Medic248

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Quick clinical question for you folks:

Had a patient the other day with what I thought was a classic presentation of pneumothorax, but turned out to be a massive PE.

35 year old female hx cervical CA with mets to lymph. CC of severe, sudden-onset shortness of breath. Auscultation of the lungs showed clear lungs on the right with good air movement and totally absent left-sided fields. She had sternocleidomastoid retractions and +JVD, but she was normotensive and tracheal deviation was not appreciated. SpO2 was around 80% on 15 lpm, which did not provide any relief of symptoms. Non-invasive EtCO2 was 15mmHg with a "normal" (but obviously hypocapnic) waveform. 12-lead was unremarkable (Sinus tach, I believe).

She denied all other symptoms.

Am I missing anything in the differential here? I was kind of expecting a two-part waveform on the EtCO2, showing delayed (or no) emptying of the left lung. I considered the low, short waveform to possibly be indicative of either 1) small amount of CO2 being exhaled, or only from one lung, or 2) V/Q mismatch secondary to PE. But she lacked any symptoms other than SOB to differentiate.
 

Medic248

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Additional: This is in the prehospital setting, so any aides to assessment would have to be without x-ray, CT, ultrasound, labwork, etc.
 

Tiger26

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Quick clinical question for you folks:

Had a patient the other day with what I thought was a classic presentation of pneumothorax, but turned out to be a massive PE.

35 year old female hx cervical CA with mets to lymph. CC of severe, sudden-onset shortness of breath. Auscultation of the lungs showed clear lungs on the right with good air movement and totally absent left-sided fields. She had sternocleidomastoid retractions and +JVD, but she was normotensive and tracheal deviation was not appreciated. SpO2 was around 80% on 15 lpm, which did not provide any relief of symptoms. Non-invasive EtCO2 was 15mmHg with a "normal" (but obviously hypocapnic) waveform. 12-lead was unremarkable (Sinus tach, I believe).

She denied all other symptoms.

Am I missing anything in the differential here? I was kind of expecting a two-part waveform on the EtCO2, showing delayed (or no) emptying of the left lung. I considered the low, short waveform to possibly be indicative of either 1) small amount of CO2 being exhaled, or only from one lung, or 2) V/Q mismatch secondary to PE. But she lacked any symptoms other than SOB to differentiate.
1) Cancer is a gigantic risk factor for hypercoagulability
2) PEs are often sudden onset
3) Retractions and +JVD fit with PE causing R ht failure
4) No tracheal deviation
5) Pulse ox didn't improve w/O2
6) ET CO2 was low because she was hyperventilating
7) Sinus tach is the most common EKG finding in PE. The S1Q3T3 thing only happens 30% of the time. Did she have R axis deviation?


Was there a history of trauma at all to suggest pneumo? Otherwise, could have been a pneumo from bleb rupture, but I think most signs point to PE given the pt history
 

Tiger26

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With all that said, it's much easier to explain away findings when you already have an imaging diagnosis as opposed to being in the field and trying to put it all together amidst the chaos.
 

Rendar5

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1) Cancer is a gigantic risk factor for hypercoagulability
2) PEs are often sudden onset
3) Retractions and +JVD fit with PE causing R ht failure
4) No tracheal deviation
5) Pulse ox didn't improve w/O2
6) ET CO2 was low because she was hyperventilating
7) Sinus tach is the most common EKG finding in PE. The S1Q3T3 thing only happens 30% of the time. Did she have R axis deviation?


Was there a history of trauma at all to suggest pneumo? Otherwise, could have been a pneumo from bleb rupture, but I think most signs point to PE given the pt history
Only thing to add is that we're taught that tracheal deviation, while classic, is an extremely rare sign of tension pneumo as it is a very late sign. So absence of it really doesn't say much for anything +JVD is a sign of a number of things and it's good that you noticed it. It'll be + in both PE and tension pneumothorax (though not likely non-tension) as well as in CHF exacerbations and cardiac tamponade.
 

canjosh

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As the others have said, you really can't narrow this differential much in the field. The only other thing worth pointing out is that spontaneous pneumothorax is much more common in males (6:1 male:female). The true classic presentation would be the young, tall, and thin male smoker.
 

Jeff698

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Her decreased breath sounds are likely from atelectasis. There was a study I read once that showed the lung exam to be unreliable in 60% of patients in detecting pneumothorax. Of course they included minor pneumothoraces.
Pleural effusion also popped into my mind as a reason for decreased breath sounds.

If I really want to know what the lungs sound like, I'll get an XRay.

