 MFS lecture series. Our new topic is orophacial and neck infections. This lecture is intended to introduce you to the facial layers of the neck which is also called as cervical fascia. First you should understand what the term fascia means. Fascia is a band or sheet of connective tissue primarily of collagen and it is found beneath the skin and what are its functions? The fascia attaches, stabilizes, encloses and separates the muscles and other internal organs. There is one more term that you need to be familiar with that is facial space. These are potential spaces that exist between the fascia and underlying organs and other tissues and they are separated from each other by barriers which may be a muscle, a bone or fascia. A neurontogenic infection can reach these facial spaces resulting in space infection. Generally the spread of infection is determined based on whether the anatomical barrier, it can be a muscle, bone or fascia. So it depends on the anatomical barrier whether it is breached or not. What is the significance of these facial spaces or space infection? Space infections are relatively common sequelae of odontogenic infection and rapidly progressing which results in prolonged morbidity. There are long-term complications associated with space infections which are potentially life threatening. The treatment of space infections are also considered to be difficult due to various factors like the complexity of the anatomy of neck, the deeper location of the spaces, limited access, proximity to vital structures and communication of spaces with each other. So that said let's have a look at the cervical fascia in detail. Cervical fascia is divided into superficial cervical fascia and deep cervical fascia. Superficial cervical fascia is a thin layer of subcutaneous connective tissue that lies between the dermis of the skin and the first layer of deep cervical fascia which is the investing layer. It contains the following. The neurovascular supply to the skin, superficial veins and lymph nodes, fat and platysma muscle. Superficial cervical fascia is thinner on the anterior aspect of the neck and it has usually got very thin amount of fat which is its distinguishing characteristic. At the anterior neck the superficial fascia blends with the platysma. Platysma is a broad superficial muscle which originates from the fascia over the pectoralis major and deltoid. The fibers of platysma then causes the clavicle and meat in the midline fusing with the muscles of the face. It is beneath the superficial cervical fascia that you can find the external jugular vein. Beneath the superficial cervical fascia you find the deep cervical fascia. The deep cervical fascia as its name suggests lies deep to the superficial cervical fascia and the platysma muscle. This fascia is organized into several layers and each of these layers have role in supporting the neck structures. We shall now have look at each of these layers in detail. From here onwards you will see the same diagram in every following slide throughout this presentation because this is the best way to visualize and compare the facial layers at a glance. Before looking into the diagram let us understand that any object or human body can be visualized in three different planes the sagittal, coronal and transverse planes. The sagittal plane divides the human body into equal right and left halves through the midline. Sagittal plane is shown in right color here. The coronal plane divides the human body into anterior and posterior halves or anterior and posterior parts. Transverse plane also called the axial plane or cross sectional plane divides the body into inferior and superior portion. So this is applicable to human body as well as any object. So keep this image in mind while discussing the topic proper images. This figure shows the cross sectional image of neck at the level of seventh cervical vertebra of the C7. You have sectioned the neck at the level of C7 and you are viewing it from above. This is a superior view. So let's see what all structures you can identify here because this is sectioned at C7 level. Here is the seventh vertebra and through the center runs the spinal cord. This is the spinal cord. This is the C7 vertebra. So to identify the structures, let's move from anterior to posterior. This is the anterior aspect. This is the posterior aspect. So anteriorly you can visualize the superficial cervical fascia with the platysma. This muscle is the platysma. The thin muscle over here is the platysma and around it you have the superficial cervical fascia. You know from the previous slide that platysma is the limit of superficial cervical fascia. Beneath the platysma you can identify the external jugular vein. The deep cervical fascia begins at the investing layer which is shown in green colour. So investing layer surrounds the entire neck. As you can see very clearly here the investing layer which is green in colour surrounds the entire cross section of the neck. You can see the sternocleidomastoid muscle on either side and also the smaller infrahiroid muscles. These are the infrahiroid muscles, the ones smaller in size. As you move further deeper the structure in pink here is the thyroid. This overlies the trachea which is blue in colour. This is thyroid, this is trachea and the structure behind the trachea in red colour is the esophages. So the thyroid, the trachea and esophages are enclosed within the second layer of deep cervical fascia which is the pre tracheal layer that is illustrated in blue colour here. As you still go posteriorly there is carotid sheet which is red in colour on either side and the carotid sheet encloses the common carotid artery the internal jugular vein and the vagus nerve. Orange coloured layer here is the pre vertebral fascia. There are different groups of muscles around the cervical vertebra which is enclosed by the pre vertebral fascia and most posteriorly you can see that the investing layer of deep cervical fascia has split itself to enclose the trapezius muscle. So this is the description of deep cervical fascia in a nutshell. Moving on to the investing layer of deep cervical fascia which is depicted in blue colour here. It is the most superficial aspect of the deep cervical fascia and is clearly seen in the diagram here that it surrounds all the structures in the neck like a collar. Here again is a cross sectional view of the neck at C7 level. This is the anterior posterior part and where the investing fascia meets the trapezius muscle and the sternocleid or mastoid muscle it splits into two and it completely surrounds both the muscles. So imagine the investing fascia as a cube with superior inferior anterior and posterior attachments. In the cross sectional image you cannot see the superior and inferior limits. Therefore here is the sagittal view. The green colour here is the investing fascia. Superiorly