The following case is part of the Sermo Case Conference Series. This case will unfold over several days - feel free to ask for additional data, test results, or supporting materials you think would be most appropriate. A 43 year-old female had a Mastectomy in 2005, which revealed a 3.5cm Invasive Ductal Carcinoma, ER/PR/Her2neu negative; 2 of 15 Axillary Nodes were ¨positive; margins were negative. She received 4 cycles of adjuvant Adriamycin, Cytoxan, and Taxol chemotherapy. She was not referred for Postmastectomy Radiotherapy. She now presents with a 2 month history of a 1.5cm tender, mobile nodule along her Mastectomy scar. Interested in leading a Case Conference like this in your specialty? Email Sermo at clinicalcase@sermo.com.

In the new green journal, from the 2007 Ostheimer Lecture Review Article, it was stated that "the latest Confidential Enquiries into Maternal Deaths has reported that cardiac diseas is now the most common cause of maternal death." I read that last week and found it very hard to believe, until I heard of a case over the weekend. A 277 pound 5' 8" woman had a C-section for a failed induction. She reportedly had a functioning spinal anesthetic. After delivery of the infant, the patient developed profound hypotension and a junctional rhythm that alternated with atrial fibrillation. She required intravenous epinephrine plus a phenylephrine drip to maintain any kind of blood pressure. Postoperatively her Troponin I was over 3. A cardiac cath was done that showed no coronary lesions. Ever heard of this?

I am interested in hearing the opinions of other electomyographers on classifying radiculopathies, particularly old or chronic conditions that may or may not have much in the way of spontaneous activity to help identify the underlying entity and on the practice of using MUAP morphology to assist in diagnosis. A recent example of mine that prompted this post was a 59 yr old male with a +/- 2 yr history of neck and radiating arm pain. He had just had a C7 and C8 nerve root block by an interventionalist but was seeing me for an EMG due to some persistent medial forearm and hand paresthesias. He has a history of CTS as well, but never had any treatment. Reportedly, this was about 8 years ago and the symptoms had settled down until the above more recent issues started 2 yrs ago. Both the ulnar and Median NCS were normal. I saw only 2+ psw's and fibs in the FDI. I felt there were neurogenic MUAPs in the FDI, ADM as well as the APB and the pronator quadratus, so I was drawn to conclude that this was likely a C8/T1 radic as opposed to an ulnar neuropathy or CTS issue and likely chronic in nature given the history and the motor unit remodeling. However, the psw's/fibs in the FDI had amplitudes greater than 100 microvolts so I had difficulty convincing myself to use the term "chronic" as I would more readily with smaller amplitude potentials. I am struggling with how best to classify this. Could it be a resolving condition since there is only membrane instability distally. I was hesitant here without polyphasic MUAPs more proximally. In summary my question is: Is it old or chronic, or subacute or some kind of mixed thing? Or am I crazy to make an attempt at a diagnosis without more specific findings? For those interested, His MRI shows DDD causing severe foraminal stenosis at C4-5 on the contralateral side and severe bilateral foraminal stenosis bilaterally at C5-6 with slight retrolisthesis of C7 on T1 and no upper thoracic or spinal cord abnorms noted. Any comments welcome, Thanks!

We saw a cute little 5 month old Asian child today with a one week history of a rash. The rash has been present for about a week. Started on the back as a series of circles. The circles have not moved or grown on the back. Some later showed up on the neck and face and these seem to come and go. They do not seem to be itchy. They are not raised nor raised border. They blanch on pressure. Pressure on the childs skin shows dermatographism. No prior history of the same in this child or other family members. Family denies contact with metals, no coin rubbings, or suction cups. I asked another pediatrician of 50 + years on the job to take a look and it stumped him as well.

