuscular infusion of the Lysozyme (200 mg 2 times a day on first three days, 100 mg 2 times a day the next 3 days) without combination with antibiotics. Blockades are useful because sympathetic fibres of cervical ganglions innervate smooth muscule elements being in a capsule and trabeculas of lymph nodes of the maxillofacial area and the neck that provides contraction of the latter and promotes pushing through of lymph to revehent vessels. In the inflammatory area nervous fibres are in a state of parabiosis the rate of which depends on the severity of the inflammatory process. Novocaine has antiparabiotic property.

It is very useful to apply warming compresses with 30% solution of dimeth- ylsulfoxide. If the source of infection is not revealed and suppuration of a node (or a package of nodes) occured, it is necessary to dissect the abscess and drain it. In some cases it is possible to manage with aspiration of pus and filling of the cavity of an abscess with a solution of antibiotics. If the source of an infection is revealed, it is necessary to eliminate it with antibacterial preparations or surgical intervention (removal of tooth with periodontitis, husking of festered cyst, removal of hanging inflamed hood above cutting tooth, treatment of antritis, osteomyelitis, periostitis, etc.).

If there is interrelation between suppurated lymph node and odontogenic source of an infection, it is as usually enough to eliminate the latter to stop lymphadenitis

or perilymphadenitis. However, in some cases besides intervention on a tooth (its removal, replantation, apical resection etc.) it is necessary to do an incision throughout the mucogingival fold to dissect granular-inflammatory bundle from a tooth to the focus of suppuration in soft tissue. An incision throughout mucogingival fold is drained by rubber strip. As a result, entry of new portions of infection from dental-maxillary systems completely stops. If lymph node suppuration resulted in destruction and cicatricial deformation of the skin, it is necessary to dissect cicatrical changes of tissue, to remove whole granulation tissue both in the depth of the focus of injury and on the internal surface of the dissected skin, to rinse the wound and layer by layer to take it in.

Specific tubercular lymphadenitis should be treated in specialized medical establishments. Sanitation of the oral cavity is obligatory. Immunotherapy is successful for adenoactinomycosis as well as hypodermic form of actinomycotic injuries of the face and the neck; in case of lymph nodal suppuration dissection of the focus, scraping of granulations and administration of antibiotics (locally and intramuscularly) is indicated. However, it is necessary to remember, that a source of a specific infection quite often is gangrenous tooth. Therefore the treatment of specific lymphadenitis should be started with sanitation of the oral cavity.

Prevention of acute sharp and chronic limphadenitis consists of general and local anticarious actions: duly treatment of caries of teeth and its complications, elimination of non-odontogenic sources of infection (treatment of stomatitis, rhinitis, gingivitis, glossitis, otitis, furuncules, carbuncules, etc.), treatment of traumatic injuries of the mucous membrane of a mouth and skin of face, increase of resistance of human organism, etc.

Specific inflammatory processes

(actinomycosis, tuberculosis, syphilis): etiology, classification, clinical course, diagnostics, treatment.

Tuberculosis (tbc.)

Mycobacterium Tbc. (human — 92 %, bovine — 5 %, intermediate — 3 %). Droplet type of transfer, contact, alimentary factor. Immunity and firmness of an organism to Tbc, premobid background, social conditions of a life of the patient. Tbc. bacilli are partially persist in a place of penetration, the others — are

transferred by a current of a lymph to the nearest lymph nodes. Further duplication of microbacilli takes and granuloma is formed — Tbc tubercule. Tubercule (Tbc) decays with formation of the cheesy decay focus 4-8 weeks after an organism sensitizes to tuberculoprotein.

Tbc can affect any human system or organ, remaining thus systemic disease.

Tbc of the maxillofacial area can be primary, when there is no pulmonary focus and secondary — when active Tbc process occurs in lung, bones, etc.

Clinic

Tbc. injury of the maxillofacial area includes injuries of the skin, mucous membranes, hypodermic cellular tissue, jaws, lymph nodes and salivary glands.

Primary Tbc injury is usually formed in the region of lymph nodes amounts up to 60%.

Classification including:

Hyperplastic (infiltrative) form — Tbc granulomas against the background of lymphoid tissue proliferation. Fibrous-cheesy form — cheesy necrosis numerous combined Tbc granulomas. Fibrous — cicatricial hardenings, development of a connecting fabric.

1 i Tbc of jaws — secondary, with mucous, in hematogenous spread (lympho

genous) spread, Ro — in a jaw foci of exhaustion take place.