it is attached to the external occipital protuberance, the superior nuclear line of the skull, the mastoid process and the base of the mandible. That is the superior limit and anteriorly the limit is the hyoid bone and the symphysis mentee. Posteriorly it is attached along the nuclear line of the vertebral column and the spine of C7. This is attached to the ligamentum nuke and the spine of seventh cervical vertebra. Inferiorly the limit is the manubrium sternum. So these are the attachments of investing layer of deep cervical fascia. Just like the investing fascia splits to enclose two muscles that is the sternocleid or mastoid muscle and the trapezius muscle. Similarly the fascia also splits to enclose two glands. Those are the submandibular and submental glands and two spaces the suprasternal and supraclavicular spaces. So these are the structures or the regions surrounded by or enclosed by the investing layer of deep cervical fascia. The second layer or the pre tracheal layer of deep cervical fascia. In the sagittal view here the pre tracheal layer is depicted in blue color. This is situated in the anterior neck and it extends between the hyoid bone and the oblique line of thyroid cartilage superiorly and tracts inferiorly where it blends with the pedicardium of the arch of the iota. In the car sectional image the pre tracheal layer fuses with the carotid sheath deep to the sternocleid or mastoid muscle. So here is the carotid sheath to which the pre tracheal layer is blended on either side. So here in this diagram you can see that the pre tracheal layer has enclosed few muscles over here. These are the infrahioid muscles. It has also enclosed the thyroid gland the trachea and the esophages. Therefore anatomically pre tracheal fascia can be divided into two parts the muscular part and the visceral part. The muscular part encloses the infrahioid muscles and the visceral part encloses the thyroid trachea and the esophagus. There are few other features of the pre tracheal layer. On either side of the thyroid gland it forms a suspensory ligament for the gland which is known as the ligament of berry. This ligament is attached to the cricoid cartilage and also to the thyroid cartilage. So its function is to support the thyroid gland and the thyroid doesn't sink into the medias genome. This fascia also provides a slippery surface for the free movement of the trachea during swallowing. Moving on to the pre vertebral layer as the name suggests it lies in front of the pre vertebral muscles and forms the floor of the posterior triangle of the neck. As you can see here the purple colored is the pre vertebral fascia and the pre vertebral muscles lie between the fascia and the vertebra which is colored in pink. There are three sets of muscles associated with this fascia. The first group of muscles is located anterior to the vertebra and it includes the longest capitis and longest scaly muscles. The second group of muscle is the scaliness muscles which include the anterior, middle and posterior scalenes as well as the levator scapulae which is located lacquely to the vertebra and posteriorly the deep muscles or intrinsic muscles of the back are located. The sagittal section shows the pre vertebral fascia in brown color. Superiorly it is attached to the skull base and inferiorly it extends to the superficial mediasenium where it is attached to the body of the fourth thoracic vertebra. Anteriorly the pre vertebral fascia is separated from the pharynx and buccopharyngeal fascia by the retropharyngeal space containing loose adiola tissues. This is the sagittal view and here is the cross sectional view of the same region. So pre vertebral fascia is illustrated in blue color and the orange color shows the retropharyngeal space. Anterior to the retropharyngeal space is the buccopharyngeal fascia. So this space differentiates or separates the buccopharyngeal fascia from the pre vertebral fascia. This region is of utmost importance in dealing with or while dealing with space infections. The importance of this region will be dealt in detail in the subsequent lectures. The next layer of deep cervical fascia is the carotid sheath. It is paired and present on either side of the neck. The carotid sheath encloses the internal jugular wing, the common carotid artery and the vagus nerve. In addition it has relations to ansa cervicalis anteriorly and the cervical sympathetic chain posteriorly. The carotid sheath is formed by the fusion of pre-veical, investing layer and the pre-vertible layers of deep cervical fascia. It is within this carotid sheath that the common carotid artery bifurcates into the internal and external carotid artery. It is only the internal carotid artery that is present within the sheath. The same diagram is depicted here. This is the internal jugular wing, the common carotid artery, the ansa cervicalis and the sympathetic trunk. As you can see here the carotid sheath is organized into a column. So the superior limit of the sheath is the base of the skull and the inferior limit is the thoracic mediasthenum. And this particular organization is of clinical significance as a pathway for the spread of infection. Bacopharyngeal fascia wraps around the lateral and posterior sides of the pharynx and it lies on the superficial side of the pharyngeal constrictor muscle. It was told earlier that the pre-vertible fascia is separated from the bacopharyngeal fascia by the retropharyngeal space. Again there is aller fascia which is red in color which is present between the retropharyngeal space and the pre-vertible fascia. As you can see here the red colored structure is the aller fascia which lies just posterior to the retropharyngeal space. So these structures will prevent the meeting or communication between the two fascias that is a pre-vertible fascia and the bacopharyngeal fascia. But there is one point where the aller fascia fuses with the retropharyngeal space. As you can see here at this particular point the aller fascia and the retropharyngeal space or it is retropharyngeal fascia as you can call it either way. So at this point both the fascias meet and here ends the retropharyngeal space. So it is probably at this level that the pre-vertible fascia communicates with the bacopharyngeal fascia. As you can see in this diagram here is the midline fusion between the pre-vertible fascia and the bacopharyngeal fascia which is at a variable level between the sixth cervical vertebrae that is C6 and the fourth thoracic vertebrae T4. So this meeting point of the pre-vertible fascia and the bacopharyngeal fascia is somewhere between C6 and T4. Faryngeal basilar fascia is a thickened part of the deep cervical fascia between the upper border of the superior constrictor muscle and the base of the skull. This lies deep to the pharyngeal muscles. This figure again depicts the relationship between the pre-vertible