So, I admitted a patient last night --a 38 y.o. G3P1 with abdominopelvic pain, leukocytosis (WBC 21 with left shift), and h/o abnormal vaginal d/c and negative HCG. she's had constipation (x 4days), nausea/vomiting yesterday, but pain is really what brought her in. no fever. in monogamous, married relationship, and recent GC/CT cultures two days ago are negative. she was diagnosed with BV and started on an unknown medication. on exam, i thought she had guarding, some rebound, no CVA tenderness. +CMT, vag d/c and generally tender throughout pelvis. what's unique about her is that she clearly has a dirty U/A (but i've never seen a patient with her symptoms be solely attributed to cystitis), normal CT (including appendix/GI system), other than "fat stranding" in pelvis. her pelvic u/s showed "prominent ovaries/tubes" consisent with inflammation and suspicious for PID with scant free fluid, no obvious TOA, with normal blood flow to ovaries, and a mildly enlarged left ovary with what radiologists call a probable hemorrhagic cyst. The patient is on Yasmin and has no known history of STDs. General Surgery saw her prior to me being consulted in the ED and punted to Gyn. there are no other identifiable risk factors, and she has no significant medical/surgical history. She's was placed on broad spectrum antibiotics, including cefotetan, doxycycline, and metronidazole (given h/o BV), intermittent dilaudid last night. repeat labs showed continued leukocytosis. urine culture still pending. other labs include normal LFTs. i don't think she has pyelonephritis. We are going to have the General Surgeon follow with us, but I have concerns as to what time frame we should allow for improvement before doing a laparoscopy. She said her pain has improved a small bit, but on exam, she still has peritoneal signs. When would you reimage her? Give it at least 24 hours to watch closely with serial exams? Why has she had no fever despite significant WBC and left shift? (perhaps, it's inevitable...) I've had one atypical PID patient while a resident, of a woman in her 40's without risk factors for PID --with negative cultures and presumably a polymicrobial, ascending infection. Admittently, in my practice, i simply haven't seen much PID the last three years --maybe two cases... Any thoughts Gyn or Gen Surgery colleagues?

I have been a doc for over 20 years. The degradation in our profession has been outrageous. For instance... I get one sided non negotiable "contracts" from third party payers that don't even have a fee schedule--they say that their fee schedule is proprietary so I can't see it until after I sign the contract. After I sign it, get a "sample" fee schedule. For the fees not on the fee schedule, I have to wait and see what I get paid. The insurance company can announce changes to the contract when ever they want to, my only recourse is to quit taking their insurance. But I can't just stop seeing the patients or I become guilty of abandonment. The insurance companies have some idiot who could not make it in private practice called a medical director that they use to tell me I can't order a test, and yet I can be sued for not fighting hard enough with this idiot to get the test approved. We can be sued because our names are on the chart of a patient who had a bad outcome whether or not we contributed to that bad outcome. We are forced to pay to defend ourselves against a lawyer who has the right to "stir the pot" just in case he can find a reason to perform this legal form of extortion. If nothing is found, oh well, too bad for us. We don't have any way of getting back the time, money or mental anguish we paid for that defense. We are prohibited from selling products to our patients at a reasonable profit (such as vaccines), yet we are expected to eat the cost of the storage, handling, expiration, etc. Name another profession that is prevented from buying at wholesale and selling at retail to make a living? WHY JUST US??? THIS IS BULLSH_T! No other profession would put up with this crap. We keep putting up with this insanity so that patients don't get hurt. Well I have some sobering news for you...the patients don't give a rats ass about any of us. Oh sure, they say they love us, respect us, etc. But what are they doing to fight for us? Nothing. They have no incentive to fight for us. They bitch about their $10 copays because they feel they have already paid for their insurance, so why should they have to pay again. They want us to address multiple medical problems at the same time for the same price as if they had just one problem, yet expect us to assume the liability for all of their problems. They want us to excuse them from jury duty, justify their purchase of a hot tub for some BS medical excuse and get them out of paying for airline tickets because they want to change their plans. And we put up with this crap in the name of patient care. Now Sermo is sending out an open letter to the public. I strongly respect the content of the letter and the authors of the letter. On the other hand, the letter does not even suggest what we might do to solve the problem. I suspect that the lawyers and inurance companies will snicker and giggle when they read it, if they read it all. So what can we do? We can't negotiate as a group, that is illegal. Something called the Sherman Anti Trust Act of 1890--yeah it is 118 years old and we still live with it, makes it illegal for us to negotiate as a group. We can't negotiate as individuals, we have no power. We have been begging for relief in the name of patient care and we get nothing...in fact it is getting worse. Unfortunately we only have one weapon...we can boycott. We can stop negotiating with insurance companies. We can all choose to pick one evil insurance company and refuse to accept their contracts. If we all pick the same insurance company, they will go out of business. When they go out of business, we can choose another and do the same thing. If we can't pass laws to help us get tort reform, then we can stop providing care to PI lawyers, their families. their employees and their employees families. Make it highly undesirable to be associated with a med mal lawyer firm. When they can't get employees, they will find it undesirable to be in the business of suing doctors. I would rather see professional juries, made up of practicing physicians. Med mal cases would not take months, they would take hours. Bad docs would be out of business after being found negligent, good docs with bad outcomes would go back to work. I would like insurance companies to be forced to have their contracts, policies and behaviors be monitored by a board of practicing physicians that don't work for the insurance companies. Stupid policies and predatory behavior would be stopped instantly. Insurance companies would make reasonable profits, not insane profits. Patients would get the care they need. Docs would get paid more of those premiums. Administrative costs would go down for docs and insurance companies. But none of this will ever happen until we force the issue.

