what is the diagnosis?

[ihindash]

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a 24 year old smoker with a strong family history of ischemic heart disease, and relates an unexplained, sudden left-sided, severe chest pain, shortness of breath, and a temperature of 101.1 F . He now has a dry cough. He also smokes one pack of cigarettes a day and has done so for the past year, His cough was productive of a green and brown-streaked sputum. He denies wheezing and hemoptysis. He has no occupational exposure to dusts or fumes, has never been exposed to anyone with TB, and does not frequently suffer from respiratory infections.
along with the severe left-sided chest pain, he has a shortness of breath which has worsened over the past week to the point that speaking becomes difficult. but he denies sortness of breath with activity or exertion.
his physical had the following results:
Temp 101.1F
Resp 18, regular resp rythm
Pulse 72, regular pulse rythm
BP 118/80

his pulmonary exam revealed the following: Chest was normal to inspection with no obvious deformity. Palpation revealed mild left-sided chest tenderness. Lungs are clear to auscultation on the right side, but increased breath sounds are present on the left including rhonchi in the lower lung fields. The upper left lung is also dull to percussion.

his EKG reveals right axis deviation, an S wave in I and a Q in III, as well as inverted T wave in III.

his chest film was normal.

his pulmonary angio results were:
- right atrium: 3mmHg
- right ventricle: 26/6 mmHg
- pulmonary capillary wedge: 6 mmHg
- pulmonary artery: 13 mmHg

his labs showed the following:
white blood count (WBC) is 12,000 (normal is 3.2-9.8X10^9/L)
Polymorphonucleotide (PMN) 90% (normal is 50-70%)
Lymph 7.3% (normal 15-40%)
Eosinphils 0.5 (normal 1-4)
Prothrombin Time (PT) 13.2 (norm 10-12 secs)
Aspartate Aminotransferase (AST) 642(5-40) (normal 0-35U/L)
Alanine Aminotransferase (ALT) 229 (38-126) (normal 0-35U/L)
Total Bilirubin 76 (38-126) (normal 0-1.0 mg/dL)

Sputum Culture:
PMN 1+
Epithelial Cells 1+

Few mixed bacteria strep pneumo:
PCN Intermediate -Sensitivity
Erythromycin -Resistant
Vancomycin -Sensitive
Chloramphenicol -Sensitive
Sulfoximethasole -Sensitive
Clindamycin -Sensitive
Ampicillin -Sensitive
Rifampin -Sensitive
Levofloxacin -Sensitive

WHAT is THE DIAGNOSIS?

 

[robotsonic]

This guy's not doing too well. Let's review: he has the "classic" EKG for pulmonary embolism, he's got strep pneumo growing from sputum, and he has markedly elevated LFTs, suggesting hepatitis. Although the ratio of AST:ALT is over 2:1, which can often indicate alcohol abuse, alchoholic hepatitis rarely has such high AST and ALT values (usually <300). I think these values are more like viral hepatitis.

The thing that is concerning is how a 24-year-old got a PE - that is, how he ended up in a hypercoagulable state. I'm moving toward some hereditary hypercoagulable disorder. This might be exacerbated by the liver disease, which could produce decreased Protein C and S. As for how he got hepatitis and what his specific hypercoagulable disorder is, I'm not sure.

 

[virilep]

he's got herpes

 

[robotsonic]

he's got herpes

Like HSV hepatitis? HSV pneumonia? He doesn't really fit either of those, and if he did he would most likely be immunodeficient in some way. We don't have other evidence for an immunodeficiency disorder, although I guess he needs to be checked.

I'm glad these zebras weren't on step 2ck 😛

 

[werd]

a 24 year old smoker with a strong family history of ischemic heart disease, and relates an unexplained, sudden left-sided, severe chest pain, shortness of breath, and a temperature of 101.1 F . He now has a dry cough. He also smokes one pack of cigarettes a day and has done so for the past year, His cough was productive of a green and brown-streaked sputum. He denies wheezing and hemoptysis. He has no occupational exposure to dusts or fumes, has never been exposed to anyone with TB, and does not frequently suffer from respiratory infections.
along with the severe left-sided chest pain, he has a shortness of breath which has worsened over the past week to the point that speaking becomes difficult. but he denies sortness of breath with activity or exertion.
his physical had the following results:
Temp 101.1F
Resp 18, regular resp rythm
Pulse 72, regular pulse rythm
BP 118/80

his pulmonary exam revealed the following: Chest was normal to inspection with no obvious deformity. Palpation revealed mild left-sided chest tenderness. Lungs are clear to auscultation on the right side, but increased breath sounds are present on the left including rhonchi in the lower lung fields. The upper left lung is also dull to percussion.

