Case #1 (2-1-2004)

[Andrew_Doan]

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CC: 29 y.o. man with HA, hematuria, and visual obscurations.

HPI: 29 y.o. man complained of headache (HA) for several weeks. HA was worse the day before presentation (8/10) and was associated with nausea & vomiting (N/V). He went to the local ER and was noted to have hematuria. The patient was told he was "dehydrated" from the N/V, given pain meds, and sent home.

On the next day, he awoke feeling weak and complained of HA and N/V. He noticed visual field (VF) obscurations in the left eye (OS). He then presented for formal ophthalmology evaluation.

PMH: Poorly controlled HTN (160/108) with losartan & amlodipine.

EXAM:

-Ill looking man with BP 160/108.
-Best corrected visual acuity (BCVa) 20/20 OD & OS
-Extraocular motilities (EOM) FULL OU
-Intraocular pressures (IOP) were 18 mmHg OU
-Pupils equal and reactive. No RAPD.
-VF full OD.
-VF OS had small paracentral scotoma on Amsler grid.

Dilated fundus exam (DFE) showed multiple cotton wool spots (CWS) OU with normal optic nerves without optic nerve edema/papilledema or pallor OU:

Figure 1: View of CWS using the 90D lens and slit lamp.

Feel free to discuss the following:

What tests should you order (I'll post labs when asked for them)?

What's the differential diagnosis?

What's the diagnosis?

What is the treatment of choice?
______________________________

Requested labs and work-up:

Urinalysis indicated 3+ hematuria and proteinuria. Not gross.

CBC:
platelet count: 32K/mm3
hemoglobin: 14.1 g/dl
WBC: 4.8K/mm3

His electrolyte panel was notable for:
Na: 143 MEQ/L
K: 3.7 MEQ/L
Cl: 108 MEQ/L
-CO2: 21 MEQ/L
creatinine: 1.6 mg/dl
BUN: 26 mg/dl

ESR 1 mm/hr
CRP < 0.5 mg/dl

HIV NEGATIVE

Head CT negative

The peripheral blood smear showed:
1+ schizocytes & helmet cells, and significantly reduced numbers of platelets.

LDH was 752.

The patient was admitted, and the following day, his hemoglobin dropped from 14.1 g/dl to 9 g/dl.

 

[dread]

Interesting case. I'm taking this approach from a non-ophthamologists perspective, so you will have to excuse my ignorance. My thought that is that maybe he has some sort of nephritic syndrome going on causing him to develop malignant hypertension which is causing retinal hemorrhages, headache, nausea and vomiting. Or maybe he doesn't have a nephritic syndrome and he simply has malignant hypertension due to some unknown cause causing his hematuria as well. Even though a BP of 160/100 isn't all that high (particularly given that he's stressed), given his young age and the fact that he is on 2 BP med's already, it'd be enough to raise my eyebrows. I don't know how to account for his paracentral scotoma. Could that be from papilledema? Anyways, to begin his work up, I'd like to see a complete urinalyisis, CBC with a CMP to evaluate organ function. I will offer further lab testing after I get those. While drawing initial labs, I'd probably also ask to draw an HIV test just in case this was some sort of weird presentation of some infectious disease too.

 

[imtiaz]

Is it gross hematuria? Do you see blood in the cup?

 

[Andrew_Doan]

Originally posted by imtiaz
Is it gross hematuria? Do you see blood in the cup?

Originally posted by dread
Anyways, to begin his work up, I'd like to see a complete urinalyisis with a CMP to evaluate organ function.

Urinalysis indicated 3+ hematuria and proteinuria. Not gross.

CBC:
platelet count: 32K/mm3
hemoglobin: 14.1 g/dl
WBC: 4.8K/mm3

His electrolyte panel was notable for:
Na: 143 MEQ/L
K: 3.7 MEQ/L
Cl: 108 MEQ/L
-CO2: 21 MEQ/L
creatinine: 1.6 mg/dl
BUN: 26 mg/dl

ESR 1 mm/hr
CRP < 0.5 mg/dl

HIV NEGATIVE

 

[JR]

There is obviously impaired kidney function most likely from HTN. I'd do a full work up to r/o 2' causes of HTN in this guy. The ddx includes coarctation, renal artery stenosis, intrinsic renal disease, pheo, 1' hyperaldo, Cushings, hyperCa++, alcohol, neurologic process, thyroid dz, etc. So, next I'd measure bp/pulses in upper vs lower extremities, get more precise hx (episodic sx? alcohol hx? thyroid problems?), do a physical (stigma of Cushings? abdominal bruit?) . Also, check if he is taking some herbal junk or does drugs (cocaine). That should be a good strat.