2. Tbc of salivary glands are rare, often in parotid, foci of necrosis appear.

3. Tbc of skin and hypodermic cellular tissue:

Primary Tbc (Tbc chancre) — erosion and ulcers with harden bottom; Tbc lupus — Tbc tubercule (lipoma) soft; scrofuloderma — intrascutaneous nodes sized 1-3 cm, dense; lupus verucosis Tbc — small, dense, painless node of pinkish- cyanotic color; milliary-ulcer Tbc — small yellowy-red nodes, ulcerating conjugate and superficial very painful ulcers are formed; disseminated milliary Tbc (milliary lupus) — small nodes are painless, they are ulcering, cicatrize or resolve; roseola tu- berculitis — pinkish-brown papulae with drying up crusts; papulo-necrotic Tbc — small roundish paulae (2-3 mm).

Treatment

Dissection of the purulent foci,biopsy (incisional, excisional), sequestectomy, etc. Sanitation of the oral cavity. Systemivc treatment: PAS(A), phtivazid, rifam- picin.

Syphilis (LuES)

It is caused by pale treponema. A venereal and domestic way of transmission.

It can be congenital, a superinfection — pale treponemas get into an organism (repeated infection of not cured patient) — overlay of syphilitic infection on the already available ones, clinically — erupt during the period when repeated infection occured.

Clinic consist of the primary, secondary and tertiary periods.

The incubatory period is 3 weeks and is completed with formation of primary syphiloma. Primary — a spot of red color or papulae — in the center is necrosis — an ulcer (hard chanre), 5-7 days after enlargement of regional lymph nodes — syphilitic scleradenitis 3-4 weeks after — polyadenitis painless.

Seronegative and seropositive period 6-7 weeks later.

Secondary — occurrence of roseolas, papulae, pustules (syphilides) on the skin and mucous membrane.During this period the greatest contagiosa occures. Sometimes periosteum is injured, more often on the lower jaw, thickening.

The tertiary period occurs 3-6 years later and is characterized by grumous tubercle and gummatous formations. In tubercle syphilide in dermal thickness rounded dense raised formation are detected.

Formation of grumous infiltrate, necrosis, ulcers is possible. Gumma is a painless node densely elastic consistence up to 1.5 mm in diameter, contains viscous substance — a deep ulcer, cicatrizes slowly — deformed scars. They are in the region of hard and soft palates in the thickness of the tongue, the back wall of the throat, the nose, frequently in nasal septum. Foraminous defects in bone are formed.

Dental treatment includes the following stages: antiseptic care of syphilitic elements. Sanitation of teeth.Surgical treatment of deformations after the performed course of treatment.

Actinomicosis

Radiant-fungoid diseases — is ray fungus. In 85% maxillofacial area is affected. Ray fungus — saprophyte, mainly in stroma of dental calculus.

The entrance gate of an infection — carious teeth, pathological dentalgingival pockets, the mucous membrane of the oral cavity, pharynx, nose, throat, salivary glands. The incubation period — from some days up to 2-3 weeks, but sometimes it can last for months. Ray fungus can develop in friable cellular tissue, in tissue layers of muscles and organs, i.e. in good vascularized environment. Specific granuloma is formed. Robustova distinguishes the following forms of actinomycosis of the face, neck, jaws and oral cavity: cutaneous; hypodermic; submucosal; mucous;

odontogenic actinomycosis granuloma; hypodermical-intermuscular; actinomycosis of lymph nodes; actinomycosis of jaw periosteum; actinomycosis of jaws; atinomycosis of the oral cavity, tongue, tonsils, salivary glands, maxillary sinus.

The diagnosis is verified by analysis reaction:

• 1) - negative reaction — only a site of needle prick is visible; 2) ? doubtful reaction — hardly appreciable pink erythema; 3) +? poorly positive — clear erythema; 4) + positive reaction — brightly-pink erythema up to dark red color; 5) + + strongly positive reaction — brightly-red erythema with skin edema, painful; 6) + + + systemic or local reaction — systemic or focal changes.

Treatment may consist of surgical: removal of teeth — an entrance gate of infection; surgical processing of infection foci, removal of neoplastic bone. Influence on specific immunity;increase of general resistance of organism; influence on accompanying purulent infection; anti-inflammatory, desensibilizing, symptomatic treatment, treatment of concomitant diseases; physical methods and exercise therapy.

Complications of inflammatory processes of the maxillofacial region and neck

Sepsis

Sepsis is a serious medical condition characterized by a whole-body inflammatory state (called a systemic inflammatory response syndrome or SIRS) and the presence of a known or suspected infection. Septicemia is a related but deprecated (formerly sanctioned medical) term referring to the presence of pathogenic organisms in the blood-stream, leading to sepsis. Severe sepsis occurs when natural immune response to an infection goes into overdrive, triggering widespread inflammation and blood clotting in tiny vessels throughout the body. One or more organs may stop working properly or fail. Sepsis can lead to a dangerous drop in blood pressure (septic shock).