his EKG reveals right axis deviation, an S wave in I and a Q in III, as well as inverted T wave in III.

his chest film was normal.

his pulmonary angio results were:
- right atrium: 3mmHg
- right ventricle: 26/6 mmHg
- pulmonary capillary wedge: 6 mmHg
- pulmonary artery: 13 mmHg

his labs showed the following:
white blood count (WBC) is 12,000 (normal is 3.2-9.8X10^9/L)
Polymorphonucleotide (PMN) 90% (normal is 50-70%)
Lymph 7.3% (normal 15-40%)
Eosinphils 0.5 (normal 1-4)
Prothrombin Time (PT) 13.2 (norm 10-12 secs)
Aspartate Aminotransferase (AST) 642(5-40) (normal 0-35U/L)
Alanine Aminotransferase (ALT) 229 (38-126) (normal 0-35U/L)
Total Bilirubin 76 (38-126) (normal 0-1.0 mg/dL)

Sputum Culture:
PMN 1+
Epithelial Cells 1+

Few mixed bacteria strep pneumo:
PCN Intermediate -Sensitivity
Erythromycin -Resistant
Vancomycin -Sensitive
Chloramphenicol -Sensitive
Sulfoximethasole -Sensitive
Clindamycin -Sensitive
Ampicillin -Sensitive
Rifampin -Sensitive
Levofloxacin -Sensitive

WHAT is THE DIAGNOSIS?

concur with robotsonic about the PE. coupla things...1)i'm curious why the dullness to percussion in the upper left wasn't visible on a chest film; 2)the pain is consistent with pleural inflammation but 3) i'm not convinced of pneumococcal pneumonia... sputum cultures are a little questionable in general and this one had as many epithelial cells as poly's, and there's a normal carrier rate for strep pneumo in the URT. temp 101 and worsening over a week don't ring true for strep pnuemo. the increased poly's in the lab suggest he's got some kind of bacterial challenge but i'm not ready to set sail in the step pneumo boat.

 

[imnodr]

if he's got a PE, what's the possibility of a clot in the liver somewhere causing the elevated labs and hypercoag??

 

[group_theory]

alpha-1 antitrypsin deficiency

*although I will still do the workup --> Cardiac enzymes x 3, BNP, CT Chest r/o PE, BMP, and probably a CT abd, hepatitis panel, d-dimer?

 

[UCLA2000]

I'm with the rest of you on this. Sudden onset cp c s1q3t3 classic for PE. Pt does not however have tachy (which is pretty common for pe).

Pt is a smoker (destroys cilia) c brown/green sputum. Cx grew strep pneumo.

Also note the 2:1 ast/alt suggestive of etoh. I'd consider covering the pt for anaerobes etc (aspiration?)

Why is pt throwing a clot? Who knows. Note that his PT is actually slightly elevated. Does he have a malignancy?

If he is throwing clots it raises the question could the pt be throwing clots to the liver to cause the elevated lft's?

 

[Doc Ivy]

alpha-1 antitrypsin deficiency

*although I will still do the workup --> Cardiac enzymes x 3, BNP, CT Chest r/o PE, BMP, and probably a CT abd, hepatitis panel, d-dimer?

I'm inclined to agree with this--it is a parsimonious dx that would explain both his liver and lung path-- alpa1AT along with his smoking would explain the sputum stuff-- COPDers are very susceptible to infections. And it seems clear that he has some intrinsic liver dz which can cause a coagulopathy affecting all of your factors (pro and anti coagulants) and therefore elevate your PT even though you may also be hypercoagulable.

 

[DarksideAllstar]

alpha-1 antitrypsin deficiency

*although I will still do the workup --> Cardiac enzymes x 3, BNP, CT Chest r/o PE, BMP, and probably a CT abd, hepatitis panel, d-dimer?

I could potentially see where you are going with this, but his CXR was read as "normal", I would imagine that this person would have emphysematous changes by now (if you are assuming that his liver damage is a result of AATD.) I place this way down on my differential.

As an aside what does this guys heart sound like? Are there murmurs or rubs? Has he been sick recently?

I like PE given the S1 Q3 T3 and RAD on EKG.