 

[Andrew_Doan]

Originally posted by JR
There is obviously impaired kidney function most likely from HTN. I'd do a full work up to r/o 2' causes of HTN in this guy. The ddx includes coarctation, renal artery stenosis, intrinsic renal disease, pheo, 1' hyperaldo, Cushings, hyperCa++, alcohol, neurologic process, thyroid dz, etc. So, next I'd measure bp/pulses in upper vs lower extremities, get more precise hx (episodic sx? alcohol hx? thyroid problems?), do a physical (stigma of Cushings? abdominal bruit?) . Also, check if he is taking some herbal junk or does drugs (cocaine). That should be a good strat.

Good thoughts about the secondary causes of HTN.

BP/pusles in upper vs lower ext equal.
no EtOH use. no drug use.
no abdominal bruits
no Thyroid dz
no signs of Cushings
no other episodic symptoms than what was discussed in the HPI.

 

[JR]

Well, given the negative work up so far plus n/v/HA for several weeks I would scan his head as a next step.

 

[TulaneKid24]

Sounds like this could be some vasculitis (extrapulmonary/extrarenal manifestation of Wegeners), systemic collagen vascular disease (read SLE) or some autoimmune dz.

I would want to see a full autoantibody panal: i.e. ANA, pANCA, cANCA, thryoid autoantibodies, etc

I would also want to see a ESR or CRP (which ever one you have).

CBC and Chemistry would be nice. HepB panel (there is a loose association between HepB and systemic vasculitis)

If this is some sort of vasculitis, I would start the patient on Steroids, prednisone.

I know this my be off in left field, but its a try!

 

[Andrew_Doan]

Originally posted by TulaneKid24
Sounds like this could be some vasculitis (extrapulmonary/extrarenal manifestation of Wegeners), systemic collagen vascular disease (read SLE) or some autoimmune dz.

I would want to see a full autoantibody panal: i.e. ANA, pANCA, cANCA, thryoid autoantibodies, etc

I would also want to see a ESR or CRP (which ever one you have).

CBC and Chemistry would be nice. HepB panel (there is a loose association between HepB and systemic vasculitis)

If this is some sort of vasculitis, I would start the patient on Steroids, prednisone.

I know this my be off in left field, but its a try!

Head CT was negative.
ESR/CRP normal.

CBC shows thrombocytopenia as indicated above. Chemistry demonstrates mild renal insufficiency.

At this point, the autoantibodies are low yield and was not ordered. However, they're all normal.

 

[Gottschalk]

I think it is TTP, especially if he has purpura. Does he? Also, check LDH for hemolyis.

 

[dread]

Originally posted by Gottschalk
I think it is TTP, especially if he has purpura. Does he?

I don't think that it's TTP because he's not anemic. Can we see a peripheral smear? I'd also like to see a 24 hr urine protein, urine cytology looking for red cell casts, renal ultrasound, ASO titers, and CT of the abdomen without contrast. I really have no idea what's going on in this patient. If everything is negative, I'd like to get a renal biopsy too.

 

[TomOD]

This is a very interesting case. Thanks for posting it Andrew. Any chance a F/A was done (academic I guess)?

How about an ELISA, IgG, IgM (if they have not already been mentioned)?

Any chance of a tick-borne disease- Lyme disease, human babesiosis, human granulocytic erlichiosis, Rocky Mountain Spotted fever etc...?

 

[Andrew_Doan]

Originally posted by Gottschalk
I think it is TTP, especially if he has purpura. Does he? Also, check LDH for hemolyis.

Originally posted by dread
Can we see a peripheral smear? I'd also like to see a 24 hr urine protein, urine cytology looking for red cell casts, renal ultrasound, ASO titers, and CT of the abdomen without contrast. I really have no idea what's going on in this patient. If everything is negative, I'd like to get a renal biopsy too.

Originally posted by TomOD
This is a very interesting case. Thanks for posting it Andrew. Any chance a F/A was done (academic I guess)?

