Universal Journal of Pharmacy

Shamimul Hasan et al. UJP 2013, 02 (05): Page 1-4

Universal Journal of Pharmacy

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Review Article ISSN 2320-303X

Take Research to New Heights

LUDWIG’S ANGINA- AN ALARMING MULTIDISCIPLINARY CHALLENGE - OVERVIEW OF LITERATURE Shamimul Hasan1*, Sarah Asif2, Shakeba Quadri3 *1

MDS; Assistant Professor Deptt of Oral Medicine and Radiology Faculty of Dentistry Jamia Millia Islamia New Delhi, India 2 BDS Z.A Dental College & Hospitals Aligarh Muslim University Aligarh, India 3 BDS Z.A Dental College & Hospitals Aligarh Muslim University Aligarh, India

Received 12-07-2013; Revised 10-08-2013; Accepted 12-09-2013

ABSTRACT Ludwig’s angina is a rare, potentially life threatening diffuse cellulitis, usually originating from odontogenic infection. It usually involves bilateral deep tissue spaces and causes elevation of the tongue, woody brawny induration of the floor of the mouth, trismus and laryngeal edema. Airway obstruction and cavernous sinus thrombosis are serious complications and the condition may be fatal. Early diagnosis, prompt airway control, aggressive antibiotic administration and surgical intervention is essential to combat an unfavourable outcome. Keywords: Ludwig’s angina, airway obstruction, antibiotics.

INTRODUCTION The clinical entity now known as Ludwig angina (LA) was described in the times of Hippocrates and Galen. This serious and potentially fatal disease continues to be discussed in the otolaryngology and oral surgery literature. Karl Friedrich Wilhelm von Ludwig provided a clear description of this disease process in 1836 after careful observation over time of its clinical course and postmortem findings. He described the pathophysiology as rapidly progressive gangrenous cellulitis that began in the vicinity of the submandibular gland and spread via continuity rather than through the lymphatic system 1,2,3 .Ludwig’s angina is a potentially life threatening diffuse cellulitis involving the floor of the mouth, submandibular regions bilaterally and causing progressive airway obstruction3, typically; ludwig’s angina is characterized by fever, malaise, dyspnea, dysphagia as well as brawny hard tender swelling of the floor of the mouth and neck 4,5,6. Etiology of Ludwig’s angina includes odontogenic infection, penetrating injury of the floor of the mouth, osteomyelitis, compound fracture of the jaw, otitis media, submandibular gland sialidenitis, sialolithiasis *Corresponding author: Dr Shamimul Hasan C/O Mohd Javed Khan C-4, Duplex Quarters, New Sir Syed Nager, Aligarh 09953290676; 09411467630 Email:[email protected]

and tongue piercing2,7,8,9. Of all these, the major cause is of odontogenic infection, mainly around the second and third lower molar teeth7,10. Most odontogenic infections are uncomplicated resolving following the removal of the cause and sometimes with antibiotic therapy. However, a few cases of odontogenic infections do get complicated by Ludwig’s angina amongst others. Several factors which may either act locally or systemically are responsible for these complications11,12,13. Treatment invariably consist of securing the airway where necessary , aggressive broad spectrum antimicrobial therapy, and surgical decompression of the facial planes with removal of source of infection5,6,14.

DISCUSSION The danger of airway obstruction from soft tissue swelling in the head and neck has been appreciated since antiquity, with specific references being made by Hippocrates, Galen, Aretius, and Paulus of Aegin. Wilhelm Frederich von Ludwig in 1836 described “repeated recent occurrence of a certain type of inflammation of the throat, which, despite the most skillful treatment, is almost always fatal.” 15 It was known as Morbus Strangulatorius and Garotillo (Spanish for hangman’s loop); all names alluding to the respiratory obstruction so prominent in disease morbidity16. Ludwig’s angina is a serious and rapidly progressive infectious process that spreads by the floor of the