If I really want to know what the XRay shows, I'll get a CT scan.

I joke, I joke. Sort of.

Take care,
Jeff
 

Arcan57

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Jeff, I've never heard that saying before. At 0100 on the undifferentiated dyspneic patient, that line of thinking becomes almost gospel. Especially since the mean time from when a patient gets into the room until they get undressed and in a gown is... infinite.
 

docB

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Some interesting points come up in this discussion. To recap: Sick, young F patient will exam findings concerning for pneumothorax prehospital but turned out to have a PE.

If this patient suddenly crumps in the back of the ambulance she's going to get a needle decompression of the chest. Was there a rush of air? If you said you could really tell going code 3 you're lying. You would notice that the patient didn't improve as you'd expect with a tension PTX. So intubation, ACLS and you arrive at the hospital. Let's say we get her back. Now she gets a chest tube and a trip to the scanner. Uh oh! Big saddle embolus. That was the problem. Did she eve have a PTX? Hard to say now, maybe, maybe not. She does now have a big hole in her chest and a tube hanging out. That will make any TPA or even heparin she gets more interesting.

You can do the right thing and screw the guy down the road.
 

WilcoWorld

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...and the next day, once the prior records are available, the family is present to give a history and a full list of meds, the CT is read by the Rads attending, the blood cultures have shown no growth x 24 hours, three sets of enzymes are back, and the patient is stable your consulting service will lament how glaringly obvious the correct diagnosis was, and how terribly the ED mismanaged this patient. Then, when the patient takes a turn for the worse while still waiting for a bed, and she needs acute intervention, all of a sudden the all-knowing consultants will be nowhere to be found.

sigh...guess it's time to mismanage the patient again
 

esperRN

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6) ET CO2 was low because she was hyperventilating
I believe the decrease in ETCO2 is from the inability of the blood to reach the pulmonary capillaries and exchange CO2. Can't blow off what you are exchanging.
 

Tiger26

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I believe the decrease in ETCO2 is from the inability of the blood to reach the pulmonary capillaries and exchange CO2. Can't blow off what you are exchanging.
You're right in that you would have a difficult with gas exchange, however, the body hyperventilates as a compensatory mxm
 

proman

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You're right in that you would have a difficult with gas exchange, however, the body hyperventilates as a compensatory mxm
Not really. The EtCO2 drops in a step-wise manner within 3-5 breaths from the sudden increase in dead space ventilation (ventilation without perfusion). The EtCO2 slope of the expiratory plateau (which represents alveolar emptying) does not change.
 

esperRN

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You're right in that you would have a difficult with gas exchange, however, the body hyperventilates as a compensatory mxm
I agree that the body hyperventilates in response to increase PaCO2, I just thought it would be important to note that the initial decrease in ETCO2 is from lack of gas exchange. I know pre-hospital personnel don't deal with this, but if say you have a vented patient, then you can compare the ETCO2 to the PaO2 and see impaired gas exchange if the difference is greater that 5mmHg 02. This can be the very first sign of PE in an unconcious/vented patient.

Really applies more to the OR where you have constant ETCO2 monitoring, but I thought I would mention it.
 

ER-ER-Oh

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Not really. The EtCO2 drops in a step-wise manner within 3-5 breaths from the sudden increase in dead space ventilation (ventilation without perfusion). The EtCO2 slope of the expiratory plateau (which represents alveolar emptying) does not change.
Uh, yeah.

Stick a needle in her if her systolic drops. No improvement...something else, probably, maybe. That's just how it is. ABC's, ABC's, ABC's, that's what I'm thinking as I'm thinking. Hints are in the history of CA, and that's probably where my head would have gone first, even with the lack of breath sounds. But doesn't mean I wouldn't stick a needle in her chest with a low systolic BP first.

It's great to exercise the intellect with the physiology, and it builds intuition and adds to our ability to quickly think things through. But it's still ABC's, ABC's, ABC's that keep you out of the most trouble.
 
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if you have a portable US in the ambulance, you can r/o PTX in a about 30 sec. (look for "sliding lung sign"); it's better than cxr
 

tncekm

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I believe the decrease in ETCO2 is from the inability of the blood to reach the pulmonary capillaries and exchange CO2. Can't blow off what you are exchanging.
Okay, so I haven't dealt with this as an MS1 (still basic science work *sigh*), so I'm just waxing hypothetical to try to work out some questions I have, if you all don't mind :)

Assuming the patient has a unilateral pneumothorax, could that actuall increase the EtCO2? My logic is this: the other lung is functioning, and the PaCO2 will be elevated due to the shunting. The elevated PaCO2 will lead to elevated PACO2 (due to increased A-a gradient) in the functioning lung, and the collapsed lung will not be moving much volume since it's collapsed. So, because the PACO2 in the functioning lung is elevated, couldn't the EtCO2 also increase, which would mean that, if EtCO2 were low and respiratory rate was high the decreased EtCO2 would be the result of compensatory hyperventtilation?
 