This is a girl that has been a mystery to me for the past few years: 6 year old female presented to ER after she complained of left elbow pain. There was no history of trauma. X-rays were normal and she was sent back to me for followup. Left elbow had full range of motion with some swelling. Serial repeat x-rays eventually showed maybe a healing small supracondylar fracture. She was never casted or splinted. Ortho saw her but discharged her without doing anything. A few months go by and her left arm is STILL larger than the other. There is a 2 cm difference in cirumference above and below the elbow. The compartments are soft, but the left arm definitely felt tighter and fuller. While waiting for an outpatient MRI, she presented to the ER for increased swelling of left (ipsilateral) side face, chest, and thigh swelling. ER did head, chest, and pelvic CT looking for compressing mass. All negatvie. Upper arm ultrasound did not show any clots. By the time she came to see me for follow up, I did not see any face asymmetry. Her arm was still the same, and maybe her pectoral muscle was more prominent. MRI of left arm finally done which showed non-specific edema. The radiologists recommended a MRA, which was also normal. My read of the literature was not all that revealing. Hemihypertrophy can be related to Wilms and other tumors. (She had normal CTs). She is a normal and bright girl otherwise who does not fit Proteus or Beckwith-Wiederman syndromes. I sent her to the geneticist recently. We are currently awaiting a nuclear medicine imaging of her lymphatics (lymphoscintography). Meanwhile, she continues to do well. I see her every few months for measurements and nothing else has changed. PMH/FH significant for mom with seizure disorder and borderline IQ. She seized a couple times in our clinic. 3 other older sisters all healthy. This girl is very bright. The only other health issue in the past were frequent UTIs which seems to have resolved. Renal ultrasounds and VCUGs were normal. Routine labs including CBC, Chemistry were all normal. Am I missing something? Am I making something out of nothing? One paper I read said up to 2 cm difference can be within normal. But she had edema on the MRI. Did this all happened after the "fracture" or was that just the event that made mom and me pay attention to the size difference?? What should I do if the lymphatic imaging is normal? I was think of another MRI, MRA since it's been almost 2 years.

I have a severely ill 52 yo M, who has severe aortic regurg s/p bacterial endocarditis, who now has VRE empyema. He has multiple comorbidities, many of which revolve around his heart and lungs: CHF leading to Pulmonary edema leading to severe dyspnea and repeated diuresis w. prerenal failure. He's also severely malnurished with an albumin of 1.4. He's been on some extreme antibiotic regimens for 2 wks now as well as having had multiple chest tubes w/ thrombolysis placed for drainage. On the most imaging he has large loculated effusions bilaterally, with apparent bronchopleural fistulas. I've looked into the articles and the reviews on this subject, and I really don't know what I can offer this guy anymore. His latest pleural tap is still positive for VRE and the 4th CT surgeon I consulted will not take him to the OR for decortication - siting that his surgical risk is too high. He's condition is declining despite maximum medical managment. Do I just let him die?