Universal Journal of Pharmacy, 02(05), Sep-Oct 2013

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Shamimul Hasan et al. UJP 2013, 02 (05): Page 1-4 mouth affecting simultaneously to submandibular, sublingual and submental spaces. The infection generally begins as cellulites, then it turns into fasciitis, and finally, into real abscess that results in a woody and hard swelling of the floor of the mouth and suprahioid region in a bilateral form, with displacement of the tongue and airway affectation17. ETIOLOGY Ludwig’s angina usually originates from an odontogenic infection, especially from the second or third lower molars. These teeth have roots that lie at the level of the mylohyoid muscle, and abscesses here can spread to the submandibular space. Other less commonly reported causes of Ludwig’s angina include sialadenitis, peritonsillar abscess, open mandibular fracture, infected thyroglossal duct cyst, epiglottitis, intravenous injections of drugs into the neck, traumatic bronchoscopy, endotracheal intubation, oral lacerations, tongue piercing, upper respiratory infections, and trauma to the floor of the mouth. Predisposing conditions include diabetes mellitus, neutropenia, alcoholism, aplastic anemia, glomerulonephritis, dermatomyositis, and systemic lupus erythematosus18. PATHOPHYSIOLOGY The development of Ludwig’s angina is facilitated by the anatomy of the floor of the mouth. Periapical dental abscesses of the second and third molars penetrate the inner cortex of the mandible. Because these roots extend inferiorly to the mandibular insertion of the mylohyoid muscle, submandibular infection ensues. Communication around the posterior margin of the mylohyoid muscle produces rapid involvement of the sublingual and contralateral spaces. The mandible, hyoid, and superficial layer of the deep cervical fascia limit tissue expansion as edema develops. This leads to superior and posterior displacement of the floor of the mouth and tongue base. The resulting airway compromise can be insidious until it is nearly complete, when abrupt asphyxiation occurs1. The organisms most commonly cultured from oral infections include Streptococcus viridans and Staphylococcus aureus, as well as anaerobic B. melaninogenicus and peptostreptococcus19. Isolation of gram-negative organisms like H. influenza, E. coli, Pseudomonas, and Neisseria are not frequent. CLINICAL FEATURES Most cases of Ludwig’s angina occur in previously healthy persons. Most affected patients are between age 20 and 60 years, although an age range from 12 days to 84 years has been reported 18. There is a male predominance (3:1 to 4:1) of the disorder. Patients with Ludwig’s angina typically have a history of recent dental extraction or of poor oral hygiene and dental pain. Clinical findings are consistent with sepsis and include fever, tachypnea, and tachycardia. Patients

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may be anxious, agitated, and confused. The disease is recognized by 5 identifiable characterstics: (1) Submandibular cellulitis; (2) Involvement of more than 1 space; (3) Progression of cellulitis to gangrene with serosanguineous infiltration and minimal purulence; (4) Extension of cellulitis to connective tissue fascia; and (5) Spread of cellulitis by continuity, not via the lymphatics2. Many patients with Ludwig’s angina demonstrate a “Bull neck” appearance as the inflammation spreads to the submandibular region, giving the appearance of a large “Double chin”. Hoarseness, stridor, respiratory distress, decreased air movements, cyanosis, and a “sniffing” position (characterstic position assumed by patients with impending upper airway compromise consisting of an upright posture with the neck thrust forward and the chin elevated) are all signs of impending airway catastrophe. More specifically, they may have a muffled tone at higher registers (“Hot potato” voice) caused by edema of the vocal apparatus; this finding should be a warning to clinicians of potentially severe airway compromise. Adenopathy and fluctuance are not usually seen in patients with ludwig’s angina. DIAGNOSIS AND INVESTIGATIONS Awareness and recognition of the possibility of Ludwig’s angina is the first and most essential step in the diagnosis and management of this serious condition. The presence of brawny induration of the floor of the mouth in a suggestive clinical presentation should prompt the clinician to move rapidly toward airway stabilization first, followed by further diagnostic confirmation. Plain radiographs of the neck and chest often show soft-tissue swelling, the presence of gas, and the extent of airway narrowing. Sonography has been used to identify fluid collections in the soft tissues, as has gallium citrate Ga-67 scanning. Panoramic radiographic views of the jaw may show a dental focus of infection. After the airway patency is assured, CT scanning is a valuable modality to show the extent of soft-tissue swelling, the presence of gas, fluid collection, and airway compromise. Magnetic resonance imaging is another elegant modality that can be considered in some patients18. DIFFERENTIAL DIAGNOSIS The differential diagnosis of Ludwig’s angina includes angioneurotic edema, lingual carcinoma, sublingual hematoma (following anticoagulation), salivary gland abscess, lymphadenitis, cellulitis, and peritonsillar abscess. TREATMENT OPTIONS Ludwig's angina was formerly invariably fatal but now, with adequate surgical and antibiotic treatment, has a much reduced rate of mortality6. It remains, however, a potentially life-threatening condition because of the risk of impending airway obstruction. Thus, because of