Sepsis is usually treated in the intensive care unit with intravenous fluids and antibiotics. If fluid replacement is insufficient to maintain blood pressure, specific vasopressor drugs can be used. Artificial ventilation and dialysis may be needed to support the function of the lungs and kidneys, respectively. To guide therapy, a central venous catheter and an arterial catheter may be placed. Sepsis patients require preventive measures for deep vein thrombosis, stress ulcers and pressure

ulcers, unless other conditions prevent this. Some patients might benefit from tight control of blood sugar levels with insulin (targeting stress hyperglycemia), low- dose corticosteroids or activated drotrecogin alfa (recombinant protein C).

Severe sepsis occurs when sepsis leads to organ dysfunction, low blood pressure (hypotension), or insufficient blood flow (hypoperfusion) to one or more organs (causing, for example, lactic acidosis, decreased urine production, or altered mental status). Sepsis can lead to septic shock, multiple organ dysfunction syndrome (formerly known as multiple organ failure), and death. Organ dysfunction results from sepsis-induced hypotension (< 90 mm Hg or a reduction of > 40 mm Hg from baseline) and diffuse intravascular coagulation, among other things.

Bacteremia is the presence of viable bacteria in the bloodstream. These term says nothing about the consequences this has on the body. For example, bacteria can be introduced into the bloodstream during toothbrushing. This form of bacteremia almost never causes problems in normal individuals. However, bacteremia associated with certain dental procedures can cause bacterial infection of the heart valves (known as endocarditis) in high-risk patients. Conversely, a systemic inflammatory response syndrome can occur in patients without the presence of infection, for example in those with bums, polytrauma. At higher risk for sepsis are

• Very young people and elderly people.

• Anyone who is taking immunosuppressive medications (such as transplant recipients).

• People who are being treated with chemotherapy drugs or radiation.

• Patients who have no spleen.

• Patients taking steroids (especially over the long-term).

• People with long-standing diabetes, AIDS, or cirrhosis.

| Someone who has very large bums or severe injuries.

In addition to symptoms related to the provoking infection, sepsis is characterized by evidence of acute inflammation present throughout the entire body, and is, therefore, frequently associated with fever and elevated white blood cell count (leukocytosis) or low white blood cell count and lower-than-average temperature. The modem concept of sepsis is that the host’s immune response to the infection causes most of the symptoms of sepsis, resulting in hemodynamic consequences and damage to organs. This host response has been termed systemic inflammatory response syndrome (SIRS) and is characterized by hemodynamic compromise and resultant metabolic derangement. Outward physical symptoms of this response frequently include a high heart rate (above 90 beats per minute), high respiratory rate (above 20 breaths per minute), elevated WBC count (above 12G) and elevated or lowered body temperature (under 36 °C or over 38 °C). Sepsis is differentiated

from SIRS by the presence of a known pathogen. For example, SIRS and a positive blood culture for a pathogen indicates the presence of sepsis. Without a known infection you can not classify the above symptoms as sepsis, only SIRS. This immunological response causes widespread activation of acute-phase proteins, affecting the complement system and the coagulation pathways, which then cause damage to the vasculature as well as to the organs. Various neuroendocrine counter-regulatory systems are then activated as well, often compounding the problem. Even with immediate and aggressive treatment, this may progress to multiple organ dysfunction syndrome and eventually death.

Definition of sepsis

Sepsis is considered present if infection is highly suspected or proven and two or more of the following systemic inflammatory response syndrome (SIRS) criteria are met:

• Heart rate > 90 beats per minute (tachycardia).

• Body temperature < 36 °C (97 °F) or > 38 °C (100 °F).

• Respiratory rate > 20 breaths per minute or, on blood gas, a PaC02 less

• than 32 mm Hg (4.3 kPa) (tachypnea or hypocapnia due to hyperventilation).

• White blood cell count < 4.000 cells/mm3 or > 12,000 cells/mm3 (< 4x 109 or > 12 x 109cells/L), or greater than 10% band forms (leukopenia, leukocytosis, or bandemia);

Fever and leukocytosis are features of the acute-phase reaction, while tachycardia is often the initial sign of hemodynamic compromise. Tachypnea may be related to the increased metabolic stress due to infection and inflammation, but may also be an ominous sign of inadequate perfusion resulting in the onset of anaerobic cellular metabolism.

To qualify as sepsis, there must be an infection suspected or proven (by culture, stain, or polymerase chain reaction (PCR)), or a clinical syndrome pathognomonic for infection.

The more critical subsets of sepsis are severe sepsis (sepsis with acute organ dysfunction) and septic shock (sepsis with refractory arterial hypotension). Patients are defined as having “severe sepsis” if they have sepsis plus signs of systemic hypoperfusion: either end-organ dysfunction or serum lactate greater than 4mmol/dL. Other signs include oliguria and altered mental status. Patients are defined as having septic shock if they have sepsis plus hypotension after aggressive fluid resuscitation (typically upwards of 6 liters or 40 ml/kg of crystalloid).