fascia, the bacopharyngeal fascia and the pharyngeal basilar fascia. The dark blue color is a pre- vertebral fascia. The light blue is the bacopharyngeal fascia which will eventually meet somewhere between C6 and T4. Between the pharyngeal basilar and the bacopharyngeal fascia lies the constrictor muscles of the pharynx. So this is how all the three fascia the bacopharyngeal pharyngeal basilar and pre-vertible fascia are related. So that's all about the facial layers of neck in brief. In subsequent lectures we shall discuss in detail the clinical significance of important facial spaces and how adentrogenic infections spreads to each of them. Thank you. MFS lecture series. We shall continue with orophacial and neck infections. This lecture will cover the classification of facial spaces, the anatomy and infections of submental, sublingual and submandibular spaces. We had seen in the previous lecture that fascia is a band or sheet of connective tissue primarily made up of collagen and it is found beneath the skin that attaches, stabilizes, encloses and separates muscles and other internal organs. We had also discussed that facial spaces are potential spaces that exist between the fascia and underlying organs. They are separated from each other by barriers which may be muscle, bone or fascia. How exactly does a space get infected? Here you need to understand that no such space exists unless pus gets accumulated in these specific regions referred to as tissue spaces. Some of these potential spaces are compartments which contain structures like submandibular salivarid glands, buccal pad of fat or a group of lymph nodes. So normally these structures are surrounded by loose connective tissue and this connective tissue is thin and very fragile and it is easy to strip off these tissues using finger. The pus which is formed within these spaces will destroy the loose connective tissue around it and it separates the anatomical boundaries of the compartment as it increases in its volume. Thus an abscess cavity is created which is bounded by muscles and tissues. So it is now understood that orophacial infections do not spread haphazardly through the loose connective tissue but they tend to accumulate in these potential spaces around the jaws. Many of these spaces also communicate with each other. Therefore a detailed knowledge of the surgical anatomy, the boundaries and the related anatomical structures is important as it facilitates planning of proper surgical drainage. Coming to the classification of spaces Grodinski and Holiok used numbers to indicate the various deep neck spaces. Space 1 it lies superficial to the superficial fascia here and this is synonymous with the subcutaneous space. Space 2 is a group of spaces surrounding the cervical strap muscles. The strap muscles are the sternothyroid, thyroid hyoid, sternohyoid and omohyoid. Therefore space 2 surrounds the cervical strap muscles. Space 3 is the potential anatomical space which is superficial to the visceral division of pre tracheal layer. It was discussed in the previous lecture that the pre tracheal layer of the deep cervical fascia is divided again into visceral and muscular divisions. Therefore space 3 is related to the visceral division of the pre tracheal layer and space 3a. Space 3a is the carotid sheet. Here is the carotid sheet. Space 4 is the potential space that lies between the lr fascia and the pre vertebral fascia. This is the pre vertebral fascia which lies just in front of the vertebral column. And here is the lr fascia. Therefore danger space or space 4 is lying between the lr fascia and the pre vertebral fascia. Space 4a this is associated with the posterior triangle and it lies posterior to the carotid fascia or the carotid sheet. Space 5 is pre vertebral space and space 5a is enclosed by the pre vertebral fascia which is posterior to the transverse process. If this is the vertebral and this is the transverse process space 5a is formed by the pre vertebral fascia which lies in the posterior aspect of the vertebrae surrounding the scalene muscles. We had seen the cross sectional image of the neck at the level of C7 vertebrae. Here is the sagittal section. You can see that the buccal pharyngeal fascia is separated from the pre vertebral fascia by retro pharyngeal space. What is danger space? It is a potential space between the lr fascia and the pre vertebral fascia and it extends from the base of the skull to the posterior medial stenum as far as the diaphragm. The lr fascia fuses with the retro pharyngeal fascia at a variable level between the sixth cervical vertebrae and the fourth thoracic vertebrae. That means the lr fascia and the retro pharyngeal fascia fuses in between somewhere in between C6 and T4. So this fusion forms the base of the retro pharyngeal space somewhere over here. Infections of the retro pharyngeal space can rupture the lr fascia thus entering the danger space which is continuous with the posterior medial stenum. So this is the significance of danger space. If there is an infection of the retro pharyngeal space it will rupture or tear the lr fascia thus entering the danger space which extends up till the posterior medial stenum. Let us see how these facial spaces are classified. Facial spaces can also be divided based on its mode of involvement to the niudice of infection. It is divided into primary space or spaces with direct involvement and secondary spaces or those with indirect involvement. Spaces involved in autotogenic infections can again be classified into primary maxillary spaces that means those spaces associated with the upper jaw or maxilla. Primary mandibular spaces those involved in lower jaw infections and secondary facial spaces. All these spaces will be discussed in detail individually. Based on clinical significance facial spaces are classified into those present on face in the supra hyoid region, in the infra hyoid region and spaces of total neck. First facial space we are going to discuss is the submental space which is a potential primary space related to the mandible. In this image we are viewing the submental space from below. Imagine you are standing at the hyoid bone and looking up to see the submental space. Here you can see that the space is bounded laterally by the lower border of mandible and anterior bellies of digastric muscle. Superiorly is the mylohyoid muscle which forms the floor of the mouth. Inferiorly is the investing layer of deep cervical fascia. Superiorly you have the mylohyoid muscle. Inferiorly the investing layer of deep cervical fascia and laterally the lower border of mandible and the anterior bellies of digastric muscle. The submental space contains submental lymph nodes and anterior jugular veins. Submental space is involved most frequently by the infections originating from the six anterior mandibular teeth. Infected skin wounds or anterior mandibular