My hypothesis (given no other physical exam findings):
Fibrolamellar HCC with tumor emboli to the lungs as cause of this "PE".

 

[Paws]

Infection, blood in the sputum? Hx of cardiac ischemia in family? PE? would that be a sharp pain on inhalation? Liver panel? (We haven't done GI, etc yet.)

I dunno, ask the guys over in the Emergency Med forum and see what they say. They could nail it pretty quick.

 

[Paperboy!]

/

 

[Paws]

Paws has been listening to Dr Goljan's lecture about cardiovascular stuff and now I want to say that I think this is some kind of left-sided heart failure with pulmonary edema. There is dyspnea, rust colored streaking in the sputum and lower lung sound weirdness. Cough could be from the lower lung edema. If there is a history of cardiac ischemia (for whatever reason), this could be part of the package. I might do an echocardiogram to look and see. Could the ecg be showing the cardiac activity?

I don't know enough about liver enzymes to talk about these. Is the venous system backed up and affecting the liver? Alpha-1, well that sounds likely, altho he denies shortness of breath on exertion, which would be a symptom of emphysema. Is there a family history of pulmonary problems? Liver disease?

I have no idea really, what this is but it's fun to try and figure it out based on 1.5 years of medical education.

 

[liveandlearn]

just to put everyone's opinions together... what about shock liver syndrome?

 

[UCLA2000]

d-dimer?

This guy sounds so high risk that a negative D-Dimer wouldn't change my management.

 

[Hawkeye Kid]

This guy sounds so high risk that a negative D-Dimer wouldn't change my management.

He's also so sick that his D-dimer wouldn't be negative. Agreed, it's useless in this case, unless we use it in conjunction with an ESR and CRP

 

[UCLAstudent]

I agree that his EKG suggests pulmonary embolism, but wouldn't his right atrial/right ventricular/pulmonary artery pressures be higher if that were the case? They're pretty normal. The pulmonary artery pressure is actually kind of low.

 

[Seaglass]

Bronchitis, alcholism

S1Q3T3 is really a non-specific finding. It suggest right heart strain but that is all. Since you often get right heart strain in PE it is associated with PE but angio is the gold standard for PE and if there is no PE on angio then for all intents and purposes there is no PE. A complete PE eval also includes lower ext doppler US for DVT.

Alph 1 antitrypsin is a good DX but rare. A work-up would probably be indicated after a few recurrent infections but normal PA pressures suggests that is is less likely because you would expect ot see pulmonary hypertension IIRC. Also a significant percentage of the populace has elevated LFTs for no reason, although given that this is a case presentation it probably means something.

The fever and lung findings on physical exam plus sputum culture for S. Pneumo suggest a lobar pneumonia but the CXR was "normal" so that would be somewhat less likely.

Bottom line: Vitals are OK, guy is young, EXTREMELY unlikely to have ischemic heart disease - no enzymes, doxycycline for bronchitis x 2 weeks, follow up with your PCP, stop drinking.

 

[Seaglass]

With regards to being high risk for PE:
The missing key info is an O2 Sat but assuming that that is normal the only risk factor for PE that this guy has is smoking. He has an excellent alternative dx: infection. He would get by with a dimer at the max.

With regards to ischemic cause: 24 years old, reproducible chest pain. The only other possiblilty is pericarditis but a truly ischemic cause is so unlikely that I wouldn't test for it.

With regards to failure: On cath had normal pressures. Failure excluded.

With regards to being sick: Young, healthy except for smoking, elevated LFTs but no complaint, white count with productive sputum. Assuming not hypoxic this guy is almost as healthy as they come.

With regards to his chest pain: Probable chostochondritis or other musculoskeletal chest pain. It would help to know if the pain is positional, pleuritic, and modifying factors.

 

[ERMudPhud]

I'm a little confused. How the heck did a young guy with essentially normal vitals other than a bit of a fever end up with Swan catheter and a wedge pressure but not have a pulse ox reading. This must be one of those made for testing type cases that has too little relationship with real medicine. I certainly don't go putting Swans in every slightly febrile young smoker I see with a cough and SOB.

If he really had a pulmonary angio we should know if has PE's or not. Assuming he just got a Swan for some reason and no pulmonary angio then in the modern day he would have had a chest CT by now. With that many abnormalities on exam he should have something abnormal on chest imaging.