Diagnosis

The medical history and clinical examination can provide, important elements regarding the cause and severity of sepsis.

The identification of the causative microbe in sepsis can provide useful information. The exact causative organism is confirmed by microbiological culturing in the laboratory (blood cultures and cultures from suspected sites of infections). However, this is a slow process, as it takes a few days to grow up the cultures and correctly identify the pathogens. New molecular diagnostic tests are now available that use genetic material from the pathogen to quickly (within hours) provide results. However, current practice is to directly prescribe broad spectrum antibiotics to the patient.

The effects of the condition on the function of the organs should be documented to guide therapy. This can involve measurement of blood levels of lactate, blood gas sampling, and other blood tests. Because patients on the intensive-care unit are predisposed to hospital-acquired infections (especially related to the presence of catheters), they may require surveillance cultures.

Treatment

The therapy of sepsis rests on antibiotics, surgical drainage of infected fluid collections, fluid replacement and appropriate support for organ dysfunction. This may include hemodialysis in kidney failure, mechanical ventilation in pulmonary dysfunction, transfusion of blood products, and drug and fluid therapy for circulatory failure. Ensuring adequate nutrition — preferably by enteral feeding, but if necessary by parenteral nutrition — is important during prolonged illness.

During critical illness, a state of adrenal insufficiency and tissue resistance (the word “relative” resistance should be avoided to corticosteroids) may occur. This has been termed critical illness-related corticosteroid insufficiency. Treatment with corticosteroids might be most beneficial in those with septic shock and early severe acute respiratory distress syndrome (ARDS). A number of different types of medications are used in treating sepsis, such as:

• Antibiotics. Treatment with antibiotics begins immediately — even before the infectious agent is identified. Initially “broad-spectrum” antibiotics are used, which are effective against a variety of bacteria. The antibiotics are administered intravenously (IV).

• Vasopressors. If the blood pressure remains too low even after receiving intravenous fluids, the patient may be given a vasopressor medication, which constricts blood vessels and helps to increase blood pressure.

• Activated protein C. People with severe sepsis whose organs are failing or who are at high risk of dying may receive a newer drug called activated protein C. This drug interferes with some of the body’s responses to severe infection, helping to curb the overactive inflammatory reaction; but it can cause serious bleeding.

• Others. Other medications include low doses of corticosteroids, insulin to help maintain stable blood sugar levels, and painkillers or sedatives.

People with severe sepsis usually receive supportive care. Depending on the condition, the patient may need mechanical ventilation (respirator) in case of breathing problems or dialysis for kidney failure.

Possible complications: death; disseminated intravascular coagulation; impaired blood flow to vital organs (brain, heart, kidneys); septic shock.

Mediastinitis

Mediastinitis is inflammation of the tissues in the midchest, or mediastinum. The mediastinum lies between the right and left pleura in and near the median sagittal plane of the chest. It extends from the sternum in front to the vertebral column behind, and contains all the thoracic viscera excepting the lungs.

Mediastinitis can be either acute or chronic. Acute mediastinitis is usually bacterial and due to rupture of organs in the mediastinum. As the infection can progress rapidly, this is considered a serious condition. Chronic sclerosing (or fibrosing) mediastinitis, while potentially serious, is caused by a long-standing inflammation of the mediastinum, leading to growth of acellular collagen and fibrous tissue within the chest and around the central vessels and airways. It has a different cause, treatment, and prognosis than acute infectious mediastinitis.

Before the development of modem cardiovascular surgery, cases of acute mediastinitis usually arose from either perforation of the esophagus or from contiguous spread of odontogenic or retropharyngeal infections. However, in modem practice, most cases of acute mediastinitis result from complications of cardiovascular or endoscopic surgical procedures.

Treatment usually involves aggressive intravenous antibiotic therapy and hydration. If discrete fluid collections (such as abscesses) have formed, they may have to be surgically drained. Chronic mediastinitis is usually a radiologic diagnosis manifested by diffuse fibrosis of the soft tissues of the mediastinum. This is sometimes the consequence of prior granulomatous disease, most commonly histoplasmosis. Other identifiable causes include tuberculosis and radiation therapy. Fibrosing mediastinitis most frequently causes problems by constricting blood vessels

or airways in the mediastinum. This may result in such complications as superior vena cava syndrome or pulmonary edema from compression of pulmonary veins. Treatment for chronic fibrosing mediastinitis is somewhat controversial, and may include steroids or surgical decompression of affected vessels.

Meningitis

Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The inflammation may be often caused by bacteria of odontogenic origin. Meningitis can be life-threatening because of the inflammation’s proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.

The most common symptoms of meningitis are headache and neck stiffness associated with fever, confusion or altered consciousness, vomiting, and an inability to tolerate light (photophobia) or loud noises (phonophobia).