fractures can also cause infections of the submental space. How does an autogenic infection in the anterior mandible cause infection of the submental space? For the space to get infected the infection has to first perforate the cortical plate and this perforation is just below the attachments of the mantalis muscle labially and mylohyoid muscle lingually. If the perforation of the cortical plate is below the attachments of these muscles then that will result in submental space infection. Extraoral findings of submental space infection is distinct firm swelling in the midline beneath the chin as you can see in the diagram here. The skin overlying the swelling is hard and taut. Fluctuation may be present. Intraoral findings include the anterior teeth which are either non-vital, fractured or carious. The offending tooth may exhibit tenderness to percussion and it may also show mobility. The patient will also experience considerable discomfort on swallowing. This diagram shows the incision needed for drainage of a submental space infection or a submental abscess. The drainage is performed by making a transverse incision in the skin just below the symphysis of the mandible. A blunt dissection is carried out by inserting a sinus forceps through this incision in upward and backward direction. Later a small piece of corrugated rubber drain is inserted into the abscess cavity and is secured to one of the margins of the wound using a suture. The next potential primary space associated with the mandible is the sublingual space. This space is V shaped and it lies lateral to the muscles of tongue. The teeth which frequently gets involved in sublingual space infection are the mandibular incisors canines, premolars and sometimes the first molars. The apices of these teeth are superior to the myelohyoid muscle. Therefore the ordentogenic infections from these teeth are confined to the sublingual space whereas if the root apices extends beyond the myelohyoid muscle then the infection will spread into the submandibular space which lies just beneath the sublingual space. The boundaries of the sublingual space are the mucosa of the flow of the mouth which is just superior to the sublingual space. So above the sublingual space it is only the mucosa of the flow of the mouth which is present. Inferiorly is the myelohyoid muscle. Laterally there is medial side of the mandible above the myelohyoid muscle. Medially is the tongue muscles, all the hyo glosses, genio glosses and genio hyoid muscles and posteriorly is the hyoid bone. So this is the sublingual space bounded by the mucosa of the flow of the mouth, superiorly, inferiorly by the myelohyoid muscle, laterally by the medial side of the mandible just above the myelohyoid muscle, the tongue muscles medially and posteriorly by the hyoid bone. Then of the sublingual space include the tongue muscles also deep part of the submantibular salivary gland and its duct, sublingual salivary gland, the lingual nerve and the hypoglossal nerve. Extraorally there is little or no swelling. The lymph nodes may be enlarged and may be tender. Pain and discomfort is experienced by the patient on weed rotation. Speech also may be affected. Extraorally a firm painful swelling is seen in the flow of the mouth on the affected side. The flow of the mouth may be raised and the tongue may be pushed superiorly. Elevation of the tongue is the clinical hallmark of the sublingual space infection. This will bring about airway obstruction if the tongue and the flow of the mouth is raised that can cause airway obstruction. The ability to protrude the tongue beyond the vermilion border of the upper lip is also an important sign in sublingual space infection. Surgical drainage of sublingual axis can be performed both incra and extraorally. Incraorally an incision is made close to the lingual cortical plate lateral to the sublingual plica. The important structures to be taken care here are the lingual nerve, the water duct and the sublingual vessels. Extraoral approach is preferred when both the submental and sublingual spaces contain pus and it can be drained via skin incision placed in the submental region. Similarly when submandibular space is also involved, a sublingual space axis can be approached and drained through an incision in the skin overlying the submandibular space. The spread of infection from the sublingual to other spaces or region is possible. The infection always crosses the midline and it can affect the space on the opposite side. Infection from the posterior inferior part of the space can spread around the submandibular gland into the submandibular space. Similarly infection can also spread via lymphatics to the submendial or submandibular lymph nodes. The sublingual space is separated from the submandibular space by myelohyoid muscle in the anterior region. Therefore the spread to the submandibular region occurs most often as a result of lymphatic spread to the submandibular lymph nodes. The diagram here shows that the sublingual space is evacuated. Incision was placed, drainage is performed and the space is evacuated following which a corrugated rubber grain is inserted into the space through the extraoral incision. So it passes the anterior belly of digastric, the myelohyoid muscle and it emerges into the submlingual space. So this is performed on either side, it is performed bilaterally through the same incision you can place two rubber grains into the submlingual space on either side. Moving on to submandibular space, the submandibular and submlingual spaces are quite distinct anatomically. Still they are considered as a single surgical unit because of their proximity and frequent dual involvement in adentrogenic infections. Let's have a look at the boundaries that form the submandibular space. Antidomedially the floor of the submandibular space is formed by the myelohyoid muscle anteriorly and posterior medially the floor is formed by the hyoglossus muscle. So there are two muscles which form the medial extant of the submandibular space which are the myelohyoid and the hyoglossus muscle. Myelohyoid muscle also form the separation between the submlingual and submandibular space. As you can see in this diagram this is the myelohyoid muscle which separates the submlingual space from the submandibular space. Supido-lactoily the medial surface of the mandible forms the limit. So if this is the mandible the medial aspect of this mandible below the myelohyoid ridge it forms the supido-lactyl boundary of submandibular space. Postero-superially is the anterior belly of digastric. Here is the anterior belly of digastric and posterior superior is the posterior belly of digastric. Laterally the space is covered by platysma and skin. The submandibular space contains the superficial lobe of submandibular salivarid land and the submandibular lymph nodes. It also contains facial, artery