How about an ELISA, IgG, IgM (if they have not already been mentioned)?

Any chance of a tick-borne disease- Lyme disease, human babesiosis, human granulocytic erlichiosis, Rocky Mountain Spotted fever etc...?

All good thoughts. There's no history of exposure to tick-borne diseases. A FFA was not done.

The patient did not have any rash, joint pains, fevers, or purpura on exam.

The peripheral blood smear showed:
1+ schizocytes & helmet cells, and significantly reduced numbers of platelets.

LDH was 752.

The patient was admitted, and the following day, his hemoglobin dropped from 14.1 g/dl to 9 g/dl.

 

[dread]

Please draw coags, D-dimers, coombs test. Also, 🙄 for giving your patient anemia. 😉 I'm thinking HUS/TTP (depending on his renal function the following day) with retinal hemmorhage now too. I'd treat his BP first, maybe with labetelol, lowering it 25-30% and seeing what happened.

 

[Andrew_Doan]

Originally posted by dread
Please draw coags, D-dimers, coombs test. Also, 🙄 for giving your patient anemia. 😉 I'm thinking HUS/TTP (depending on his renal function the following day) with retinal hemmorhage now too. I'd treat his BP first, maybe with labetelol, lowering it 25-30% and seeing what happened.

This is how the patient presented to me. Sorry if there was delayed anemia. 😉

Coags and D-dimers normal. Renal U/S was negative, and HTN treated in house without problems. Detailed discussion to follow later this week. Any thoughts on treatments?

 

[dredd]

Alright, well, given that the patient's renal function isn't all that bad, I would go ahead and give him a presumptive diagnosis of TTP and treat him emergently with large volume plasmaphersis. I would not treat him with prednisone right now because his ESR and CRP are so low that I don't think that he has a lot of inflammation for some reason and I would not treat him with an anti-platelet agent because I can't imagine that being good for his retinal hemmorhages. The evidence for prednisone and anti-platelet agents in addition to plasmapheresis is weak anyways, according to my CMDT. Thanks for the case! Please adjust your presentation to fit my diagnosis and treatment if they are incorrect. That's what I do when patient's don't fit my differential anyways, I change their history and physical 😉 .

 

[MD'05]

Just curious ... how long has the pt had poorly controlled htn?

Is he morbidly obese? Has he had a gradual weight loss? Has he had changes in his frequency of micturation?

Did he have a 24-hr urine done?

Since his serum cr is only 1.6, this could be due to the htn although he is approaching nephrotic range proteinuria.

When his hgb dropped, did you see an increase in urine RBCs??

Any ultrasound or CT scan of the urinary tract (including bladder)? -- never mind (saw renal u/s above - must have included bladder??)

I am leaning toward adding pheochromocytoma to the differential dx especially with the headaches, htn, urine RBCs.

 

[Andrew_Doan]

Originally posted by MD'05
Just curious ... how long has the pt had poorly controlled htn?

Is he morbidly obese? Has he had a gradual weight loss? Has he had changes in his frequency of micturation?

Did he have a 24-hr urine done?

Since his serum cr is only 1.6, this could be due to the htn although he is approaching nephrotic range proteinuria.

When his hgb dropped, did you see an increase in urine RBCs??

Any ultrasound or CT scan of the urinary tract (including bladder)? -- never mind (saw renal u/s above - must have included bladder??)

I am leaning toward adding pheochromocytoma to the differential dx especially with the headaches, htn, urine RBCs.

We're not sure how long he had poorly controlled HTN. It may have been just the recent illness that made him have high BP in the ER. The patient didn't have any retinal hemorrhages or optic nerve swelling, just cotton wool spots OU. Cotton wool spots are microinfarctions of the retinal nerve fiber layer resulting in swelling and 'cotton wool' appearance.

The patient was not obese. Complete workup for secondary causes of hypertension by Internal Medicine was negative. His BP was well-controlled with a single medication in the hospital, amlodipine.

 

[Richard_Hom]

Originally posted by Andrew_Doan
CC: 29 y.o. man with HA, hematuria, and visual obscurations.

HPI: 29 y.o. man complained of headache (HA) for several weeks. HA was worse the day before presentation (8/10) and was associated with nausea & vomiting (N/V). He went to the local ER and was noted to have hematuria. The patient was told he was "dehydrated" from the N/V, given pain meds, and sent home.

