POTD: Ludwig’s Angina

History: Named after German physician, Wilhelm Frederick von Ludwig, who first described this condition in 1836.

Overview:

•        Submandibular Space Cellulitis

•        Bilateral

•        Aggressive, fast spreading

•        70% of Ludwig’s angina is dental in origin

•        Real risk of airway compromise: This can result in rapid airway decompensation.

Physical Exam (useful things to document the presence of absence of in the chart):

•        Floor of the mouth: is described as: “woody,” which means firm, indurated, taut

•        Tongue: displaced superiorly and posteriorly

•        This result in: Slow suffocation, drooling, sniffing position, muffled voice, stridor

•        Labs

•        Vbg, cbc 7, blood cultures

•        Imaging

•        CT face and neck with IV contrast

•        Be very cautious if you are sending them to CT without airway secured

•        Consults

•        ENT, anesthesia

Treatment

•        ABCs…A! Airway obstruction in 33%

•        sit upright

•        Secure/verify integrity of airway

•        Awake fiberoptic nasal intubation

•        Mentally prepare yourself for a surgical airway. This is the time to have the materials set up at the bedside.

•        Abx: polymicrobial

• Oral anaerobes and aerobes

• PCN G + flagyl

• Unasyn

• Clinda

• Immunocompromised? Cefepime +flagyl

•        Steroids

• Dexamethasone  8-12 mg IV

•        Dispo

• ICU

• 3-4 day process, gets worse before better

Complications

•        Mortality usually associated with airway compromise

•        with appropriate treatment, 8% mortality

•        Spread of infection: IJ thrombophlebitis, intracranial infection, mediastinitis

Brush up!

Sources: LIFL https://lifeinthefastlane.com/ccc/ludwigs-angina/

Uptodate Lugwig’s angina

Tintinelli’s Lugwig’s angina

POTD: Young woman with upper abdominal pain clinical vignette

25-year-old woman presents with RUQ abdominal pain she has had for 1 week. She denies fever and vomiting. She also describes some vague pelvic pain for the past month. She is unsure if her vaginal discharge is abnormal. She thinks she was treated for an STI a few years ago, also unsure. No urinary symptoms.

Examination reveals tenderness to palpation in the right upper quadrant, negative murphy’s sign. You do a bedside u/s that does not show GS/cholecystitis. LFTs/lipase are nl. GI cocktail doesn’t help. Being a thorough emergency physician you decide to do a pelvic exam and find +purulent discharge with an erythematous cervix and mild cervical tenderness to palpation. No adnexal ttp b/l.

Dx? Management?

Fitz-Hugh-Curtis syndrome (FHCS).

FHCS is a relatively rare secondary infection of the perihepatic region following pelvic inflammatory disease (PID). Patients generally have mild to moderate PID findings on pelvic examination. Most infections are chlamydial; gonococci are another infectious etiology. Because the infection does not affect the liver or biliary system itself, liver function test results and ultrasound examination results are normal. Abdominal CT can be diagnostic for FHCS; perihepatic inflammation will be noted.

Outpatient treatment for Fitz-Hugh-Curtis syndrome is similar to that for PID: ceftriaxone, 250 mg IM once, and doxycycline, 100 mg PO twice daily for 14 days, with or without metronidazole, 500 mg PO twice daily for 14 days. Patients who are hemodynamically stable may be discharged home with OBGYN f/u.

Although this is a rare diagnosis just keep it in the back of your mind. Chlamydia and gonorrhea are often asymptomatic in women, undiagnosed and lead to infertility (vs men where they tend to have symptoms).  So if the clinical scenario fits, do the pelvic exam.

Sources: Peer IX, uptodate

POTD: Cavernous sinus thrombosis (CST)

Clinical Scenario:

A 30-year-old woman presents with headache, fever, and decreased vision in her right eye over the past 24 hours. Examination reveals exophthalmos of the right eye and no pupillary reflex and a clear anterior chamber. When asked, she denies weakness and numbness.

What is the most likely diagnosis?

Last week we talked about cerebral venous sinus thrombosis (CVST), today let’s talk about cavernous sinus thrombosis (CST), or the infected subset of cerebral venous sinus thrombosis.

What is it?

• Cavernous sinus thrombosis (CST) is a rare condition, defined as a septic thrombophlebitis of the cavernous sinus. It is caused by a bacterial infection that typically originates in the face, sinuses, ears, or orbits. Most infectious etiologies in cavernous sinus thrombosis are from Staphylococcus or Streptococcus species. 

• The two cavernous sinuses are located on both sides of the sella turcica. Important structures are located in, or run through, the cavernous sinus, including the pituitary gland, cranial nerves III, IV, V and VI, and the internal carotid arteries (ICA). 

• It causes significant morbidity and the mortality rate is at 20-30%.

Risk Factors

• Sphenoid and ethmoid sinusitis are the most common causes of CST. 

• Other risk factors include dental infections, facial cutaneous infections, otitis media, maxillofacial surgery, and trauma.

Presentation

• Most patients will have fever, headache, and vision changes/ocular complaints (proptosis, periorbital edema and/or chemosis). 

• Most will also have external ophthalmoplegia, due to venous congestion of orbital tissues, extra-ocular muscle inflammation and/or inflammation of cranial nerves III, IV and VI. 

• Other symptoms include eyelid erythema, autonomic dysfunction, sensory changes in the ophthalmic and maxillary trigeminal nerve distributions, pupillary abnormalities, and papilledema. 

• Vision loss is rare as the orbital nerve lies outside the cavernous sinus. 

• CST commonly spreads from one eye to both within 24 to 48 hours.

Evaluation

Blood cultures, CBC, and coagulation studies (PT and PTT) should be ordered, as well as CT of the head and orbits with contrast.

Treatment

• Parenteral antibiotic treatment should be started with gram-positive coverage (nafcillin plus a third-generation cephalosporin or vancomycin if concerned for MRSA). The patient should be admitted with neurology and ophthalmology consultations

• Anticoagulation and steroids, remain controversial.

  • Steroids may confer improved cranial nerve function.

  • Anticoagulation may confer a risk of systemic and intracranial bleeding and may result in dissemination of septic emboli. Consider anticoagulation only if there is no evidence of severe bleeding risk or current hemorrhage.

Differences between CVST and CST

References

PEER IX

http://www.emdocs.net/cavernous-sinus-thrombosis/