A lumbar puncture may be used to diagnose or exclude meningitis. This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid (CSF), the fluid that envelops the brain and spinal cord. The CSF is then examined in a medical laboratory. The usual treatment for meningitis is the prompt application of antibiotics. In some situations, corticosteroid drugs can also be used to prevent complications from overactive inflammation. Meningitis can lead to serious long-term consequences such as deafness, epilepsy, hydrocephalus and cognitive deficits, especially if not treated quickly.

Clinical features

In adults, a severe headache is the most common symptom of meningitis — occurring in almost 90 % of cases of bacterial meningitis, followed by nuchal rigidity (inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 44-46% of all cases of bacterial meningitis. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises).

Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis. Other signs of meningism include the presence of positive Kemig’s sign or Brudzinski’s sign. Kemig’s sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kemig’s sign, pain limits passive extension of the knee. A positive Brudzinski’s sign occurs when flexion of the neck

causes involuntary flexion of the knee and hip. Although Kemig’s and Brudzinski’s signs are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases.

People with meningitis may develop additional problems in the early stages of their illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature and rapid breathing. Disseminated intravascular coagulation, the excessive activation of blood clotting, may cause both the obstruction of blood flow to organs and a paradoxical increase of bleeding risk.

The brain tissue may swell, with increasing pressure inside the skull and a risk of swollen brain tissue getting trapped. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal positioning. Inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus).

The types of bacteria that cause bacterial meningitis vary by age group. In premature babies and newborns up to three months old, common causes are group B streptococci (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and those that normally inhabit the digestive tract such as Escherichia coli (carrying Kl antigen). Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics. Older children are more commonly affected by Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination). In adults, N. meningitidis and S. pneumoniae together cause 80% of all cases of meningitis, with increased risk of L. monocytogenes in those over 50 years old.

In some proportion of people, an infection in the head and neck area lead to meningitis. Recent trauma to the skull gives bacteria in the nasal cavity the potential to enter the meningeal space. In these cases, infections with staphylococci are more likely, as well as infections by pseudomonas and other Gram-negative bacilli. The same pathogens are also more common in those with an impaired immune system.

Recurrent bacterial meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system. Anatomical defects allow continuity between the external environment and the nervous system. The most common cause of recurrent meningitis is skull fracture, particularly

fractures that affect the base of the brain or extend towards the sinuses and petrous

pyramids.

Diagnosis

In someone suspected of having meningitis, blood tests are performed for markers of inflammation (e.g. C-reactive protein, complete blood count), as well as blood cultures.

The most important test in identifying or ruling out meningitis is analysis of the cerebrospinal fluid through lumbar puncture (LP, spinal tap). However, lumbar puncture is contraindicated if there is a mass in the brain (tumor or abscess) or the intracranial pressure (ICP) is elevated, as it may lead to brain herniation. CT or MRI scans are performed at a later stage to assess for complications of meningitis.

Treatment

Meningitis is potentially life-threatening and has a high mortality rate if untreated; delay in treatment has been associated with a poorer outcome. Thus treatment with wide-spectrum antibiotics should not be delayed while confirmatory tests are being conducted. Intravenous fluids should be administered if hypotension (low blood pressure) or shock is present. Given that meningitis can cause a number of early severe complications, regular medical review is recommended to identify these complications early, as well as admission to an intensive care unit if deemed necessary.

Mechanical ventilation may be needed if the level of consciousness is very low, or if there is evidence of respiratory failure. The structural formula of ceftriaxone, one of the third-generation cefalosporin antibiotics recommended for the initial treatment of bacterial meningitis.

Empiric antibiotics (treatment without exact diagnosis) must be started immediately, even before the results of the lumbar puncture and CSF analysis are known. The choice of initial treatment depends largely on the kind of bacteria that cause meningitis in a particular place.

The results of the CSF culture generally take longer to become available (24- 48 hours). Once they do, empiric therapy may be switched to specific antibiotic therapy targeted to the specific causative organism and its sensitivities to antibiotics. For an antibiotic to be effective in meningitis, it must not only be active against the pathogenic bacterium, but also reach the meninges in adequate quantities; some antibiotics have inadequate penetrance and therefore have little use in meningitis.

Adjuvant treatment with corticosteroids (usually dexamethasone) reduces rates of mortality, severe hearing loss and neurological damage. The likely mechanism is suppression of overactive inflammation.

Prognosis

Untreated, bacterial meningitis is almost always fatal. With treatment, mortality (risk of death) from bacterial meningitis depends on the age of the patient and the underlying cause and is about 19-37% in adults. Risk of death is predicted by various factors apart from age, such as the pathogen and the time it takes for the pathogen to be cleared from the cerebrospinal fluid, the severity of the generalized illness, decreased level of consciousness or abnormally low count of white blood cells in the CSF.