On the next day, he awoke feeling weak and complained of HA and N/V. He noticed visual field (VF) obscurations in the left eye (OS). He then presented for formal ophthalmology evaluation.

PMH: Poorly controlled HTN (160/108) with losartan & amlodipine.

EXAM:

-Ill looking man with BP 160/108.
-Best corrected visual acuity (BCVa) 20/20 OD & OS
-Extraocular motilities (EOM) FULL OU
-Intraocular pressures (IOP) were 18 mmHg OU
-Pupils equal and reactive. No RAPD.
-VF full OD.
-VF OS had small paracentral scotoma on Amsler grid.

Dilated fundus exam (DFE) showed multiple cotton wool spots (CWS) OU with normal optic nerves without optic nerve edema/papilledema or pallor OU:

Figure 1: View of CWS using the 90D lens and slit lamp.

Andrew,

Has there been a history of foreign travel?
Any stool samples?

Regards,
Richard_Hom

 

[Andrew_Doan]

Originally posted by Richard_Hom
Andrew,

Has there been a history of foreign travel?
Any stool samples?

Regards,
Richard_Hom

Hi Richard,

No foreign travel ever, and we didn't take stool samples. There was no change in his bowel habbits.

 

[I Surgeon]

You might want to get a Hgb electrophoresis on this patient to r/o Sickle cell Disease, since it can present with cotton wool spots, anemia, renal failure, and schistocytes. There is also thromboctopenia due to splenic sequestration. Dehydration is a risk for a vasoocclusive event.

 

[questionguy]

I sincerely doubt that a 29 y/o with sickle cell would have enough of a spleen left to sequetser anything.

 

[Andrew_Doan]

Although a nonspecific finding, the presence of cotton wool spots in an ill, young patient should elicit a careful review of systems and consideration of a thorough medical evaluation. Table 1 details common and uncommon diagnoses for cotton wool spots of the retina.

Given the clinical presentation, our patient was diagnosed with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS), see Table 2. Although, once thought to be separate pathologic entities, it is now felt that these entities represent a spectrum of a single disorder. TTP-HUS presents as a thrombocytopenia and microangiopathic hemolytic anemia associated with thrombi composed primarily of platelets in affected organs. Patients may present with: thrombocytopenia, microangiopathic hemolytic anemia, neurologic signs and symptoms (e.g., headache, vision changes, paresthesias), renal insufficiency, and fever. TTP-HUS is a deadly disorder with mortality rates over 90% in untreated patients. Plasma exchange with fresh frozen plasma is the treatment of choice and reduces the mortality rate to below 50%. Patient survival is dependent on prompt diagnosis, hospital admission, and treatment.

While this patient came to our attention due to a new scotoma in his visual field from large cotton wool spots, other ophthalmic manifestations in patients with TTP-HUS include: serous macular detachments, choriocapillaris occlusion due to fibrin-platelet thrombi, retinal or vitreous hemorrhages, optic disc edema, neovascularization of the disc, and central retinal vein occlusion.

Cotton wool spots can be a sign of serious systemic disease and warrant further evaluation in certain clinical scenarios. Initial testing should include blood pressure measurement, complete blood count with platelets and differential, and evaluation for diabetes. In this patient, a life-threatening illness was discovered. Although TTP-HUS is a rare disorder, it should be considered in patients who present with vaso-occlusive disease of the retina, neurologic decline, renal insufficiency, and hematologic abnormalities (such as anemia and/or thrombocytopenia). Evaluation and management of TTP-HUS should be done in conjunction with internists and hematologists. Because the mortality rate of this condition can be exceedingly high without prompt intervention, ophthalmologists may play a key role in its timely diagnosis and thus improve the likelihood of patient survival.




TABLE 1: Differential diagnoses for cotton wool spots.
__________________________________
COMMON

Diabetes
Hypertension
Retinal arteriole occlusion
Retinal vein occlusion
Collagen-vascular diseases
AIDS retinopathy

LESS COMMON

Cardiac valvular disease
Carotid artery obstruction
Hematologic abnormalities: Anemia, Leukemia, Thrombocytopenia, Thrombocytosis
Purtscher?s retinopathy
Lymphoma

TABLE 2: Key features of TTP-HUS.
____________________________________
Symptoms
Thrombocytopenia
Hemolytic anemia
Kidney failure
Neurologic abnormalities
Fever

Age and Sex
All ages, typically younger
Women, particularly during pregnancy and immediately post-partum.