As long as we are talking hypothetical why not legionella
-fever
-pleuritic chest pain
-LFT abnormalities
-bradycardia relative to fever
-coagulopathy
-cough
-variable CXR findings
-variable lung exam findings

are all features of legionella

While you are doing this huge work up. First make sure he really didn't have a PE as that is still a simple unifying diagnosis then add an LDH and urine legionella antigen and bronch him.

 

[UCLA2000]

With regards to being high risk for PE:
The missing key info is an O2 Sat but assuming that that is normal the only risk factor for PE that this guy has is smoking. He has an excellent alternative dx: infection. He would get by with a dimer at the max.

Agreed. The thing that is really weighing on my mind is the "sudden onset" of the CP. Argues against infection as the primary cause of the CP.

 

[ERMudPhud]

Agreed. The thing that is really weighing on my mind is the "sudden onset" of the CP. Argues against infection as the primary cause of the CP.

Actually if you read the "classic" descriptions of pneumococcal pneumonia a very acute onset is often described. Patients can sometime tell you to the minute when they suddenly felt sick. I think the S. pneumonia in his sputum cuture with "mixed bacteria" is probably a red herring here but sudden onset doesn't always rule out infection.

I thought Seaglasses evidence based approach to the work up was very solid and consistent. Without more info the patient has few if any risks for PE and a presentation inconsistent with acute MI. Given this evidenced based approach I was surprised by his advocating doxy for bronchitis. Most of the available evidence for antibiotic treatment of bronchitis is specifically for acute exacerbations of chronic bronchitis (AECB) a very different entity from the typical viral bronchitis. To have AECB you first have to have CB which means emphysema with symptoms of CB. Just being a 24 year old smoker with a normal CXR doesn't count.

 

[funkless]

Should we be answering this sort of question from somebody with only 10+ posts?

To quote Yaah and Stoic:

Don't give medical advice - people register on this site to ask medical questions for legal reasons, advice, whatever. Don't get involved.

he's not kidding. there have several malpractice lawyers that have signed on and ask questions "innocently" hoping that they could then show even a mere medical student should know the answer to some medical issue....

 

[ERMudPhud]

Should we be answering this sort of question from somebody with only 10+ posts?

To quote Yaah and Stoic:

I think its more likely we were doing someones homework for them. The question reads more like a poorly written test question than a lawyer looking for advice. Check the identical thread on pre-Allo.

If you are going to have us do your homework for you than you should at least be good enough to post your grade and the answer when you get your test back

 

[ozarka]

Should we be answering this sort of question from somebody with only 10+ posts?

To quote Yaah and Stoic:

but even if, theoretically, a malpractice lawyer posts cases on sdn, would the weight of anonymous posters in an online forum really count as viable evidence in a trial?

 

[Callogician]

I'm a first year student, and although I recognize the majority of the terms and can make basic inferences, I am having a lot of trouble integrating the information and making a reasonable hypothesis.

I agree with UCLAstudent in that the low to normal PCWP is contraindicative of left acute MI, pulmonary edema, and [major] pulmonary embolism. However, I like the idea of disseminated intravascular coagulation being the connection between the ECG results (assuming pulmonary embolism) and the elevated liver function tests. This might be confirmed by d-dimer, but high bilirubin can cause a false positive, and based on what UCLA2000 said, d-dimer might not be clinically worthwhile. It seems to me that constituitive alpha-1 antitrypsin deficiency is a questionable hypothesis because this would marginalize the contribution of smoking to COPD. Wouldn't you expect frequent respiratory tract infections and hyperreasonance to percussion? Also, what is the connection between absent AAT and liver function tests?

By the way, the suggestion that a lawyer would present a particularly sophisticated response in this thread as evidence isn't entirely absurd. My father is an attourney, and he once had my sister (an actress) leave a message on the opposing council's client's voicemail right before the subpeona for the phone records went through. The intention was to demonstrate that the man in question was receiving solicitations for a particular service he had advertised.

 

[UCLA2000]

However, I like the idea of disseminated intravascular coagulation being the connection between the ECG results (assuming pulmonary embolism) and the elevated liver function tests.

All of the cases of DIC that I have seen have been very obvious. The patient presented with obvious petechiae/purpura etc. Easily confirmed with low platelet count and high fibrin split products. The patients should also have increased pt and ptt. In addition they were oozing from venipuncture sites.

 

[Seaglass]

COPD is a condition that, in the absence of a congenital abnormality like alpha-1 antitrypsin, takes years to develop. This person is unlikely to have significant COPD.