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Shamimul Hasan et al. UJP 2013, 02 (05): Page 1-4 its invasive nature, early recognition and treatment of Ludwig's angina is extremely important. The first therapeutic consideration in patients with Ludwig’s angina is the airway management, because it is mandatory to preserve it early by means of a fiberoptic nasotracheal intubation or tracheostomy. Medical management with antibiotics, improved dental care and dexamethasone in the early stages of the disease has minimized the need for surgical intervention to control the airway10. Different antimicrobial regimen have been recommended to cover in broad-spectrum the polymicrobial aetiology (gram - positives, gram-negatives, aerobes and anaerobes). Antibiotics used before obtaining the culture and the antibiogram results, have been penicillin G intravenous, clindamycin or metronidazole20. Aminoglucosides have been also associated in some studies 21. Other alternatives described are ticarcilin, sulbactam-ampicilin or piperacilin-tazobactam. Cervical incision and surgical débridement are indicated when there is suppurative infection, radiologic evidence of fluid collection or soft-tissue air, clinical fluctuance, crepitus, or a purulent needle aspirate. Drainage is also indicated when there is no clinical improvement after 24 at 48 hours of intravenous antibiotics. The delay in the realization of the surgical intervention has been related to mortality increase. It has been demonstrated that early elimination of the dental focus of the infection reduces the time of recovery17. Intravenous dexamethasone and nebulized adrenaline have been used to reduce upper airway edema in such cases to defer or avoid airway instrumentation altogether22 . In an exhaustive review of the literature, from 1945 to 1979, 75 cases of Ludwig angina were found, and the authors strongly advocate elective tracheostomy under local anaesthesia. However, there may be good reason to avoid tracheostomy7. Cellulitis of the neck with in volvement of the tracheostomy site makes it a more difficult procedure. Moreover, surgical dissection of the fascial planes in the neck may actually open and contaminate the pathways, leading to life-threatening mediastinal invasion19. More recent reviews of anesthesia management report good results without the use of tracheostomy15. Other options for airway management may include orotracheal, blind nasotracheal, and fiber optic intubation or cricothyroidotomy with jet insufflation. The prognosis in Ludwig’s angina depends primarily on immediate protection of the airway and then on prompt antibiotics, and possibly surgical treatment of the infection. Mortality in the preantibiotic era was 50% but, with the advent of current therapies, has declined to less than 5%. COMPLICATIONS The most serious complication of Ludwig's angina is asphyxia caused by expanding edema of soft tissues of

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the neck23. Another common cause of death is the acute loss of airway during interventions to control the condition24. The possible serious complications include sepsis, pneumonia, empyema, pericarditis, mediastinitis, and pneumothorax .

CONCLUSION Ludwig’s angina, a potentially alarming condition, is a deep tissue infection that causes respiratory distress. Clinical manifestations are bizarre, hence, accurate diagnosis and treatment planning is required for the survival of the patient. Mutidisciplinary approach involving the dental surgeons, anaesthetists and ENT (Ear Nose and Throat) specialists play an important role in managing this fatal disease. Aggressive antibiotic intervention, adequate hygiene maintainence may be sufficient in the early stages, if correct diagnosis is established.

REFERENCES 1.

2.

3.

4.

5. 6.

7.

8.

9.

10.

11.