Treatment
Without treatment, mortality rates can be as high as 90%.
Plasma exchange with fresh frozen plasma can reduce mortality rates below 50%.
Steroids
Splenectomy

Long-Term Outcomes
Recurrence can occur in one-third of treated patients.
Chronic renal failure can occur in one-fourth of patients.
Long-term support and care may be necessary.

 

[Visionary]

Originally posted by Andrew_Doan
This is how the patient presented to me.

Andrew-

By the above statement, I assume this was an actual patient of yours, yes? If so, what is his current status?

I enjoy hearing examples of ophthalmologists' involvement in the diagnosis and management of systemic diseases. It reinforces the idea of an ophthalmologist as a physician rather than simply an eye care professional.

[To head off any of the nasty rhetoric that tends to be generated by posts like this, I must qualify my statement by saying this is not intended as a slight against optometrists. I am referring to the attitude held by many physicians in other specialties with regard to the professional status of ophthalmologists. Example: a general surgery attending I rotated with, upon hearing of my desire to pursue ophthalmology, said "I don't know why you guys even need to go to medical school."]

 

[jse75]

to put case summaries on a separate thread or a separate website, so we can all refer to them later as time goes by.

This was a great case!

Thanks Andrew!

-jason

 

[Andrew_Doan]

Originally posted by Visionary
Andrew-

By the above statement, I assume this was an actual patient of yours, yes? If so, what is his current status?

Yes, this patient is doing well. He presented to me on call when I was a first year. I saw 15 patients that evening including 2 open globes and a lady who faked losing vision. The functional vision loss patient, by far, was the most tedious patient! 😉

These cases are linked on a posting in the Ophthalmology FAQ. You'll see an index and will be able to reference the cases.

If you have cases you want to present, then send me the images and post the case.

 

[Andrew_Doan]

Originally posted by Visionary
Example: a general surgery attending I rotated with, upon hearing of my desire to pursue ophthalmology, said "I don't know why you guys even need to go to medical school."]

Because you'll find that ophthalmologists diagnose systemic diseases that are missed by other physicians.

I have heard similar ridiculous comments from surgery and medicine attendings. Then I pull out my ARCHOS AV 320 with my cases that their physicians missed. They don't have much to say after that! 😉

 

[eyedocmaggie]

CBC
ESR
Carotid Doppler
Cholesterol screening

DDX:
I dont have very many.... still thinking... this one would be referred out by me for further testing with a PCP and probably Ophtho ... and I would seek the above tests.
Grade III Hypertensive Retinopathy
Vascular Disease
Ischemia of some kind (if he were older and had an APD I might look at some form of Ischemic Optic Neuropathy as a possibility)


Questions:
Was there any retinal edema? Was the CWS the only retinal pathology? Does the patient have any other systemic disorders such as neurofibromatosis? Does this patient suffer from Migraines?

 

[Andrew_Doan]

Originally posted by eyedocmaggie
Questions:
Was there any retinal edema? Was the CWS the only retinal pathology? Does the patient have any other systemic disorders such as neurofibromatosis? Does this patient suffer from Migraines?

Welcome to the ophthalmology forum! 🙂

There was no retinal edema, only CWS. There is no history of systemic disorders or migraines, other than HTN.

 

[jjwiiwi]

Originally posted by Andrew_Doan
Because you'll find that ophthalmologists diagnose systemic diseases that are missed by other physicians.

I have heard similar ridiculous comments from surgery and medicine attendings. Then I pull out my ARCHOS AV 320 with my cases that their physicians missed. They don't have much to say after that! 😉

Dr. Doan,

What do you use the ARCHOS for? How do you show ophthalmology cases on it?

 

[Andrew_Doan]

Originally posted by jjwiiwi
Dr. Doan,

What do you use the ARCHOS for? How do you show ophthalmology cases on it?

www.archos.com

The ARCHOS AV320 is a 20 GB harddrive (avail up to 80 GB) that has a 3.5 inch screen that plays MPEG4 video, displays photos, plays MP3, etc...

