 The topic for this lecture is Ludwig's angina. Ludwig's angina 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 the submandibular, sublingual and submental spaces bilaterally. So this is the definition of Ludwig's angina. 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 Ludwig's angina. All other types of presentations though massive are not considered as Ludwig's angina. The word angina 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 fatal. Many other terminologies were also used for this condition which include Marbelle's triangulatories. It is also called angina maligna and gadotilo. There are various causes attributed to Ludwig's angina. For example, Audentogenic Infection. These infections in the form of acute dental alveolar abscess, acute pedodontal abscess or acute pericoronal abscess. All these can lead to Ludwig's angina. As already told in the lecture on tergomandibular space infection, pericoronal abscess in relation to erupting third molars can extend into sublingual, submandibular and tergomandibular spaces. Thus resulting in Ludwig's angina. Use of a contaminated needle for giving local anesthesia is an iatrogenic 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 secondary to compound mandibular fractures or an acute exacerbation of chronic ostromylitis of mandible may develop into Ludwig's angina. Acute or chronic infections of salivary glands. For example, sublingual and submandibular phyladenitis are also causes of this condition. The malignancies of oral region. It can give rise to secondary infection thus leading to this condition. The miscellaneous causes of Ludwig's angina include infections in the tonsils or pharyngeal area, foreign bodies such as fish bone or oral soft tissue lacerations. So this is regarding the etiology of Ludwig's angina. Here you need to understand that the condition of Ludwig's angina 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. Such type of spreading infection occurs in the presence of organisms that produce significant amounts of hyaluronidase 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 Ludwig's angina. Few of the microorganisms which were able to be isolated from the culture specimen include Staphylococci, Streptococci, E. coli, Bacteroids, anaerobic Streptococci, Peptostreptococcus and Fusospyrotids. The condition of Ludwig's angina usually follows a submandibular space infection caused by a pediapycle infection or pedicoronitis 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 Ludwig's angina are present with varying degree of severity. Upon general examination, the patient looks toxic, very ill and dehydrated. There is pyrexia, anorexia, chills and malaise. There is dysphagia or difficulty in swallowing. The speech is impaired and there is hoarseness of voice. Upon external examination, there is a firm, hard brownie swelling in the bilateral submandibular and submandible regions, which may extend down to the anterior neck to 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 vault. There is airway obstruction and the respiratory rate may seem to be raised, breathing being shallow with accessory muscles of respiration being used. Sinosis may occur due to the progdaseive hypoxia. Ultimately, fatal death may occur in untreated case of Ludwigs angina within 10 to 24 hours due to asphyxia. Intraordinary 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 backwards 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 trachea or larynx. Strider is an alarming sign of Ludwigs angina, 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 submalubular space, the infection may spread posteriorly to the mastectric spaces and the pedopharyngeal spaces, thus worsening the airway compromise. Infection from the submalubular region can also spread downwards beneath the investing layer of deep cervical fascia towards the clavicle and towards the mediastinum, thus causing mediastinitis. Less commonly, infection can spread below towards the catarotid sheet also, which leads to cavernous sinus thrombosis with subsequent meningitis. Ludwigs angina, 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 endotracheal intubation is performed using fibroptic laryngeoscope and nasopharyngeal airway is maintained. In case of Ludwigs angina, 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. Naso-endocrine 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 specimens 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 Ludwigs angina. Usually, IV antibiotics with proper dosage and frequency are necessary. Pencilins are the first line of antibiotics in treating Ludwigs angina 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 erythromycin. Antibiotics should be changed subsequent to the result of bacterial culture and sensitivity testing. The therapy should also be changed if the favorable vessels are not observed after 48 to 72 hours of therapy. Most cases of Ludwigs angina are dehydrated. This is because of two reasons. Diminished liquid intake due to pain and discomfort associated with dysphagia. 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 Ludwigs angina include a pre-peri 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 diabetes 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 pre-operative protocol includes incubation, removal of the cause and surgical drainage and appropriate antibiotics. The post-operative considerations include extubation after confirming an adequate airway, periodic irrigation of the drains, obtaining culture reports to adjust the antibiotics accordingly, evaluation of lab reports, monitoring the colds of infection and re-exploration and drainage if necessary. And finally, following up the patient regularly. Ludwigsangina continues to be a cause of significant morbidity and mortalities. The various complications associated with Ludwigsangina 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, mediastionitis, pedicarditis, internal jugular vein thrombosis, several neurological complications, involvement of carotid shape and ultimately death. Talking a little more about mediastionitis. The mediastionum is the sexual portion of the thorax. It is bounded bilaterally by the pleura, lengthally by the sternum, dorsally by the vertebrae and inferiorly by the diaphragm. Vital structures located within the mediastionum 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 mediastionum is a life-threatening complication. And it should be suspected in the patient who exhibits exacerbation of fever associated with substernal pain. Therefore, mediastionitis is an infection involving the connective mediastional tissue that fills the interplural space and surrounds the median thoracic organs. The chest x-ray will show typical widening of the mediastionum. 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.