0:00

Well, we saw a case of a fungus ball and I mentioned that

0:05

with allergic fungal rhinosinusitis, you generally see a more diffuse process

0:10

that may lead to polyps in the nasal cavity or within the paranasal sinuses.

0:16

Allergic fungal sinusitis, usually immunocompetent individual, potentially

0:21

with a history of allergy or asthma or aspirin sensitivity, it's unilateral

0:28

or in the nasal cavity in six out of seven cases,

0:32

usually high density on all the CT scans in the nasal cavity as

0:36

well as in the paranasal sinuses. And this may have intermediate or high

0:41

signal intensity on T1 weighted scan, so, bright on T1. Again,

0:45

we are going to think about hemorrhage, we're going to think about the

0:48

presence of fat. In the sinonasal cavity, we also worry about melanin and

0:54

the potential for a sinonasal melanoma. However, inspissated secretions

0:59

and allergic fungal sinusitis with paramagnetism secondary to manganese

1:05

or magnesium, might also be a potential etiology. By and large,

1:10

this is going to be dark in signal intensity on T2 weighted scan, and

1:13

usually, without showing gadolinium enhancement. So here is the stereotypical

1:18

feature of the allergic fungal sinusitis. You see central hyper density

1:24

to the secretions. You see expansion of the sinus with a polypoid look to

1:30

it. And yet there is this periphery of lower density along the peripheral

1:36

mucosa. This is affecting bilaterally. You see ethmoid sinus involvement,

1:43

again, with the periphery of the low density.

1:46

And you also see involvement of the nasal cavity, so not just the

1:51

ethmoids but coming down into the nasal cavity with polyposis. This is another

1:56

example where you have a opacified maxillary antrum, which is protruding

2:03

into the nasal cavity. This is not a bilateral process, this is not

2:08

a diffuse process. This is an example, again, of a fungus ball where

2:12

you have complete opacification and expansion of one of the paranasal sinuses,

2:17

usually not bilateral process. Hyper attenuating; in this case, without

2:23

calcification, showed you a case previously with calcification. This also

2:28

will be dark on T2 weighted scan because of the inspissated secretions and

2:32

or the calcification. And you may also see thickening of the bony walls,

2:38

the so called osteitis that is a indicator for chronic sinusitis.

2:44

Let's move from the more benign fungal sinusitis cases to the more aggressive

2:51

fungal sinusitis. And the two things we've referred to are acute invasive

2:55

and chronic invasive fungal sinusitis. With the acute invasive fungal sinusitis,

3:01

it's usually in a patient who is immunocompromised, sometimes with diabetes,

3:06

sometimes immunosuppressed. And this is a very aggressive infection that

3:12

is associated with gross erosion of the bone and infiltration of the adjacent

3:18

tissue. By adjacent tissue, sometimes I'm referring to the orbits, which

3:23

can be devastating because you can develop a very severe, aggressive,

3:27

orbital cellulitis. But the other area where it may grow into the soft

3:32

tissues is the cavernous sinus and the intracranial compartment. In this

3:37

situation, you may show cavernous sinus thrombophlebitis. You may see carotid

3:44

artery involvement with vasculitis and thromboembolism. You may see meningitis

3:49

with associated mycotic epidural abscess. This is usually not hyper attenuating

3:56

because it's a very aggressive infection that doesn't accumulate the

4:00

hyper proteinaceous secretions associated with it. It's usually low signal

4:05

intensity on T2 weighted scan. And what's also kind of curious about this

4:10

lesion is that it shows absence of contrast enhancement, in part because

4:16

it's a necrotic or necrosing process. So look for the bone erosion,

4:22

look for low signal on T2, look for absence of mucosal enhancement,

4:27

as this fungus just goes right through the

4:31

mucosal surface. Here is example of invasive fungal sinusitis. We see the

4:38

sphenoid sinus with soft tissue within it. We also see some anterior ethmoid

4:43

and frontal sinus, but more importantly, we see the erosion of the lateral

4:48

wall of the left sphenoid sinus. From there, you see a process which

4:52

is infiltrating the left cavernous sinus, compare that with the normal right

4:59

cavernous sinus. Within the cavernous sinus is low signal intensity tissue,

5:05

and in this case, the cavernous sinus is enhancing some of the infectious

5:10

soft tissue is not showing enhancement. And you can see that this is

5:14

going from the cavernous sinus onto the surface of the pons. So this

5:19

is meningitis and spread along the blood vessel, in this case,

5:23

the posterior communicating artery, and then encasing the basilar artery.

5:29

So we have a pretty serious vasculitis. The next thing that generally happens

5:33

in these patients is that they throw septic emboli. Now for those of

5:39

you who are a little bit more observant, you might notice that there

5:42

is contrast enhancement of the cortex on the left side. And indeed,

5:47

this patient does not show a good flow void to the internal carotid artery.

5:52

Here's the black of the flow void of the normal right internal carotid artery,

5:57

here's no flow void in the left internal carotid artery. The left internal

6:02

carotid artery is thrombosed by the invasive fungal sinusitis, leading to

6:07

an infarction involving the middle cerebral artery distribution manifested

6:13

on the post gad by the gyriform enhancement of the left temporal lobe.

6:18

Very, very poor prognosis. Very hard to cure this illness once it's gotten

6:25

into the cavernous sinus and the intracranial compartment.