and vein. How do odontogenic infections extend to submandibular space? This space is involved most frequently by infections originating from mandibular molars. The pus perforates the lingual cortical plate of mandible inferior to the attachment of the myelohyoid muscle and the infection passes directly to the submandibular space. It was told earlier that the teeth responsible for submlingual space infections are the mandibular anterior teeth as well as premolars. It is because their teeth apices were confined superior to the myelohyoid muscle whereas the teeth apices of the mandibular molars extend beyond the myelohyoid muscle thus extending the infection to the submandibular space. The infection from the submandibular salivarid land may also pass through lymphatics to the submandibular region. The submandibular space infections can also be a result of infections originating from the middle third of the tongue and posterior part of the floor of the mouth. The diagnosis of submandibular space infection can be confirmed by the presence of firms swelling in submandibular region just below the inferior border of mandible. The patient will present with generalized constitutional symptoms like fever, lethargy and malice. There will be some degree of tenderness present at the overlaying skin which will be erythematous or red in color. Intraoral findings include sensitive teeth which are tender on percussion, mobile teeth, dysphagia and moderate swissness. The surgical drainage of abscess from the submandibular space can be performed by placing an incision of about 1.5 to 2 centimeters 2 centimeters below the lower border of mandible within the skin crease. The skin and subcutaneous tissues are incised. A sinus forceps is inserted through the incision in supine and posterior direction on the lingual side of the mandible below the myelohyroid. This will release pus from submandibular space. Later a corrugated rubber drain is inserted into the abscess cavity and is secured with a suture. Adversing can also be applied. Coming to the spread of infection from submandibular space. There are no major anatomic barriers between the two submandibular and submental spaces. Hence infection can extend into the submental space as well as the contralateral submandibular space. The submandibular space also communicates with sublingual space around the posterior border of myelohyroid muscle. Pediaferringal spaces can also get involved when there is a backward spread of infection. So that's all about the submental, sublingual and submandibular space infections. Rest of the facial spaces shall be explained in subsequent lectures. Thank you. MFS lecture series. The topic for the lecture is Ptergomandibular space infection. Ptergomandibular space is a part of the masticator space which apart from the Ptergomandibular space also contains other spaces like submasicric space, superficial temporal space and deep temporal spaces. All these spaces are well differentiated but they communicate with each other as well as with other spaces like buccal, submandibular and pediaferringal spaces. The masticator space is formed by splitting of the investing fascia, investing layer of deep cervical fascia into superficial and deep layers. So the fascia defines its lateral and the medial extent. The masticator spaces again divided into mesotritic compartment and tergoid compartment. Boundaries of the mesotritic compartment are the masticator muscle laterally and the mandibular ascending ramus medially. The tergoid compartment is bounded by medial tergoid muscle medially and the medial aspect of the mandible laterally. Ptergomandibular space is found to be the most frequently anatomical compartment in cases of severe odontogenic infections. The most common etiology of Ptergomandibular space infection is the pericoronitis of mandibular third molar. Infection can also be produced by a contaminated needle used for an inferior alveolar nerve block or a posterior superior alveolar nerve block injection. Talking about the boundaries of Ptergomandibular space, laterally the space is bounded by the medial aspect of the ramus of mandible. The lateral surface of the medial tergoid muscle forms the medial limit. Here is the lateral limit, this is the medial limit. Posterially the boundary is formed by the deep part of padotted gland and anteriorly there is the Ptergomandibular pathway which is formed by the superior constrictor and the buccinator muscle and the roof of the Ptergomandibular space is formed by the lateral tergoid. As already mentioned the infection of Ptergomandibular space is associated with pericoronitis of third molar. Even the established cases of Ptergomandibular space infections do not cause much swelling of the face. The clinical hallmark of every masticator space infection is prismus. If prismus is not present then it can be considered that these spaces are uninvolved in the infectious process. Tenderness can be elicited over the area which is swollen and present medial to the anterior border of ramus. Dysphagia is present, dysphagia means difficult swallowing. There is medial displacement of the lateral wall of the pharynx and redness and edema of the area around the third molar. Midline of the pallet is displaced to the unaffected side and also the uvula appears swollen. It is also associated with difficulty in breathing. Surgical access to the various compartments of masticator space is complicated by the containment of the infectious process within the muscle masses. Secher has suggested an intraoral approach to Ptergomandibular space by placing a vertical incision along the Ptergomandibular raffae on the medial aspect of the ramus. A sinus forceps is then inserted into the abscess cavity and opened and closed. It is then withdrawn. The pus is evacuated, a rubber drain is introduced and is secured in position with a suture. The oral approach is a less feasible approach in infected patient with twismis. In such patients, the oral approach can compromise the airway postoperatively because of persistent blood and pus oozing out of the incision. Also, there are chances that the drain which is sutured will get loosened and the patient can aspirate it. In such cases, an extraoral approach can be taken. An incision is taken in the skin below the angle of the mandible. A sinus forceps is then inserted towards the medial side of the ramus in an upward direction and backward direction. Pus is evacuated, a drain is inserted from an incoral approach and sutured in position. These diagrams show the pathway of spread of infection from Ptergomandibular space, which is numbered 2, to its neighboring and distant spaces. The arrow numbered 1 shows that the infection can spread posteriorly to lateral pharyngeal space and then to retropharyngeal space. In this diagram, here is the posterior spread of infection. The second path of spread