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Ludwig's Angina in a 38 year old Male with Advanced AIDS


Figure 1.
A CT of the neck
and sinuses.

By Andrea Lanctot, M.S.
Medical Student, Stanford University School of Medicine


  Ludwig's angina refers to cellulitis of the floor of the mouth in which infection spreads to submental, sublingual and submandibular spaces (1, 3, 4, 5, 7). Patients present with odynophagia, drooling, dysphonia, tachypnea, tense brawny induration, and trismus (1, 3, 4, 5). Ludwig's angina often results from an odontogenic infection (4). As a result, the bacteriology of these infections generally involves oral flora, particularly anaerobes (2, 4). Other recognized etiologies of Ludwig's angina include poor dental hygiene, intravenous drug abuse, trauma and tonsillitis (3). In today's cases there is a high incidence of associated systemic illnesses including diabetes mellitus, AIDS and HIV seropositivity (2). Airway management, antibiotic therapy and surgical incision and drainage are the mainstays of treatment (1, 3, 4, 5). This case report is used to illustrate some of the clinical features and therapeutic challenges in Ludwig's angina.


  S.P is a thirty-eight year old Caucasian man with advanced AIDS. One year ago he presented with signs of HIV dementia and wasting syndrome. At that time, his CD4 count was less than fifty. Since the initial AIDS diagnosis, he has been routinely evaluated in Stanford's Positive Care Clinic. Eosinophilic folliculitis and Candida stomatitis are his only documented opportunistic infections. His outpatient medications prior to admission included anti-retroviral D4T, itraconazole for eosinophilic folliculitis treatment and Candida prophylaxis, acyclovir for HSV prophylaxis, monthly pentamidine for Pneumocystis carinii prophylaxis, marinol for treatment of HIV wasting syndrome and pepcid for peptic ulcer disease.

  The patient had several contacts with health care providers before admission. Two months prior to admission, the patient had a tooth extraction without incident. Two weeks prior to admission, the patient complained of sore throat, sinus congestion and cough. He was seen at the Positive Care Clinic and treated with a ten day course of Cefuroxime. Following treatment, he reported some improvement. The patient returned to the emergency department two days prior to admission complaining of neck stittness, headache, sore throat and decreased appetite. Work up for meningitis was negative and the patient was discharged home.

  On the day of admission, the patient presented to the Positive Care Clinic complaining of a worsening sore throat, odynophagia, trouble swallowing his oral secretions, difficulty breathing, decreased appetite, and a fever of 102 F for three days.

  On exam, the patient was in significant distress sitting upright, drooling, with some use of accessory muscles of respiration. Due to swelling and upward/posterior displacement of his tongue, the patient was limited to one word, garbled responses to questions. Recorded vital signs were T 39 C, HR 100, R 24, BP 130/80, and 97% saturation on room air. Tender, bilateral submandibular swelling greater on the right than the left was noted. Fluctuance was insignificant. Sublingual swelling was indicated by upward displacement of the tongue. No cervical, supraclavicular, infraclavicular, pre/posterior auricular or axillary Iymphadenopathy was detected. Examination of the oropharynx was hindered by marked trismus of 25 mm. The right tonsil had a yellow-white exudate and was erythematous. The left tonsil was clear. A large area (estimated 3 x 3 cm) of the right soft palate was swollen. Due to the potential of rapid airway compromise and the need for better visualization of the oropharynx, the Otolaryngology-Head, Neck & Throat team evaluated the patient immediately in the emergency department. This examination confirmed the findings previously described and further noted normal vocal cords, a fully patent airway, right arytenoid fold swelling, and slight fullness of the right lateral pharyngeal wall. Importantly, no supraglottitis or epiglottitis were seen.

  A CT scan of the neck and sinuses demonstrated significant bilateral peripharyngeal, retropharyngeal, and paravertebral space soft tissue inflammatory change with edema. Right sicled spaces were more involved than left. Swelling distorted and compressed the oropharynx. The left common and external jugular veins were thrombosed. Finally, there was CT evidence of chronic sinusitis (Figure 1).

  The patient was admitted with a tentative diagnosis of Ludwig's angina and throat cultures were ohtained with the intent to rule out C. diphtheria infection. An attempt to incise and drain the swollen right tonsil was unsuccessful. Due to the tenuous airway demonstrated on exam, dexamethasone (20-30 mg/dose) was administered and the patient was transferred to an intensive care setting with a nasopharyngeal airway in place. The patient was not intubated. Empiric antibiotic treatment with penicillin G (2 x 106U q4*), metronidazole (500 mg q6*), and erythromycin (500 mg q6*) was instituted. The antibiotic selection was designed to cover both anaerobes and C. diphtheria.When two of four blood cultures subsequently came back positive for Pseudomonas aeruginosa, antibiotic therapy was changed to Imipenem (500 mg q6*) and gentamicin (5mg/kg qd*) and dexamethasone treatment was discontinued.