Cavernous sinus Thrombosis

Cavernous sinus thrombosis (CST) was initially described by Bright in 1831 as a complication of epidural and subdural infections. CST is usually a late complication of an infection of the central face or paranasal sinuses. Other causes include bacteremia, trauma, and infections of the ear or maxillary teeth. CST is generally a fulminant process with high rates of morbidity and mortality. Fortunately, the incidence of CST has been decreased greatly with the advent of effective antimicrobial agents.

Pathophysiology

The cavernous sinuses are irregularly shaped, trabeculated cavities located at the base of the skull. The cavernous sinuses are the most centrally located of the dural sinuses and lie on either side of the sella turcica. These sinuses are just lateral and superior to the sphenoid sinus and are immediately posterior to the optic chiasm. Each cavernous sinus is formed between layers of the dura mater, and multiple connections exist between the 2 sinuses.

The cavernous sinuses receive venous blood from the facial veins (via the superior and inferior ophthalmic veins) as well as the sphenoid and middle cerebral veins. They, in turn, empty into the inferior petrosal sinuses, then into the internal jugular veins and the sigmoid sinuses via the superior petrosal sinuses. This complex web of veins contains no valves; blood can flow in any direction depending on the prevailing pressure gradients. Since the cavernous sinuses receive blood via this distribution, infections of the face including the nose, tonsils, and orbits can spread easily by this route.

The internal carotid artery with its surrounding sympathetic plexus passes through the cavernous sinus. The third, fourth, and sixth cranial nerves are attached to the lateral wall of the sinus. The ophthalmic and maxillary divisions of the fifth cranial nerve are embedded in the wall.

This intimate juxtaposition of veins, arteries, nerves, meninges, and paranasal sinuses accounts for the characteristic etiology and presentation of CST. Staphylococcus aureus accounts for approximately 70% of all infections. Streptococcus pneumoniae, gram-negative bacilli, and anaerobes can also be seen. Fungi are a less common pathogen and may include Aspergillus and Rhizopus species.

Mortality /Morbidity

Prior to the advent of effective antimicrobial agents,® the mortality rate from CST was effectively 100%. Typically, death is due to sepsis or central nervous system (CNS) infection. With aggressive management, the mortality rate is now less than 30%. Morbidity, however, remains high, and complete recovery is rare. Roughly one sixth of patients are left with some degree of visual impairment, and one half have cranial nerve deficits .

Causes

• Most cases of septic CST are due to an acute infection in an otherwise healthy individual. However, patients with chronic sinusitis or diabetes mel- litus may be at a slightly higher risk.

The causative agent is generally Staphylococcus aureus, although streptococci, pneumococci, and Cavernous sinus thrombosis.

Clinical signs

The early signs and symptoms of cavernous sinus thrombosis (CST) may not be specific. A patient who presents with headache and any cranial nerve findings should be potentially evaluated for CST. The most common signs of CST are related to the anatomical structures affected within the cavernous sinus.

• Patients generally have sinusitis or a midface infection (most commonly a furuncle) for 5-10 days. In as many as 25% of cases in which a furuncle is the precipitant, it will have been manipulated in some fashion (eg, squeezing, surgical incision).

• Headache is the most common presentation symptom and usually precedes fevers, periorbital edema, and cranial nerve signs. The headache is usually sharp, increases progressively, and is usually localized to the regions innervated by the ophthalmic and maxillary branches of the fifth cranial nerve.

• In some patients, periorbital findings do not develop early on, and the clinical picture is subtle.

• As the infection tracts posteriorly, patients complain of orbital pain and fullness accompanied by periorbital edema and visual disturbances.

• Without effective therapy, signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus. Eye swelling begins as a unilateral process and spreads to the other eye within 24-48 hours via the intercavemous sinuses. This is pathognomonic for CST.

• The patient rapidly develops mental status changes including confusion, drowsiness, and coma from CNS involvement and/or sepsis. Death follows shortly thereafter.

Other than the findings associated with the primary infection, the following signs are typical:

• Periorbital edema may be the earliest physical finding.

* Chemosis results from occlusion of the ophthalmic veins.

* Lateral gaze palsy (isolated cranial nerve VI) is usually seen first since CN VI lies freely within the sinus in contrast to CN III and IV, which lie within the lateral walls of the sinus.

* Ptosis, mydriasis, and eye muscle weakness from cranial nerve III dysfunction

• Manifestations of increased retrobulbar pressure follow.

* Exophthalmos

* Ophthalmoplegia

• Signs of increased intraocular pressure (IOP) may be observed.

* Pupillary responses are sluggish.

* Decreased visual acuity is common owing to increased IOP and traction on the optic nerve and central retinal artery.

• Hypoesthesia or hyperesthesia in dermatomes supplied by the VI and V2 branches of the fifth cranial nerve

• Appearance of signs and symptoms in the contralateral eye is diagnostic of CST, although the process may remain confined to one eye.