For over 15 years I have succeeded in curing chronic factitious ulcerations of the legs of over 30 MRDD patients. They have these lesions for years; often wearing bandages all their waking hours. Many have been to dermatologists who have temporarily helped them with topicals and/ or a course of antibiotics -- but it has always come back. Taking a clue from a local FP's treatment if infected lighting burn scars on both lower legs, I began putting these individuals on 250mg of Pen V K daily -- essentially for life. They all healed, though it took 3-5 months, and stopping the antibiotic always caused relapse. The picture shows a very bad case. If one zooms up in the area just above the top of the lesion, you will see reddened, areas around the skin pores, Rarely there is a bit of white purulent material. It seems that the skin bacteria -staph and/ or strep, have a tiny bit of virulence, produce some inflammatory responses, scratches the areas constantly ending with a chronic desquamated inflamed lesion. Bicillin and Keflex also work in very low doses. I have seen it several times in non-MRDD patients who have something wrong -- thrombophlebitis, Alzheimer's etc?. 1) Have you seen this before? 2) Is it a recognized syndrome or disease? 3 . How should this be named? -- an eczematous dermatitis, a chronic folliculitis? 4) should the antibiotic prophylaxis be in pulses instead of all the time. 0000000000000

Thinking back in my residency training, and my experience now, I believe I had several patients who were diagnosed as major depressive disorder recurrent but if I see them now I will think of them as bipolar disorder. There are several little subtle points which are not mentioned on the DSM-IV which play a role in the diagnosis. I wonder who would agree on the following points in bipolar diagnosis. Bipolar depression is chronic long-lasting depression, in pyknic physique patients. migraine headaches is so common in bipolar disorder. Anxiety symptoms is highly comorbid with bipolar depression, if patient with depression sufferers also from panic disorder consider bipolar disorder until proved otherwise (there was studies which indicated suicide rate is higher in panic disorder patients with comorbid depression) Family history of depression or "schizophrenia" which is usually misdiagnosis of a bipolar patient. The most important factor in diagnosis of bipolar disorder is a family history of mood symptoms. But plenty of the family members may be undiagnosed , so asking only about the history can be misleading but you need to inquire about the characters of the family including sudden job changes, womanizer men, gambling, sudden traveling. Moody with periods of cheerfulness and other times of isolation. also the artistic quality and creativity can be seen in the patient or his family. Drugs especially cocaine and marijuana are so common in bipolar disorder. Irritability and insomnia are more common in bipolar depression. Postpartum depression is usually bipolar episode Labile affect which can be confused with mood reactivity Bipolar I I patients are the most missed because they present mainly with irritable hypomania for short times less than two days. These are the patients who are in their 40s, depressed since they were teenagers, low functioning, been tried on all the antidepressants with temporary responding and then losing the response to medicine. And on several other antipsychotics and sleep aids medications. The interesting thing is I noticed patients who are misdiagnosed with major depressive disorder are treated with antidepressant and atypical antipsychotic like bipolar patients. So even misdiagnosed cases are treated correctly. this reminds me of the studies done in the 60s, inpatient units which indicated that lithium was augmenting the antidepressants effects for treatment of severe depression which I will not be surprised that these patients were mainly bipolar disorder patients who merely responded to the right treatment when they took it. The last thing which I would like to put for discussion is most of the patients we see in psychiatry are actually the difficult patients who failed treatment with primary care physicians. Major depressive disorder patients respond to average doses of antidepressants (fluoxetine 20 mg, paroxetine 20 mg, sertraline 50 mg) how many of you who are in community health centers see patients who are only on one antidepressant with this dose. Me personally I had 600 patients three of them were taking only one antidepressant with average dose.