is superiorly along the medial aspect of the ramus to involve the infratemporal fossa. Through this region, the infection can spread to infratemporal fossa. Through the lateral aspect of the ramus, submesitvic space can get involved. Infection can spread along the front of the ramus to involve the buccal space. Number 4 is to involve the buccal space. It can also spread anteriorly below the lower border of mandible and also under the superior constrictor muscle to involve the submandibular space. So, this is regarding the spread of infection from Ptergomandibular space to the neighboring spaces as well as distant spaces. Therefore, Ptergomandibular space infection should be diagnosed and managed at an early stage considering its potential communication with other spaces and also associated complications. So, that's all for this lecture. Thank you. Welcome back to OMFS lecture series. In this lecture, let us discuss cavernous sinus thrombosis. As its name suggests cavernous sinus thrombosis is a serious condition consisting of formation of thrombus in the cavernous sinus or its communicating branches. Infection of head, face and intra-ory structures. In particular, the structures above maxilla. It is the infection of these structures that lead to this condition. Now, let's have a brief description about the anatomy of cavernous sinus. Each cavernous sinus is a large venous space situated in the middle cranial fossa on either side of the body of the spinoid bone. A closer look at the sinus shows that the optic chiasma, the internal carotid artery and the optic crack are present superior to the cavernous sinus. The structures in the lateral wall of the cavernous sinus from above downwards are the oculomoto nerve, the cochlear nerve, the ophthalmic and maxillary division of the fifth cranial nerve. All these structures are present in the lateral wall of the cavernous sinus. Structures passing through the center of the cavernous sinus are the internal carotid artery and the sixth cranial nerve which is the abducent nerve. There are a few incoming channels to the cavernous sinus. That means there is blood flow from different regions into the cavernous sinus. From the orbit, the superior of dalmic vein, the inferior of dalmic vein and central vein of retina, drain into the cavernous sinus on either side. The meninges drain into the cavernous sinus via spino-padital sinus and middle meningeal vein. This is the drainage from meninges to the cavernous sinus. Similarly, drainage from the brain reaches the cavernous sinus through superficial middle cerebral vein and inferior cerebral vein. There are communications between the cavernous sinus and other distant veins through which their contents get exchanged. For example, the cavernous sinus drains into the transverse sinus through superior petrosal sinus. It also drains into internal jugular vein through the inferior petrosal sinus. This communication is into the internal jugular vein. Also, the cavernous sinus drains into the pterigoid plexus of veins through emissary vein that passes through the furamen, ovale and spinosum. Here is the communication from the cavernous sinus into the pterigoid plexus of veins through the emissary vein. The cavernous sinus also flows or drains into the facial vein through superior of dalmic vein. Here is another communication where the cavernous sinus drains into the facial vein via superior of dalmic vein. Also, the right and left cavernous sinus communicates through intercavernous sinuses. Here is the intercavernous sinus that forms a communication between the left and right cavernous sinuses. So, all these communications are valueless and the blood can flow through them in either direction. The main causative factors of cavernous sinus thrombosis are infections arising from the face, maxillary sinus and maxillary teeth. The less common causes are the infections arising from tonsils, soft palate, middle ear and orbit. Complications of cavernous sinus thrombosis are rapid and occasional death can result due to the infections arising from the upper part of the face. The three possible reasons for this complications are the short distance from the facial regions to the sinuses, frequent and complicated anastomosis of these veins leading to direct communications with the sinuses and also lack of protective valves. Unlike other venous systems of the body, the veins in the facial region are valueless. So, all these factors account for the complications arising from cavernous sinus thrombosis. The various bacteria implicated in the sinus thrombosis are strutococci and staphylococci along with some gram narrative bacteria. Moving on to the clinical features, generalized constitutional symptoms like high fluctuating fever, chills, rapid pulse and sweating are frequently associated with cavernous sinus thrombosis. The initial symptoms present with swelling of the face and edematous involvement of the eyelids. There is pain in the eye and it is also tender to pressure. There is venous obstruction that leads to marked edema and congestion of eyelids. Edema of conjunctiva due to impaired venous return is also observed. There is pulsating X of thalamus and involvement of the third, fourth, fifth and sixth cranial nerves. So, this will result in of thalamoplegia and paracis or paralysis of the lateral rectus muscle of the eye. This is also papillodema with multiple retinal hemorrhage. Epitaxis or nose bleeding is also found due to increased intracranial pressure. These are the initial symptoms associated with cavernous sinus thrombosis. If left untweeted, the late symptoms develop which include thrombophlebitis which spread to the other side or there is bilateral signs that can be made out. In advanced stage of cavernous sinus thrombosis, there may be signs of toxemia and meningitis. Positive kerinic sign can also be elicited. What is kerinic sign? It is severe stiffness of the hamstrings. Hamstrings are nothing but posterior thigh muscles. So, there are stiff hamstrings which cause an inability to straighten the leg when the hip is flexed to 90 degree. When there is a hip flexion at 90 degree, there is stiffness of the hamstring muscle. It is called positive kerinic sign. What is positive grudinski sign? It is the passive flexion of the neck which causes flexion of both legs and the thighs. As you can see in this diagram, as the neck is flexed, there is flexion of the thighs and legs as well. Another positive sign is Biods respiration. It is an abnormal pattern of breathing characterized by regular deep inspirations followed by a period of apnea. This sign is seen in patients with acute neurological diseases. It is named after the person who characterized the condition. There is also septicemia with leukocytosis and severe acidosis with a positive blood culture. So, unless it is treated early, the prognosis of the condition is