ER-ER-Oh

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Okay, so I haven't dealt with this as an MS1 (still basic science work *sigh*), so I'm just waxing hypothetical to try to work out some questions I have, if you all don't mind :)

Assuming the patient has a unilateral pneumothorax, could that actuall increase the EtCO2? My logic is this: the other lung is functioning, and the PaCO2 will be elevated due to the shunting. The elevated PaCO2 will lead to elevated PACO2 (due to increased A-a gradient) in the functioning lung, and the collapsed lung will not be moving much volume since it's collapsed. So, because the PACO2 in the functioning lung is elevated, couldn't the EtCO2 also increase, which would mean that, if EtCO2 were low and respiratory rate was high the decreased EtCO2 would be the result of compensatory hyperventtilation?
Well, in theory, you may be correct. But taking into effect the fact that certain other elements of the good lung will be shunting blood across the other regions that are still within the confines of the returning blood flow you'll have to guess that any time additional blood comes into contact with alveoli that are adjusting their compression and filling times against the new gradient you'll have to keep that adjustment as part of the new paradigm.

Therefore, just imagine what kind of mess you'll have trying to rearrange the parenchymal elastic tissue gap while at the same time keeping certain regional flow mechanisms at bay. It's a nightmare, believe me, just tube em.
 

tncekm

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Well, in theory, you may be correct. But taking into effect the fact that certain other elements of the good lung will be shunting blood across the other regions that are still within the confines of the returning blood flow you'll have to guess that any time additional blood comes into contact with alveoli that are adjusting their compression and filling times against the new gradient you'll have to keep that adjustment as part of the new paradigm.

Therefore, just imagine what kind of mess you'll have trying to rearrange the parenchymal elastic tissue gap while at the same time keeping certain regional flow mechanisms at bay. It's a nightmare, believe me, just tube em.
Thanks!

And, I definitely wasn't trying to make any suggestions for treatment. Can't suggest what I haven't learned (unless, of course, it's in the form of a multiple choice exam where treatment options are provided for me, haha). So, I'll take your word for it on what to do. I was just curious about espeRN's statement about EtCO2.
 

ER-ER-Oh

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Thanks!

And, I definitely wasn't trying to make any suggestions for treatment. Can't suggest what I haven't learned (unless, of course, it's in the form of a multiple choice exam where treatment options are provided for me, haha). So, I'll take your word for it on what to do. I was just curious about espeRN's statement about EtCO2.
Hey, I'm just teasing you. Like I said in an earlier post, I think it's great to wax intellectual on these issues, it really, really does help create intuition later on...IF, and this is a big IF, IF you can let go intellectually when it's time to ACT!!

As a med student in 1st year I know how it is. Good luck my friend, keep up the right attitude.
 

tncekm

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Hey, I'm just teasing you. Like I said in an earlier post, I think it's great to wax intellectual on these issues, it really, really does help create intuition later on...IF, and this is a big IF, IF you can let go intellectually when it's time to ACT!!

As a med student in 1st year I know how it is. Good luck my friend, keep up the right attitude.
Ha, ha... thanks. But, it's hard to keep the right attitude in first year. SOOOOO BORRRIIINGGG!! AAHHHAHAA. Okay, now that I got that out, I promise I'll always wax intellectual and remember my ABC's (once I've learned them, that is).
 

proman

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End tidal CO2 is reduced in pulmonary embolism from increased dead space. PaCO2 may be decreased somewhat from hyperventilation but is usually (in massive PE) increased from the reduced lung area available for gas exchange. The PaCO2-EtCO2 gradient will be increased in massive PE.

I agree differentiating between PTX and PE based on exam is challenging. EMS ultrasound would be an enormous waste of money.
 

esperRN

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Thanks!

And, I definitely wasn't trying to make any suggestions for treatment. Can't suggest what I haven't learned (unless, of course, it's in the form of a multiple choice exam where treatment options are provided for me, haha). So, I'll take your word for it on what to do. I was just curious about espeRN's statement about EtCO2.
If you ever get access to Miller's Clinical Anesthesiology, you should take a look at it. Lot's of great stuff in an easy to read format.