  After two days in the intensive care setting on parenteral antibiotics and dexamethasone, the patient improved dramatically. The submandibular swelling remained tender with brawny induration. The patient was increasingly able to phonate despite persistent palate, tonsillar, and cervical swelling. His complaint of vocal distortion was likely a consequence of the dramatic swelling of these structures.

  After the second hospital day he was transferred to the general medical floor. He had one five minute episode of acute respiratory desaturation and hyperventilation (R 40, sat 54-67% on 100% oxygen) shortly after transfer. He remained on the general medical floor with a one-on-one sitter after he refused transfer back. to intensive care. He returned to baseline within the next few hours. Aside from this unexplained desaturation event the patient continued to improve.

  On the fifth hospital day an ulcer on the right tonsil ancl a white plaque on the soft palate were noted. Over the next few days the ulcer continued to eroded into the lateral wall; the plaque became more confluent and began to ulcerate. To rule out an invasive fungal process, ENT biopsied these sites on hospital days 6 and 10. The tissue was found to contain Psudomonas aeruginaosa and candida. Pathology specimens demonstrated vascular thrombosis and mucosal necrosis. The bicpsy specimens and a repeat CT scan of the sinuses failed to demonstrate an invasive fungal process.

  The patient continued to improve with increased ahility to talk and tolerated solid foods. On hospital day 14 the patient was discharged home on intravenous ciprofloxacin and gentamicin. The plan to continue antibiotic therapy after discharge was based on the fact that treatment of pseudomonas bacteremia requires antibiotics for at least fourteen days. The mean treatment in some studics is reported to be 19 days (9).


  Ludwig's angina refers to a potentially Iife-threatening cellulitis of the floor of the mouth with infection extending into sublingual, submental and submaxillary spaces (1, 3, 4, 5, 7). Angina is derived from the latin word angere which means to strangle. Ludwig's angina appropriately describes the subset of deep neck abscesses in which swelling of critical spaces threatens to elevate the floor of the mouth displace the tongue posteriorly and, thereby strangle the patient (1, 4). Ludwig's angina was more common in the pre-antibiotic era (3). Today Ludwig's angina represents thirteen precent of all deep neck abscesses (2).

  Patients with Ludwig's angina often complain of severe dysphagia, cervical tenderness, swelling, limited range of motion and dysphonia (1, 3, 4, 5). Patients may appear quite toxic, sitting upright, drooling and tachypneic. Observed trismus, the inability to open the jaw, is the result of inflammation and edema of the masseter space which includes masseter medial pterygoid and temporalis muscles (4). Further extension of the infection to lateral pharyngeal retropharyngeal and prevertebral spaces invariably produces severe trismus. Tense brawny induration of involved spaces with little to no fluctuance is a common exam finding that partially accounts for the limited range of motion of the neck (1, 3, 4, 5).

  Grodinsky proposed four criteria to distinguish Ludwig's angina from other forms of deep neck abscesses. The infection must (a) occur bilaterally in nore than one space, (b) product gangrenous serosanguinous infiltration with or no pus, (c) involve connective tissues fascia and muscle but not glandular structures, and (d) spread by continuity, not by Iymphatics (3, 6)

  Odontogenic procedures and poor dental hygene account for seventy to ninety-five percent of the cases of Ludwig's angina (3 4). Dental procedures involving the second ancl third molars are common sources of infection (4). The roots of these molars extend into the mylohyoid muscle thereby providing a roule to the three primary mandibular spaces. Infection usually begins in the necrotic pulp of a tooth and then invades adjacent bony tissue. Alter a period of intrabony spread the infection may erode the thinnest part of the bony cortex and thereby gain access to muscle and soft tissue. If this erosion occurs above the muscle attachment site, fascial space is entered. Submandibular and sublingual spaces freely communicate. Thus once deep cervical fascia is involved, infection may spread rapidly with grave consequences (4).

  Systemic illness, trauma and intravenous drug abuse are also common precursors to todays cases of Ludwig's angina (2). In fact one third of the cases of Ludwig's angina are associated with systemic illness (2). One recent review reporting the incidence of various illnesses associated with Ludwig's angina found 18% of cases involved diabetes mellitus, 9% AIDS and another 5% were HIV positive (2).

  Deep neck abscesses generally involve oral flora (3). Obligate anaerobes constitute approximately seventy-five percent or normal oral flora (3). The most common anaerobes are anaerobic streptococci bacteriodes and fusobacterium (4). Aerobes and facultative anaerobes are also present with Streptococcus accounting for most oral aerobes (4). Based on this microbiology it is not surprising that forty percent of Ludwigs angina cases involve anaerobes (2).

  Two-thirds of deep neck abscess infections are polymicrobial (2, 4). The bacterial agents commonly isolated in order ol decreasing frequency include Streptococcus viridans, Staphylococcus aureus and Staphylococcus epidermidis. Only seven percent of cases of Ludwigs angina are due to Group A beta-hemolytic Streptococcus (2). Psuedomonas aeruginosa is cultured from only 1.1%. of deep neck abscesses (2). Blood cultures of Ludwig's angina patients are usually negative; in a recent review 83% of cases reported no growth from blood samples (2).