I use my digital camera to document cases, and then make small teaching cases from them. It's like having a mini-powerpoint machine. In addition, I copy DVD and VHS movies to it; so I can have surgeries on it for review, educate patients, share with residents, or teach medical students.

 

[Apollyon]

Originally posted by Andrew_Doan
Because you'll find that ophthalmologists diagnose systemic diseases that are missed by other physicians.

We had a woman in the Duke ED that had c/o R sided facial numbness, and visual changes in the ipsilateral eye. CT head was neg, IOP's 10/11 OD/OS. CN's intact, acuity 20/70 OD uncorrected, 20/20 pinhole, I forget the visual fields. Sounded like TIA, called neurology. They said, "no", because the vision change should be in contralateral eye. Called ophtho, and this guy did the most detailed exam I've EVER seen, and dx'd that her hypertension was so bad, she'd blown out all her circulation on the left side of her face (including a partial R CRVO).

The ophtho guy was/is a superstar.

 

[Kalel]

I'm just curious, did optho really make the diagnosis of TTP in this case? It really wasn't fair to IM if this patient was admitted to IM, because if you look up TTP/HUS (which is a syndrome and not a firm diagnosis, it's not like something you can biopsy and see a classical disease pattern); you will see that anemia is a neccessary criteria for even considering the diagnosis of TTP. Given that this patient did not present with anemia, I think that you would have been forced to consider other diagnoses higher on your differential, unless your optho exam gave you some sort of special insight into TTP.

 

[Andrew_Doan]

Originally posted by Kalel
I'm just curious, did optho really make the diagnosis of TTP in this case? It really wasn't fair to IM if this patient was admitted to IM, because if you look up TTP/HUS (which is a syndrome and not a firm diagnosis, it's not like something you can biopsy and see a classical disease pattern); you will see that anemia is a neccessary criteria for even considering the diagnosis of TTP. Given that this patient did not present with anemia, I think that you would have been forced to consider other diagnoses higher on your differential, unless your optho exam gave you some sort of special insight into TTP.

The point of the case was that IM was ready to send the patient home until we saw the CWS and elicited a history of hematuria. This history, finding, and clinical exam prompted a CBC with diff. and urinalysis. The finding of thrombocytopenia and elevated LDH as well as a very ill patient was enough to admit to IM.

Ophthalmologists should not admit nor manage TTP-HUS, but should have IM care for these patients. Furthermore, anemia was not evident because the patient was dehydrated and was in the early stages of hemolysis. In addition, the peripheral smear demonstrated evidence of hemolysis. After IVF, it was clear that the patient had anemia when the Hb dropped precipitously over night. In this case, the eye exam and clinical history obtained by ophthalmology prompted further workup and admission to the hospital. Internal medicine ended up making the final diagnosis and monitoring of treatment. Our differential was HTN, collagen vascular disease, and vascular thrombotic disease, which are all within the scope of practice for IM; thus, this is why the patient was admitted to IM for further workup and treatment.

 

[Kalel]

I think that you misunderstood me. I was just defending the IM team that missed the diagnosis, I wasn't saying that IM shouldn't have admitted and managed the patient. Anyways, this was an unusual case. I have noticed that specialists occasionally do take better histories then the generalist because they have a shorter differential that they are asking for when they are taking their history. Blood in the urine is not something that I would think about asking with visual complaints, particularly if the patient didn't bring it up. When I first started third year, I used to run through a complete ROS as we were taught to do in first year, but I quickly learned that patients, particularly the sick ones, don't like to be asked hundreds of repetetive, seemingly tangential questions while waiting for hours in the ER for a bed on the floor. I had one patient who threatened to punch me because I was asking him too many questions in ROS (I was the last in a line of people who were taking his history). Anywho, good catch optho.😉

 

[Andrew_Doan]

Kalel,

I understand you now. 😉

I always take a complete ROS for all new patients. There's a form we have the patient fill out or I review with the patient. It covers all systems.

Also, when I take the history, I start from the day the patient got sick, and I let the patient tell the story. He offered the information during the HPI.

It's also tough as a medical student because patients know you're not a physician. On the other hand, it is also tough as a physician to obtain a history when patients are irritated. I try to make the patients feel comfortable and explain to the patient that it's important for me to hear the complete story b/c I may find something that will help them. If you emphasize helping them, then most people will cooperate.