• Meningeal signs, including nuchal rigidity and Kemig and Brudzinski signs, may be noted.

• Systemic signs indicative of sepsis are late findings. They include chills, fever, shock, delirium, and coma.

FBC, ESR, blood cultures, and sinus cultures help establish and identify an infectious primary source. Lumbar puncture is necessary to rule out meningitis.

A MRI using flow parameters and an MR venogram are more sensitive than a CT scan, and are the imaging studies of choice to diagnose cavernous sinus thrombosis. Findings may include deformity of the internal carotid artery within the cavernous sinus, and an obvious signal hyperintensity within thrombosed vascular sinuses on all pulse sequences.

Treatment

Cavernous sinus thrombosis has a mortality rate of less than 20% in areas with access to antibiotics. Before antibiotics were available, the mortality was 80-100%. Morbidity rates also dropped from 70% to 22% due to earlier diagnosis and treatment.

Recognizing the primary source of infection (i.e., facial cellulitis, middle ear, and sinus infections) and treating the primary source expeditiously is the best way to prevent cavernous sinus thrombosis.

Broad-spectrum intravenous antibiotics are used until a definite pathogen is found.

Vancomycin may be used if significant concern exists for infection by meth- icillin-resistant Staphylococcus aureus or resistant Streptococcus pneumoniae. Appropriate therapy should take into account the primary source of infection as well as possible associated complications such as brain abscess, meningitis, or subdural empyema. Anticoagulation with Heparin is controversial. Retrospective studies show conflicting data. This decision should be made with subspecialty consultation. Steroid therapy is also controversial and is not recommended by many sources. All patients with CST are usually treated with prolonged courses (3-4 weeks) of IV antibiotics. If there is evidence of complications such as intracranial suppuration, 6-8 weeks of total therapy may be warranted.

All patients should be monitored for signs of complicated infection, continued sepsis, or septic emboli while antibiotic therapy is being administered.

Complications of untreated CST include extension of thrombus to other dural venous sinuses, carotid thrombosis with concomitant strokes, subdural empyema, brain abscess, or meningitis. Septic embolization may also occur to the lungs, resulting in ARDS, pulmonary abscess, empyema, and pneumothorax.

Complications in treated patients include oculomotor weakness, blindness, pituitary insufficiency, and hemiparesis.

In order to treat an acute dentoalveolar infection as well as a fascial space abscess correctly, the following are considered absolutely necessary.

Take a detailed medical history from the patient. There are following indications for hospital admission: temperature > 38.3 °C, dehydration, threat to the airway or vital structures, infection in moderate or high severity anatomic spaces, need for general anesthesia, need for inpatient control of systemic disease and other.

The most frequent cause of death in reported cases of odontogenic infection is airway obstruction. Therefore, the surgeon must assess current or impending airway obstruction within the first few moments of evaluating the patient with a head and neck infection. Complete airway obstruction is, of course, a surgical

emergency. In such cases insufficient or absent air movement in spite of inspiratory efforts will be apparent. In highly skilled hands one brief attempt at endotracheal intubation may be made, but a direct surgical approach to the airway by cricothy- roidotomy or tracheotomy is more predictably successful. In such extreme circumstances the presence of infection overlying the trachea is less important than the absence of ventilation. Therefore, infection in the region of surgical airway access is not a contraindication to an emergency cricothyroidotomy or tracheotomy Drainage of pus, when its presence in tissues is established. This is achieved by way of the root canal, with an intraoral incision, with an extraoral incision, and through the alveolus of the extraction. Without evacuation of pus that is with administration of antibiotics alone the infection will not resolve. Drilling of the responsible tooth during the initial phase of inflammation, to drain exudates through the root canal. In this way, spread of inflammation is avoided and the patient is relieved of the pain. Drainage may also be performed with trepanation of the buccal bone, when the root canal is inaccessible. In general, surgery for management of severe odontogenic infections is not difficult. Given a thorough knowledge of the anatomy of the deep fascial spaces of the head and neck, the surgeon should be able, by using appropriate anatomic landmarks, to use small incisions and blunt dissection without direct exposure and visualization of the entire infected anatomic space. Another important principle of surgical incision and drainage is the need to dissect a pathway for the drain that includes the locations where pus is most likely to be found.

On the management of deep fascial space infections of the head and neck there are two approaches to surgical drainage of deep neck infections. First strategy is to use parenteral antibiotic therapy as a means of controlling, localizing, or even eradicating the soft tissue infection. Failure of the medical approach is determined by patient aggravation, impending airway compromise, and the identification of an abscess by CT or clinical examination or both. Only then is surgical drainage undertaken. The expectant approach to management of severe odontogenic infections has not been supported by empiric investigation. The alternative strategy is the immediate establishment of airway security as necessary, and aggressive early surgical intervention. Identification of an abscess is not required before surgical intervention. This approach is predicated on the concept that early incision and drainage aborts the spread of infection into deeper and more critical anatomic spaces, even when it is in the cellulites stage.