  The free communication of potential spaces of the head and neck and the minimal resistance offered by cervical fascia can have devastating consequences. Life-threatening infections usually involve lateral pharyngeal, retropharyngeal and prevertebral spaces, often dubbed "secondary spaces". The lateral pharyngeal space is divided by the styloid process. Muscles of the medial pterygoid and superior pharyngeal constrictor lie anteriorly. The posterior compartment contains the carotid sheath and cranial nerves. Infection of the lateral pharyngeal space has three severe complications: (a) thrombosis of the internal jugular vein, (b) erosion into the carotid artery, and (c) interference with cranial nerves (especially CN 9 - CN 12) and the sympathetic chain. Three potential complications of retropharyngeal space involvement are recognized: (a) upper airway obstruction, (b) spontaneous abscess rupture leading to asphyxia, aspiration or pneumonia, and (c) infection involving the posterior mediastinum. Since the prevertebral space extends from the base of the skull to the diaphragm, infection here can spread extensively. Other reported complications include mediastinitis, septicemia, empyema and pericarditis.

  There are four principle components in the treatment of Ludwig's angina. First, adequate airway management is essential. A recent review reported that sixty-seven percent of patients with Ludwig's angina required either anticipitory or emergent intubation (2). Second, antibiotic therapy must be designed to cover both anaerobes and Staphylococcus aureus. Penicillin with or without metronidazole is the first line therapy (2, 3, 4). Clindamycin, metronidazole alone, or amoxicillin/clavulinic acid are also considered highly effective (4). Empiric antibiotic treatment in the immunocompetent host is considered safe; however, medical therapy must be guided by cultures and sensitivities in the immunocompromisecf host. Third, in the past, incision and drainage of abscesses was routine. Now, surgical therapy is usually reserved for cases of medical treatment failure (3). Finally, adequate nutrition ancl hydration can be a challenge in patients wilh significant oropharyngeal edema.

  Prior to antibiotics, the mortality associated with Ludwig's angina approached fifty percent (3). Today, mortality rates are in the range of eight to ten percent (3). The most common cause of death is respiratory compromise (4).

  In summary, the case presented here is representative of many features of modern day Ludwig's angina. The patient had a systemic illness, AIDS. He presented with bilateral swelling of mandibular spaces, odynophagia, dysphonia, drooling, severe trismus, elevation of the tongue and tachypnea. He had a history of a recent tooth extraction. Other features of this case are atypical. Notably, the microbiology of this patients infection and the clinical outcome were unusual. Pseudomonas aeruginosa, the only isolated pathogen in this case, is isolated in approximately only 1% of all deep neck abscesses. In addition, the bacteremia seen in this case is very uncommon in typical Ludwig's patients. This patient's freedom from intubation is also unusual. Finally, due to the involvement of many secondary spaces, this patient was at high risk for serious, life-threatening complications. As mentioned, the general mortality for Ludwig's angina cases toclay approaches 8-l0 percent. Fortunately, none of these complications occurred and this patient recovered after fourteen days of parenteral antibiotics.


  The teaching I received on this case from the patient, attending physicians and residents was invaluable. Special thanks should be given to Dr. Zolopa, Dr. Pearlroth, Dr. Lindsay, Dr. Patrawala, Dr. Virmani and Dr. Tinklenberg


1. Mandell, Bennett and Dolin. Principles and Practice of Infectious Disease, Fourth Edition. p. 566-571, 1870-1871, 2169, 2198.

2. Har-El, Aroesty, Shaha and Lucente. Changing Trends in Deep Neck Abscesses, Oral Surgery Oral Medicine Oral Pathology, 1994; Vol 77, No. 5, 446-50.

3. Fritsch and Klein. Curriculum in Critical Care: Ludwig's Angina, Heart & Lung, 1992, Vol 21:39-47.

4. Cummings, Fredrickson, Harker, Krause and Schuller. Otolaryngology - Head and Neck Surgery, 1993, Second Edition, Vol 2: 1199-1215.

5. Isselbacher, Braunwald, Wilson, Martime, Fauci and Kaspaer, Harrison's Principles of Internal Medicine, 1994, Thirteenth Edition, p 199, 519, 701.

6. Grodinsky, Ludwig's Angina: An Anatomical and Clinical Study with Review of the Literature, Surger, 1939, Vol 5:678-96.

7. Andreoli, Bennet, Carpenter, Plum and Smith. Cecil Essentials of Medicine, 1993, Third Edition, p. 702-723.

8. Lee, Tami, Echavez, and Wildes. Deep Neck Infections in Patients at Risk for Acquired Immunodeficiency Syndrome, Laryngoscope, Sep. 1990, p. 915-919.

9. Mendelson, Gurtman, Szabo et al. Pseudomonas aeruginosa Bacteremia in Patients with AIDS, Clinical Infectious Disease, 1994, 18:886-95.

10. Brenner, Wolf and Ophir, Eosinophilic Pustular Folliculitis: A Sterile Folliculitis of Unknown Cause?, Journal of American Academy of Dermatology, 1994; 31:210-212.

Reprinted from the Stanford Medical Student Clinical Journal

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