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%.

attachment.jpeg

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.

KeralaJOphthalmol_2016_28_1_61_193869_f1.jpg

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

table.png
 · 

Ebola virus disease

One reason I know that I went into the right speciality is that

we HAVE to know about Ebola

. Virology is uber fascinating, and we aim to hammer out everything the EP provider needs to know regarding this Ebola virus disease (EVD). 

Aside from being an interesting topic,

there is currently a budding outbreak of EVD in the Congo.

Due to armed conflict, healthcare and quarantine measures are impeded. See news article below: 

https://www.beckershospitalreview.com/quality/101-dead-in-congo-s-ebola-outbreak-as-safety-risks-mount-for-health-workers.html

If you recall from the last outbreak, there were several notable US cases, one of which  received treatment in NYC. 

It is thought that there is animal reservoir (likely fruit bats) and the animal to human transmission of the virus may come from individuals handling bushmeat. 

Ebola is a filovirus (meaning it looks like a string). It is a negative sense single stranded RNA virus. 

Below is an colorized scanning electron microscope image of the virus, (included because it is just gorgeous!)

about-ebola-medium.jpg

image curtesy of CDC

Transmission is via contact

of viral particles to mucus membranes or broken down skin.  

Incubation time is 9-11 days.

The ebola virus is one of the most infectious agents known to man.

A single ebola virion is enough to be infectious

. This is in stark contrast to most other infectious agents which typically require a large inoculum to cause clinically significant disease. 

Symptoms typically develop by infection day 5

-fever, fatigue

-GI upset: vomiting, watery diarrhea, abdominal pain

-this can progress to seizures and cerebral edema

-renal failure

-hepatic failure

-eccymoses and petechial rash are also possible

-hemorrhage is uncommon, but reported in 18% of patients (typically GI)

Patients with severe disease typically die within 6-16 days. Mortality rate in west Africa was ~40-70%. Of 27 patients treated in the United States, the fatality rate was 18.5%.

The mechanism for the hemorrhagic fever is thought to be massive activation of macrophages and other immune cells causing a cytokine storm, which then leads to break down of the vascular endothelium and results in leaking. Other research suggests the virus itself has proteins which lead to endothelial dysfunction and leakage.

You can utilize ELISA, PCR, or virus isolation to test for the disease. These

tests for ebola are only available in consultation with a governmental health agency. 

Mainstay of treatment is supportive.

However, you can transfuse convalescent serum from recovered and now immune individuals. A more elegant and certainly more expensive treatment is

ZMapp

, which is a mix of “3 humanized monoclonal antibodies” against Ebola.  There also several vaccines including rVSV-ZEBOV which have been experimentally deployed in west Africa. 

As per the CDC, travelers from endemic outbreak regions should self monitor their health for 21 days. Febrile patients who may had contact with ebola, should be placed on contact precautions and NYDOH should be immediately contacted. 

Hopefully this is something we never see. But preparedness is critical for our specialty. Thank you for taking the time to read and have a great weekend.

 ·