Dear colleagues, A 25 year old medical student has been admitted under our care for recent fever and altered sensorium and CSF revealed turbid fluid that on microscopy shows a predominantly polymorphonuclear leucocytosis of 12,000. Gram stain is negative and CSF c/s are awaited. CT head shows diffuse brain swelling. He has been started empirically on Ceftriaxone 2g 12 hourly and Vancomycin 1g 12 hourly along with dexamethasone 8mg 8 hourly. His irritabilty and drowsiness persists after 24 hours of therapy although there are no more fever spikes. A repeat CSF is planned. In your experience how long do you find it takes for a patient of severe pyogenic meningitis to recover from altered sensorium? Please do share any other line of management that you may feel would help in this particular situation. (note: posted on behalf of Dr. Rakesh Biswas)

First post. Here goes. 52 yo man whose daughter was the nurse of a former partner. He has had GI "problems" for years suggestive of diverticulitis, with more difficulty the last year, but no documentation and no primary physician. A remote X-Lap in the mid 90's elsewhere for possibly a perforated small bowel requiring a small bowel resection and two week hospital course (no records). He had been having more difficulty evacuating and had a smaller caliber stool, as well as worsening crampy lower abdominal pain. He had been diagnosed with Hepatitis C by the Red Cross in 2000 as a blood donor and refused any treatment. In early March 2008 he had a HCV RNA by PCR, Qn Rfx Geno showing Hepatitis C Quantification of 1,074,530 with a genotype of 1a. I was asked to evaluate him with colonoscopy but could not advance the scope beyond the distal Sigmoid with a single diverticulum noted (I do about 450 endoscopies a year). An ACBE revealed "marked diverticular disease in the Sigmoid and Descending Colon with diffuse spasticity and areas that did not distend well and a malignant stricture could not be ruled out". CT of the abdomen -pelvis on 3/24/08 revealed "fluid around the gallbladder, suspicious for cholecystitis, mild nodular appearance of the liver suggestive of early cirrhosis and several small nodules in the mesentery, but none significantly enlarged and borderline splenomegaly. Marked diverticular disease of the Sigmoid colon with thickening of the wall probably secondary to diverticular disease, but a mass could not be excluded". His PHx is negative except that noted above. No history of upper or lower GI bleeding, specifically no history of bleeding varices, although no EGD. He takes no meds. Long history of > 1ppd and heavy alcohol intake, but no DT's or hospitalizations for complications from alcohol abuse. PE remarkable for a healed midline incision from xiphoid to pubis, non-distended, normal bowel sounds, mild lower abdomen tenderness, no mass and normal rectal exam other than hemorrhoids. Preop CXR normal and Lab with mild increase in hepatocellular enzymes (Alkphos-257, GOT-90, GPT-64) and Total bilirubin-2.96. WBC-7.0. Hct 41. Platelets 111,000. Electrolyes, BUN/Creatinine normal. I did not have a preop PT/INR, but the POD # 1 PR/INR was 20.3/1.6. I discussed options with the Pt and his daughter and I recommended a laparotomy for resection of the involved distal colon and possibly a cholecystectomy if the GB appeared grossly abnormal (no stones by US). He is now postop day #13 and after discussion with the family he has been made a DNR patient with comfort measures. Should I have done more preop work-up or consultation. I'm usually pretty quick to consult my Internist friends for medical problems, but I did not in this case.