poor. Eagleton has suggested six criteria for the establishment of diagnosis sinus thrombosis. Those six features are a known site of infection, evidence of bloodstream infection, early sign of venous obstruction in the retina, conjunctiva or eyelids, paralysis of the third, fourth and sixth cranial nerves that result from inflammatory edema, abscess formation and involvement of neighboring tissues. There should be an evidence of meningeal irritation. So, these are the six criteria suggested by Eagleton in order to establish the diagnosis of cavernous sinus thrombosis. Cavernous sinus thrombosis management includes the use of antibiotics directed at the causative organism and surgery to remove the primary source of infection. Immediate empirical antibiotic coverages mandatory which is followed by specific antibiotics which is adjusted to the cultures and sensitivities. Heparinization followed by antibiotic therapy will help prevent extension of thrombosis. Meningitis, ophthalmoplegia, kerinic signs, all are confirmatory findings of neurological involvement. Therefore, a neurosurgical consultation is a must. IV-manitol helps reduce the brain edema. Likewise, anticoagulants prevent venous thrombosis. Surgical drainage and elimination of the primary source of infection is also very important. Hence, to conclude, cavernous sinus thrombosis is still prevalent though patients now have better survival rates. It needs an early diagnosis and prompt intervention to yield a favorable result. So, that's all about the topic. Thank you. OMFS lecture series. The topic for this lecture is Ludwigsangena. Ludwigsangena is basically a type of severe cellulitis involving the flow of the mouth. It is a name given to a massive firm brony cellulitis or induration and acute toxic stage involving simultaneously deep submandibular, sublingual and submental spaces bilaterally. So, this is the definition of Ludwigsangena. This condition was first described by Willem Frederick von Ludwig in the year 1836. So, as the definition suggests, only the bilateral involvement of the above mentioned spaces is considered to be a classical disease of Ludwigsangena. All other types of presentations, though massive, are not considered as Ludwigsangena. The word angena is derived from the Latin word angere meaning suffocation or choking sensation and the word Ludwig comes from the person to whom the credit goes for its description. This condition has established its unique identity with three Fs as it was to be feared, it rarely becomes fluctuating and it was often fated. Many other terminologies were also used for this condition, which include Marbes strangulatoris. This is also called angena maligna and gadotilo. There are various causes attributed to Ludwigsangena, for example, autotogenic infection. These infections in the form of acute dental valvular abscess, acute pedodontal abscess or acute pericoronal abscess. All these can lead to Ludwigsangena. As already told in the lecture on tergomandabila space infection, pericoronal abscess in relation to erupting third molars can extend into sublingual, submandabila and tergomandabila spaces, thus resulting in Ludwigsangena. Use of a contaminated needle for giving local anesthesia is an iocogenic cause. Traumatic injuries to the orophacial region, like a compound and communicated mandibular fractures or a deep penetrating wound, can also lead to this condition. Ostromylitis second way to compound mandibular fractures or an acute exacerbation of chronic ostromylitis of mandible may develop into Ludwigsangena. Acute or chronic infections of salivary glands, for example, sublingual and submandibular xyladenitis are also causes of this condition. The malignancies of oral region, it can give rise to second way infection, thus leading to this condition. The miscellaneous causes of Ludwigsangena include infections in the tonsils or pharyngeal area, foreign bodies such as fish bone or oral soft tissue lacerations. So, this is regarding the ecology of Ludwigsangena. Here you need to understand that the condition of Ludwigsangena is a cellulitis, which is a diffuse inflammation of soft tissues, which is not circumscribed or confined to one area. But in contrast to the abscess, it tends to spread through tissue spaces and along facial planes. So, such type of spreading infection occurs in the presence of organisms that produce significant amounts of hyaluronic days and fibrino license, which add to breakdown or dissolve the hyaluronic acid and fibrin. A plethora of microorganisms has been implicated as the causative agents of Ludwigsangena. Few of the microorganisms which were able to isolate from the culture specimen include Staphylococci, Structococci, E. coli, Bacteroids, anaerobic Structococci, Peptostructococcus and Fusospirotids. The condition of Ludwigsangena usually follows a submandibular space infection caused by a periapital infection or pericoronitis around the mandibular second and third molar. The apices of these teeth are usually placed below the myelo-hyoid line of myelo-hyoid muscle so that the infection tends to spread primarily to the submandibular spaces. The infection then spread to the sublingual space around the submandibular gland, which is present posterior to the space. The submental space is also involved by lymphatic spread. This condition can also occur in converse manner that is by spread from the sublingual space to the submandibular space. The signs and symptoms of Ludwigsangena are present with varying degree of severity. Upon general examination, the patient looks toxic, very ill and dehydrated. There is pyrixia, anorexia, chills and malaise. There is dysphagia or difficulty in swallowing. The speech is impaired and there is hollessness of voice. Upon external examination, there is a firm, hard brownie swelling in the bilateral submandibular and submandial regions, which may extend down to the anterior neck till the clavicle. There is severe muscle spasm, which may lead to Christmas or restricted jaw movements. So here, typically the mouth remains open due to edema of the sublingual tissues leading to raised tongue, which almost touches the palatal valve. There is airway obstruction and the respiratory rate may be seen to be raised. Breathing being shallow with accessory muscles of respiration being used. Sinosis may occur due to the progdosev hypoxia. Ultimately, fatal death may occur in untreated case of Ludwigsangena within 10 to 24 hours due to asphyxia. Incrowarly, the swelling develops rapidly, which involves the sublingual tissues and raises the flow of mouth. The tongue may be raised against the palate. There is increased salivation, stiffness of tongue movements and difficulty in swallowing. A backward spread of infection leads to edema of glottis, thus resulting in respiratory obstruction. Strider is a harsh vibrating noise when breathing, which is caused