It would seem logically for the ETCO2 to creep up in PTX since you have decreased gas exchanged, but there are a few factors preventing that. CO2 is VERY lipid soluble (solubility coefficient of .067) and diffuses across the alveolar membrane 20x faster than O2(solubility coefficient of .003). This really prevents buildup of CO2. The other factor (that you can see if you ever watch thoracic surgery and they perform one lung anesthesia) is the significant shifting of blood towards the inflated lung by hypoxic pulmonary vasoconstriction and decreases shunting. This will sense the decrease level of O2 in the deflated lung and shift it to the ventilated lung. Of course, this is all dependent on the patient's inflated lung status.

But you are right that the hyperventilation during a PTX (an attempt to receive more O2) could cause a decrease in PaCO2 and ETCO2.

What I was originally getting at was pulmonary embolism causes deadspace, that deadspace air mixing with alveolar air = greater than 5mmHg difference in ETCO2 and PaCO2. I would think that since a PTX doesn't increase deadspace, then there would be as great of a difference between the ETCO2 and the PaCO2.

This of course is also all speculation for me also since I'm not an EM doc nor have I ever had end tidal CO2 monitoring during a PTX. But I have seen one lung anesthesia and I would think it would be somewhat analogous.
 

dchristismi

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The lung exam can be very misleading in PE. I had a lady with what turned out to be massive bilateral PEs show up on my doorstep last night, arrived in distress, failed Bipap, tubed, sats still in 70s. Breath sounds were surprisingly clear and equal.

I thought she was dissecting, honestly. (Her mediastinum looked a little wide and her UE BPs were quite disparate)

Blood gas was roughly
7.34
PCO2 38
PO2 45
Sat 75%

The lab wouldn't release it because they didn't think it was "real." I had to call and convince them that yeah, it's real, please just tell me how bad it is.

Long story short, there are a lot of things that PE can look like, and differentiating it in the field is challenging at best. Hell, differentiating in the ED can be hard.

I could see the clots on the CT scan, which is bad. If I can see just about anything on a CT = 100% probability of badness. I think the EMS guys figured it was COPD or CHF or any number of other old-person-lung problems.

She didn't make it.

If I really want to know what the lungs sound like, I'll get an XRay.

If I really want to know what the XRay shows, I'll get a CT scan.
Maybe it's because I'm tired and switching back to days after a long string of nights, but I love this.


I'm too tired to think about Aa gradients, but carry on... ;)
 

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She didn't make it.
I assume 'she didn't make it' means dead.

Did you give lytics?
If so, when in the clinical course? (esp. in relation to the time of intubation, the sats in the 70s, the abg, and the positive CT with big PEs)

Lytics in the ED for massive PE is quickly becoming an interest of mine.

HH
 

dchristismi

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I assume 'she didn't make it' means dead.

Did you give lytics?
If so, when in the clinical course? (esp. in relation to the time of intubation, the sats in the 70s, the abg, and the positive CT with big PEs)

Lytics in the ED for massive PE is quickly becoming an interest of mine.

HH
Some background:
Well, it all played out at about 0330.
It takes my pharmacy about 20 minutes to mix TPA. Sometimes longer.

Pt is 85 years old, h/o dementia.

First 10 minutes are getting vitals, labs, lines, recognizing that her profound hypoxia isn't getting better, and intubating. I tell the patient we are going to give her medicine to go to sleep, and we'll take the mask off that she keeps pulling on. She says that it would be good to go to sleep, and please just help her breathing. She's working pretty hard, RR in 40s.

Next 10 minutes is me rechecking and rechecking to see that the tube is indeed through the cords, ordering a bunch of stuff, seeing the CXR and noting the mediastinum looks a little funny. BP falling. Sats still 70%. I have to argue with the lab to tell me the gas results, which delays that tidbit until she's in the scanner.

Then to the CT scanner, which takes a little while. I had to arrange a stat scan without labs to get it as fast as I did. (Lungs/aorta trump kidneys) I see one of the clots blocking her R main PA, order heparin immediately (still takes a little while) think about TPA, but mostly in case she codes... which will happen sooner than later. This lady isn't exactly a great candidate, and I don't know much of her medical history.

She gets back from CT and she starts to brady down. Little squirt of atropine and her family arrives not 2 minutes later. Family states that she has lived a long, good life, and wouldn't want to be kept alive like this. They get the quick "it's bad. It's Really bad" talk. After I ask, they add, "and if she dies, let her go." I really don't have time to go into my "living will vs DNR lecture" as she bradys again. BP now in the 60s, pulse to 40s.