78-y/o retiree with PMH of diabetes, hypertension, cataracts, and arthritis presented with new progressive b/l ptosis followed by an increased weakness of left hand. Denied respiratory or cardiac complaints but noted overall lack of energy. With presumed diagnosis of TIA CT without contrast was ordered. It showed no definite acute findings but several lacunar infarcts in the basal ganglia region bilaterally. Atrophy and periventricular white matter change was noted. There was a focal area of calvarial thinning, which was thought to be an incidental finding. Approximately one week later he presented for the follow up and at that time was complaining of episodes of nasal regurgitation and difficulty swallowing liquids. He also sounded somewhat nasal although without slurring. He did not complain of any sensory deficits. At that time patient was admitted to r/o stroke. EKG was normal. Carotid study was not done. Neurologist was consulted and raised the question of myasthenia gravis…He requested radiology of the chest to r/o thymoma and thought that fatigue and weakness was a result of respiratory muscle involvement...Spirometry was ordered and came back normal…As to left hand weakness he suggested it is the result of entrapment neuropathies…He specifically stated that he suspects myasthenia gravis but not stroke, TIA or Eaton-Lambert's. Is it impossible for the presentation to be a progression of lacunar infarct in basal ganglia? Something like suprabulbar palsy? I am obviously not a neurologist but I was under impression MG would reveal itself for the first time earlier in this man's life and not when he is 78… All of the above symptoms are rather new. Am I wrong? I would appreciate your opinion. Patient medications include atenolol, lisinopril, fish oil, glyburide, aspirin,hydrochlorothiazide.

Saw a 23 year old hispanic male yesterday who had a left mastectomy and liposuction at age 18 for unilateral gynecomastia. He comes in yesterday stating that the left breast has started to grow again in the last 4 months. He has not had any discharge from the breasts. Reviewing his old records, there was never a single lab test done on him. He was sent to plastics from his old PCP who just went ahead and performed the surgery. A pathology report was negative. He is not overweight. He denies any use of drugs, steroids, supplements, etc. His physical exam is normal except that his left breast is definitely enlarged, soft, no discrete masses felt. His right breast actually seems slightly larger than it should be based on his body habitus. A prolactin drawn at yesterday's visit returned at 52. This patient does not have any health insurance. What do you think would be the best cost effective step to take next?

Hi, Case I am actively seeing: 28 y/o white female with no PMHx had diarrheal illness 1 month ago. That was followed by URI about 3 weeks ago. She presented to the ER 2 days ago for new onset of brown/red urine. She is having intermittent abdominal pain. No skin rash, no joint pain, no fever. Data: cr. 1.8 on admission and up to 2.7 24 hours later (baseline is 0.8). u/a: large blood, 10-20 rbc's, 500+ protein. I looked at the urine - lots of muddy brown casts, a few epithelial cell casts, but no obvious or suggestive RBC casts. LDH is > 1000. Haptoglobin is low. Hgb is 5.5. Spleen is 15 cm in size. Renal ultrasound is completely normal. Heme x 2 reports no schistocytes on peripheral smear. Vitals are normal - SBP around 115. What do you think the diagnosis is? If it is HUS/TTP, why no schistocytes and (likely) above normal proteinuria. If it is a glomerular disease, why is there hemolysis? complements, ASO, anca, antigbm are pending. Would you biopsy? Would you start steroids now? Thanks!