Marple BF. Ludwig angina: a review of current airway management. Arch Otolaryngol Head Neck Surg. 1999: 125, 595-598 Honrado CP, Lam SM, Karen M. Bilateral submandibular gland infection presenting as Ludwig’s angina: first report of a case. Ear Nose Throat J. 2001:80, 217-218,222-223. Murphy S. The person behind the eponym: Wilhelm von Ludwig, 1790-1865. J Oral Pathol Med. 1996: 25, 513-515. Odusanya SA. Ludwig’s angina in a Nigerian with sickle cell disease. Nig Dent J. 1989: 14, 3-7. Hartmann RW. Ludwig’s angina in children. Am Fam Physician. 1999: 60, 109-112. Iwu CO. Ludwig’s angina: report of seven cases and review of current concepts in management. Br J Oral Maxillofac Surg. 1990: 28, 189-193. Hought RT, Fitzgerald BE, Latta JE, Zallen RD. Ludwig’s angina: report of two cases and review of the literature from 1945 to January 1979. J Oral Surg. 1980: 38, 849-855. Perkins CS, Meisner J; Harrison JM. A complication of tongue piercing. Br Dent J. 1997: 182, 147-148. Wong TY. A nationwide survey of deaths from oral and maxillofacial infections: The Taiwanese experience. J Oral Maxillofac Surg. 1999: 57, 1297- 1299. Kulkarni H Anand, Swarupa D Pai, Basant Bhattarai, Sumesh T Rao, M Ambareesha. Ludwig’s angina and airway considerations: a case report. Cases Journal. 2008: 19, 1-4. Baker KA, Fotos PG. The management of odontogenic infections. A rationale for


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Shamimul Hasan et al. UJP 2013, 02 (05): Page 1-4

12.

13.

14.

15.

16.

17.

appropriate chemotherapy. Dent Clin North Am. 1994: 38,689- 706. Sandor GK, Low DE, Judd PL. Antimicrobial treatment options in the management of odontogenic infections. J Can Dent Assoc. 1998: 64, 508-514. Kuriyama T, Nakagawa K, Karasawa. Past administration of beta-lactam antibiotics and increase in the emergence of beta-lactamase producing bacteria in patients with orofacial odontogenic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000: 89, 186-192. Britt JC, Josephson GD, Gross CW. Ludwig’s angina in the pediatric population: report of a case and review of the literature. Int J Pediatr Otorhinolaryngol. 2000: 52, 79-87. Loughnan TE and Allen DE. Forum: Ludwig’s angina. The anaesthetic management of nine cases. Anaesthesia. 1985: 40, 295–297 Meyers BR, Lawson W, Hirschman Z: Ludwig’s angina. Case report, with review of bacteriology and current therapy. Am J Med. 1972: 53, 257–260 Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis. 2009: 13, 327-333.

www.ujponline.com 18.

19.

20.

21.

22. 23.

24.

Nguyen VD, Potter JL, Hersh-Schick MR. Ludwig angina: an uncommon and potentially lethal neck infection. AJNR Am J Neuroradiol. 1992: 13, 215–219. Snow N, Lucas AE, Grau M, Steiner M: Purulent mediastinal abscess secondary to Ludwig’s angina. Arch Otolaryngol . 1983: 109, 53–55 Bross-Soriano D, Arrieta-Gómez JR, PradoCalleros H, Schimelmitz-Idi J, Jorba-Basave S. Management of Ludwig’s angina with small neck incisions: 18 years experience. Otolaryngol Head Neck Surg. 2004: 130, 712717. Ho MP, Tsai KC, Yen SL, Lu CL, Chen CH. A rare cause of Ludwig’s angina by Morganella morganii. J Infect. 2006: 53, 191-194. Saifeldeen K, Evans R: Ludwig's angina.. 2004: 21, 242-243. Spitalnic SJ, Sucov A: Ludwig's angina: case report and review. J Emerg Med. 1995: 13, 499503. Ovassapian A, Tuncbilek M, Weitzel EK, Joshi CW: Airway management in adult patients with deep neck infections: A case series and review of the literature. Anesth Analg. 2005: 100, 585589.

Source of support: Nil, Conflict of interest: None Declared


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