There was no talk of TPA, atropine, epi or anything else. Just "I love you mom, don't worry about us, mom." And lots of tears. A couple of minutes later she slipped into PEA. Family stroked her hair and held her hands and watched the blips fade. It was less than an hour from arrival time, all told.

So no. I don't think she would have been a candidate, and I don't think the outcome would have changed. But you asked.
 

Hamhock

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But you asked.
Yes, thanks for the answer. Not really the right case for it and therefore I will hold my other questions regarding what folks think about tpa in massive PE. The ICU vs. ED is quite different at most places.

HH
 

Arcan57

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Had a youngguy who came in looking like death, HR 170-190s, palpable pulse but couldn't get a BP, RR 30-40s. Monitor was wide complex, somewhat irregular tachycardia. He kept moaning about his back and stomach hurting, in between "I can't breathe". IV, O2, 2 lg bore IVs later, I shock him for hemodynamically unstable wide complex tachycardia. Pulse drops briefly down to 110's, 12 lead looks like RBBB with intermittent A.Fib, lateral ST depressions. Quickly speed back up to 170-180's. Pulse ox is 100% on NRB,and at this point his BP is 170/117 so I order a diltiazem bolus for rate control. I decide he need to get tube because of agitation and need for cross-sectional imaging when he gets stabilized. While waiting for the dilt and intubation equipment to arrive (~45 seconds), his monitor shows his HR slowing to 74. And then his eyes roll back and he dies. He gets the standard ACLS PEA thrash, including intubation and a blind pericardiocentesis (U/S's coming to our shop in 2 months), and eventually devolves into asystole. At this point, I'm figuring that if it's a dissection then he's going to stay dead regardless of what I do. So that left PE/ACS as the things I hadn't specifically addressed. I ordered r-PA (which is in our Pyxis). By the time it arrived, he had been in asystole for 10 minutes and I called it without giving lytics.

His ABG was one of the worst I had seen in someone that died in the ED with an airway (correct tube placement confirmed by autopsy) and decent CPR. ph <6.8/pCO2 120/pO2 5/ HCO3 0. Autopsy showed completely occlusive saddle embolus.
 

tncekm

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Ughh... this is almost overwhelming realizing these types of situations are in my near future.
 

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His ABG was one of the worst I had seen in someone that died in the ED with an airway (correct tube placement confirmed by autopsy) and decent CPR. ph <6.8/pCO2 120/pO2 5/ HCO3 0. Autopsy showed completely occlusive saddle embolus.
Dude, ONE of the worst? It couldn't GET any worse. That pO2 is going to stay there for a while after he's dead, just from residual biologic processes. That saddle just stopped everything dead.
 

roja

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...and the next day, once the prior records are available, the family is present to give a history and a full list of meds, the CT is read by the Rads attending, the blood cultures have shown no growth x 24 hours, three sets of enzymes are back, and the patient is stable your consulting service will lament how glaringly obvious the correct diagnosis was, and how terribly the ED mismanaged this patient. Then, when the patient takes a turn for the worse while still waiting for a bed, and she needs acute intervention, all of a sudden the all-knowing consultants will be nowhere to be found.

sigh...guess it's time to mismanage the patient again
This is very very cultural and very hard to fight. Where I did residency/fellowship, our ICU docs where consistantly chiding the residents for trying to 'hind sight drive', continually saying that they didn't know what the patient looked like at that moment or what was known about the patient. This goes 100 times more for EMS. The US mantra is to scoop and run, with minimal invasion; given that this shows better outcomes.

EMS functions with almost no history, little time, trying to resusc in the field or in the back of a flying ambulance. Trying to decide PTX versus giant saddle embolism is useless. If PTX is possible (and it sounded like it) and the patient looks like butt, well, then needle. The rest can be dealt with.

I see my residents try and do this second guessing with EMS also. Just had a patient with colon cancer stage 4, nothing else, and called ems for sob, they got there HR was 20, they gave atropine and got him in the bus, and started pacing. when he got to us, I looked at hte ekg and it looked like hyperK. gave calcium, etc and removed pacing pads. EMS started beating themselves up. But really, they don't have enough time or information to deal with anything other than really big life saving differential stuff.... and they kept hte guy alive and breathing with a heart beat until he got to us.

if you have a portable US in the ambulance, you can r/o PTX in a about 30 sec. (look for "sliding lung sign"); it's better than cxr


Ultrasound is always user dependent. Although I love it, I am nto sure the amount of time, etc it would take to train and maintain this level of education for the incidince of tension PTX would be a good use of time and money.