Planning of the incision and steps so that:

• Antisepsis of the area with an antiseptic solution before the incision

• Anesthesia of the area where incision and drainage of the abscess are to be performed, with the block technique together with peripheral infiltration

anesthesia at some distance from the inflamed area, in order to avoid the risk of existing microbes spreading into deep tissues.

• Injury of ducts (Wharton, Stenson) and large vessels and nerves is avoided. Incision for drainage of a sublingual abscess is performed parallel to the submandibular duct and the lingual nerve. During cutaneous incisions, the course of the facial artery and vein must be taken into consideration, as well as that of the facial nerve movement of the fluid inside the abscess. If the incision is premature, there is usually a small amount of bleeding, no pain relief for the patient and the edema does not subside.

• Sufficient drainage is allowed. The incision is performed superficially, at the lowest point of the accumulation, to avoid pain and facilitate evacuation of pus under gravity. The incision is not performed in areas that are noticeable, for esthetic reasons; if possible, it is performed intraorally.

if Placement of a rubber drain inside the cavity and stabilization with a suture on one lip of the incision, aiming to keep the incision open for continuous drainage of newly accumulated pus. The advantages of drainage are the provision of two pathways for the egression of pus, placement of the incisions in healthy tissue in cosmetically acceptable areas, and the ability to irrigate the infected wound with unidirectional flow from one incision to the other. Wound irrigation is facilitated especially by the use of tube drain, which is noncollapsible and perforated.

• Removal of the responsible tooth as soon as possible, to ensure immediate drainage of the inflammatory material, and elimination of the site of infection. Extraction is avoided if the tooth can be preserved, or if there is an increased risk of serious complications in cases where removal of the tooth is extremely difficult.

Administration of antibiotics, when swelling is generally diffuse and spreading, and especially if there is fever present, and infection spreads to the fascial spaces, regardless of whether there is an indication of the presence of pus. Antibiotic therapy is usually empiric, given the fact that it takes time to obtain the results from a culture sample. These antibiotic choices are separated by severity of infection. Penicillin group of antibiotic continues to be a highly effective for uncomplicated odontogenic infections, owing to its low cost and low incidence of unwanted side effects. Most resistance to penicillin that occurs among the oral pathogens is due to synthesis of P-lactamase. Therefore, it is reasonable to use penicillin plus a P-lactamase inhibitor such as ampicillin-sulbactam or a penicillin plus metronidazole as alternative antibiotics for serious odontogenic infections.

The penicillins and metronidazole have the advantage of crossing the blood-brain barrier when the meninges are inflamed. Clindamycin, on the other hand, does not cross the blood-brain barrier. Therefore, it is appropriate to use penicillin plus metronidazole or ampicillin-sulbactam when there is a risk of an odontogenic infection entering the cranial cavity. Few cephalosporins are able to cross the blood-brain barrier. Some third generation cephalosporins, such as ceftadizime, can do so. In addition, ceftadizime is effective against the oral streptococci and most oral anaerobes.Among the cephalosporins, therefore, ceftadizime is the alternative antibiotic of choice. A new fluoroquinolone antibiotic, moxifloxacin has great promise in the treatment of head and neck infections. Its spectrum against oral streptococci and anaerobes is excellent. Its absorption is virtually complete via either the oral or intravenous routes, and it penetrates bone readily. The tissue level of antibiotics determines their effectiveness. Those tissue levels are of course dependent on the antibiotic’s level in serum, through which the antibiotic must pass in order to achieve therapeutic levels in soft tissues, bone, brain, and abscess cavities. Administration of antibiotics by the oral route requires that the drug successfully navigate the vagaries of the highly acidic stomach, the chemical qualities of ingested foods, and the basic intestinal tract. Some antibiotics, however, are equally well absorbed intravenously and orally. The fluoroquinolones, such as ciprofloxacin and moxifloxacin, are the best examples of this. For this reason the fluoroquinolones are not given intravenously unless use of the oral route is contraindicated. Dosage intervals should not be changed from published guidelines by the surgeon. Nonetheless, the surgeon must be aware of the greater effectiveness of intravenous antibiotics over their oral counterparts.

Criteria for changing antibiotics: allergy, toxic reaction, or intolerance, culture and/or sensitivity test indicating resistance, failure of clinical improvement, given, removal of odontogenic cause, adequate surgical drainage (suggest postoperative imaging), other causes for treatment failure ruled out 48-72 h of the same antibiotic therapy. Medical supportive care for the patient with a severe odontogenic infection is composed of hydration, nutrition, and control of fever in all patients.

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