by obstruction of tuikeya or larynx. Striders and alarming sign of Ludwigsangena, which needs emergency intervention to keep the airway patent. Some of the sublingual spaces, the infection may spread backwards towards the region of epiglottis. This produces swelling around the laryngeal inlet. Due to anatomical continuity of various spaces with submallibular space, the infection may spread posteriorly to the mastectobic spaces and the pedopharyngeal spaces, thus worsening the airway compromise. Infection from the submallibular region can also spread downwards beneath the investing layer of deep cervical fascia towards the clavicle and towards the mediastenum, thus causing mediastenitis. Less commonly, infection can spread below towards the catarotid sheet also, which leads to cavernous sinus thrombosis with subsequent meningitis. Ludwigsangena, if untreated, can be fatal within 12-24 hours, death arising from asphyxia. The cases may become more complicated with involvement of other spaces. Therefore, the condition should be taken as a life-threatening emergency situation and is best treated by aggressive intervention. The treatment is based on the combination of the following factors. Early diagnosis, maintenance of patent airway, intense and prolonged antibiotic therapy, extraction of offending teeth and surgical drainage or decompression of facial spaces. Surgical drainage or decompression is performed under general anesthesia given to the patient by a skilled anesthesiologist. An awake endocracheal intubation is performed using fiber optic laryngeoscope and nasopharyngeal airway is maintained. In case of Ludwigsangena, the death can occur from asphyxia rather than the infection itself. Hence, it is advisable to observe the patient for respiratory obstruction and restlessness. Blind intubation should be always avoided. Nasoendocracheal intubation is far more reliable and it is almost predictable. Therefore, it is preferred. Surgical airway may be required in case of severe upper respiratory obstruction. Laryngeotomy or cricothyroidotomy is preferred over tracheostomy considering the complications associated with tracheostomy. The surgical intervention has two main aims. To remove the cause and surgical decompression. The advantages of early surgical decompression include the following. It reduces the pressure of edematous tissue on the airway, thus reducing respiratory obstruction. It allows prompt drainage if any separation develops. It also allows obtaining specimen or samples for staining and culture and sensitivity. It allows placement of drains which may be useful to drain the pus collection. And also it helps in irrigation of the tissues at regular intervals. Antibiotics play a vital role in managing Ludwigsangena. Usually, IV antibiotics with proper dosage and frequency are necessary. Pencilins are the first line of antibiotics in treating Ludwigsangena as it is a broad spectrum antibiotic. Semi-synthetic derivatives of penicillin like ampicillin or amoxicillin may be also used. In case of allergy to penicillin, the patient is administered Lerotromycin. Antibiotics should be changed subsequent to the result of bacterial culture and sensitivity testing. The therapy should also be changed if the favorable results are not observed after 48 to 72 hours of therapy. Most cases of Ludwigsangena are dehydrated. This is because of two reasons. Diminished liquid intake due to pain and discomfort associated with dysphagia. So due to the toxic nature of the condition, there is usually excessive urination and perspiration which further diminishes body fluids. For these reasons patients should be encouraged to have liquids frequently and if required intravenously fluids can maintain hydration and also calories. A simple protocol for the management of Ludwigsangena include a pre-pedi and post-operative protocol. Pre-operative airway assessment includes observing the signs and symptoms of obstruction. Thoroughly examine the mouth opening, the tongue mobility, the region of uvula and fascial pillars. Confirm the etiological findings using an orthopantamogram or a CT scan of head and neck. Consider the risk factors like diabetic and immunodeficiency. Check if the patient is well hydrated by monitoring the BP pulse and urine output. Check the temperature. Assess the blood and urine cultures for septicemia. Apply cold packs and use antibiotics as required. Obtain chest radiographs to rule out pneumonia. Evaluate the lab data for blood count and protein levels and also consider emergency airway preparations. The pedioperative protocol includes incubation, rimuloptic cause and surgical drainage and appropriate antibiotics. The post-operative considerations include extubation after confirming and adequate airway, periodic irrigation of the drains, obtaining culture reports to adjust the antibiotics accordingly, revaluation of lab reports, monitoring the colds of infection and re-exploration and drainage if necessary and finally following up the patient regularly. Ludwig-Sangina continues to be a cause of significant morbidity and mortalities. The various complications associated with Ludwig-Sangina are osteomyelitis, maxillary sinusitis, localized respiratory tract disturbances as well as digestive tract disturbances. Even more serious complications include life-threatening airway obstruction, septicemia, distant metastatic focus, mediastinitis, pedicarditis, internal jubilar vein thrombosis, several neurological complications, involvement of carotid shape and ultimately death. Talking a little more about mediastinitis, the mediastinum is the set well portion of the thorax. It is bounded bilaterally by the pleura, lengthily by the sternum, dorsally by the vertebrae and inferiorly by the diaphragm. Vital structures located within the mediastinum include the heart, the aortic arch, the lungs, carotid and subclavian arteries, the thoracic duct, vagus nerve, the trachea and esophages. Therefore, autotogenic infection spreading to the mediastinum is a life-threatening complication and it should be suspected in the patient who exhibits exacerbation of fever associated with substernal pain. Therefore, mediastinitis is an infection involving the connective mediastinal tissue that fills the inter pleural space and surrounds the median thoracic organs. The chest x-ray will show typical widening of the mediastina. There is also pleural effusion and obliteration of sternal spaces. Treatment includes early recognition, airway management and aggressive surgical intervention. Appropriate antibiotic therapy should be followed along with supportive systemic care and hyperbaric oxygen therapy whenever indicated. Hence, to conclude Ludwig Sangeina is a life-threatening complication associated with orophacial infections which can become fatal if not timely diagnosed and intervened. That's all for this lecture. Thank you.