Medical Image of the Month: Ludwig’s Angina

Figure 1.  A coronal reconstruction of the patient’s initial post-contrast maxillofacial CT demonstrates swelling of the soft tissues of the floor of the mouth consistent with phlegmonous changes and early abscess formation (blue arrows).  There is also swelling in the region of the vallecula and epiglottis (red arrow).

Figure 2.  A coronal reconstruction of the patient’s follow-up post-contrast maxillofacial CT after placement of a tracheostomy tube demonstrates marked progression of the swelling of the soft tissues of the floor of the mouth with development of a large, ill-defined abscess in the floor of the mouth (blue circle). Note the marked, progressive narrowing of the oropharynx (red arrow) over a period of approximately 24 hours.

Case Presentation: A 65-year-old gentleman with a history of insulin-dependent diabetes mellitus presented to the emergency room with a chief complaint of two days of difficulty swallowing and jaw pain.  Four days prior to presentation, he had extensive dental work performed to address multiple dental caries.  On arrival to the emergency room, he was noted to be tachycardic with difficulty swallowing his saliva and liquids.  On physical examination, he had difficulty opening his mouth with marked swelling of his tongue.  He also had marked swelling of the soft tissues of the floor of the mouth with palpable adenopathy.  A maxillofacial CT with contrast (Figure 1) was performed which demonstrated extensive edema and early abscess formation in the floor of the mouth.  He was initially admitted to the general medicine floor and started on broad-spectrum antibiotics.  Over the course of the next 12 hours, he began to have increased difficulty breathing and was unable to swallow his own secretions.  He was promptly transferred to the ICU where a fiberoptic nasotracheal intubation was attempted at bedside but was unable to be performed given the extensive soft tissue swelling in the posterior oropharynx.  An emergent awake tracheostomy was subsequently performed by ENT.  A repeat maxillofacial CT with contrast (Figure 2) demonstrated marked progression of the inflammatory changes and abscess formation in the floor of the mouth consistent with progressive Ludwig's angina.  The combination of prompt surgical drainage and broad-spectrum antibiotics resulted in marked clinical improvement over the next 72 hours. The patient's final tissue cultures grew Streptococcus viridans.

Ludwig's angina is a potentially life-threatening gangrenous cellulitis of the neck and floor of the mouth which is characterized by progressive submandibular swelling with elevation and posterior displacement of the tongue. Odontogenic infections are the cause for most cases. Pre-existing medical conditions which predispose patients to the development of Ludwig's angina include diabetes mellitus, malnutrition, alcoholism, and immunocompromised states (i.e. AIDS and organ transplantation).

In the early stages of the disease, patients may be managed with observation and intravenous antibiotics to cover for β-hemolytic streptococcus and anaerobic organisms. The most life-threatening complication of Ludwig's angina is airway obstruction.  Immediate involvement of an anesthesiologist and ENT are crucial in the management of this condition.  Blind nasotracheal intubation should not be attempted in these patients given the potential for bleeding and abscess rupture.  Flexible nasotracheal intubation requires skill and experience.  If flexible nasotracheal intubation is not possible, a cricothyrotomy and tracheostomy under local anesthesia can be performed in the emergent setting.  An elective awake tracheostomy is a safer and more logical method of airway management in patients with fully developed Ludwig's angina.

Lauren Estep, MD and Tammer El-Aini, MD

Department of Pulmonary, Critical Care, Allergy and Sleep

University of Arizona College of Medicine

Tucson, AZ USA

References

1. Hasan W, Leonard D, Russell J. Ludwig's Angina-A Controversial Surgical Emergency: How We Do It. Int J Otolaryngol. 2011;2011:231816. [CrossRef] [PubMed]
2. Candamourty R, Venkatachalam S, Babu MR, Kumar GS. Ludwig's Angina - An emergency: A case report with literature review. J Nat Sci Biol Med. 2012 Jul;3(2):206-8. [CrossRef] [PubMed]

Cite as: Estep L, El-Aini T. Medical image of the month: Ludwig’s angina. Southwest J Pulm Crit Care. 2019:18(4):74-5. doi: https://doi.org/10.13175/swjpcc013-19 PDF 

Medical Image of the Week: Cannon V Waves

Figure 1. Video showing jugular venous distention to earlobes with cannon V waves.

A 66-year-old man experienced recurrent ascites of unknown etiology over six months. He had previously undergone a renal transplant secondary to complications of diabetes and hypertension and had known severe coronary artery disease. His most recent paracentesis revealed an albumin 1.6 g/dL (serum albumin 2.1) and a total protein of 3.8 g/dL. His adenosine deaminase was 11.6 U/L (normal <7.6 U/L), but repeated bacterial and mycobacterial ascites cultures were negative, as were a carcinoembryonic antigen assay and ascites cytology. Computerized tomography of the abdomen showed findings consistent with cirrhosis, but an extensive workup for common causes of cirrhosis was negative.

Physical exam showed jugular venous distention with prominent V waves and a holosystolic murmur at the left lower sternal border (Figure 1). Echocardiography showed a dilated right ventricle, moderate pulmonary and tricuspid regurgitation and an estimated right ventricular systolic pressure of 87 mm Hg. Cardiac catherization confirmed the presence of an elevated right ventricular pressure of 72/10 (22) mm Hg, an elevated pulmonary artery pressure of 75/27 (45) mm Hg and a left ventricular ejection fraction of 20-25%. The right atrial pressure was 20 and the pulmonary artery occlusion pressure was 22 mmHg.  A diagnosis of pulmonary hypertension secondary to left ventricular heart disease (type 2 pulmonary hypertension) with congestive hepatopathy and cardiac ascites was made.

The patient’s physical examination provided an important clue to the etiology of the ascites – cardiac ascites is thought to be due to chronic venous congestion of the liver due to transmission of high central venous pressures. Tricuspid regurgitation can be associated with severe hepatic congestion because of retrograde transmission of right ventricular pressure directly into the hepatic veins. In some patients (although not in this patient), careful examination will reveal that the liver in such patients is palpably pulsatile.

Cardiac ascites is typically characterized by a serum albumin gradient (SAAG) >1.1 g/dL (indicative of portal hypertension) and ascites protein level of >2.5 g/dL (1). We cannot fully explain why this patient’s SAAG was low. A complete workup for infectious and oncological etiologies of low SAAG ascites was negative. It has been noted that in patients with known cirrhosis (as in this patient), the finding of a low SAAG has a low specificity for infectious and oncological etiologies of ascites (2). Serositis which can sometimes manifest as ascites can also be a complication of tacrolimus which the patient was receiving s/p renal transplant. It’s possible that tacrolimus might have changed the nature of the ascites fluid in this patient but this is conjectural. 

Robert A. Raschke, MD

College of Medicine-Phoenix

Phoenix, AZ USA

References

1. Sam AH, James THT. Rapid Medicine. Wiley-Blackwell; 2009: ISBN 1-4051-8323-3.
2. Khandwalla HE, Fasakin Y, El-Serag HB. The utility of evaluating low serum albumin gradient ascites in patients with cirrhosis. Am J Gastroenterol. 2009 Jun;104(6):1401-5. [CrossRef] [PubMed] 

Cite as: Raschke RA. Medical image of the week: cannon V waves. Southwest J Pulm Crit Care. 2017;15(2):90-1. doi: https://doi.org/10.13175/swjpcc095-17 PDF