The time has come for physicians to come together and lead a new wave of healthcare reform. The current healthcare system is strained and unsustainable. Our patients' wellbeing and the dignity of our profession are at stake. The physician community has found a powerful voice on Sermo and we can use this platform to speak with consensus and act in unity. On Sermo, the physician community has been able to start formulating strategies to refocus our misdirected healthcare system for optimal patient care. The first product of this effort is the launch of an open letter to the American public, outlining the challenges we face in delivering appropriate care. This letter also gives us the opportunity to declare our full commitment to our patients. What began with the idea of drafting a single letter has now grown into a movement that is unifying and giving voice to thousands of physicians. The "Open Letter from America's Physicians" is the culmination of months of polling, discussions, and draft revisions on Sermo, involving the active participation of over a thousand physicians. We must now drive our colleagues to sign the letter to show the strength and scope of our unity to policy makers and the public. Sermo has pledged support to distribute the signed letter broadly via the Internet, national newspapers, and downloadable materials that we can share with our patients. These strategies will give us national visibility and generate significant media attention for our efforts. We have finally been given a real opportunity to speak and act as one. There is power in our unity. We can build on this experience and create a viable mechanism for establishing a new paradigm that acknowledges the value of physician autonomy and patient-centered health care delivery, free from the intrusion of special interests and political motives. ................................ An Open Letter from America's Physicians Dear Fellow Americans, For decades the United States has led the world in healthcare. We have enjoyed the finest hospitals, medical schools, research, technology, and resources. Unfortunately, our healthcare system has lost focus to the point where patient wellbeing is placed after politics, profits, and special interests. Healthcare costs are on the rise and patients have lost their freedom of choice. These trends are hurting our economy and compromising the doctor-patient relationship. As a result, it has become difficult for physicians to deliver the best possible care. Our heavily fragmented healthcare system has made it very difficult for you, the American public, to get the care you need. As your physicians, we want to partner with you to address the critical defects of the system as outlined below: * You are paying a lot for healthcare and not receiving enough in return. Your insurance premiums continue to increase while your healthcare options are dwindling. Gatekeepers, insurance networks, and restrictive regulations limit your choice of doctors and your access to care. * You have been made dependent on complicated and expensive health insurance plans. Employers are forced to take money out of your paycheck to purchase health coverage. If you lose your job, you are left with no safety net and the money you have paid for health coverage vanishes. * The time you spend with your physician has become remarkably brief due to regulatory hurdles requiring doctors to spend more time on documentation than with you. We believe the following factors have made our current healthcare system unsustainable: * The insurance industry's undue authority and oppressive control over healthcare processes * Excessive and misguided government regulation * The practice of defensive medicine in response to a harmful and costly legal environment We, the physicians of the United States, will no longer remain silent. We will not tolerate a healthcare system where those without medical expertise or genuine interest in our patients' health have absolute control. This letter is merely a summary of the most important problems in our current system. We believe that by partnering with the public we can start to demand real change and formulate practical solutions. We invite you, our patients, friends, neighbors, and employers to unite with us at this important time in the history of healthcare in the United States. Together, we can guarantee our nation a healthier tomorrow. Please talk to your doctor about this letter and visit http://www.sermo.com/doctor... for more information. Respectfully, The Undersigned U.S. Physicians ................................ What can you do? SIGN the letter here through your vote and add your voice to this nationwide call to patients. SEND emails to colleagues and encourage them to sign. Better yet, forward this posting through "Send to Colleague". SHARE the attached flyer with colleagues. Place it in mailboxes or post it in locations that will be seen by other physicians.

Interesting case. 64 year old lady with a rapid onset a few months ago of an enlargening right breast mass. She saw a different surgeon initially who rushed her to the OR for a rather disfiguring partial mastectomy (with the incision extending far into the axilla). Pathology demonstrated high grade myofibrosarcoma (6x12cm) with multiple areas of necrosis. Margins less than 1mm in several areas. Mammography and US show three separate lesions on the contralateral breast. The other surgeon performed FNA on the two palpable ones and path came back as "spindle cells". She isn't happy with the primary surgeon and came to me as a second opinion. Given the size and grade, certainly mastectomy is warranted for the right side. The left side has me troubled though. MRI has been ordered. I did a repeat core biopsy on the two left sided palpable lesions. Path pending. Ultimately, does it seem likely that bilateral mastectomy would be best?

I need a little Sermo help for this strange huge rash. Patient is mid 40's and states since her teen years every few months she would get large strange shaped rashes on her torso and arms that last for a day or so then goes away and does not itch. Denies any relation to food or drink, and also doesn't change detergents/soaps etc. It's hard to see the picture but there is a large outline erythematous rash, easily blanchable with no scale. There are little circles within the rash. The patient also denies any contact with limes and says no one touched her in the area of the rash for dermatographism. She said sometimes it seems to come out after sun exposure, but very infrequently. We are curious what this could be, any ideas would be great, thanks.

We've all reviewed the literature. Renal artery stenosis is common among the elderly. Surgical bypass of the renal artery is not much advocated these days, but renal artery angioplasy is a growth industry, abetted by a collusion of interventional radiologists, vascular surgeons and interventional cardiologists who construe the renal artery to be fallow, but lucrative, soil for intervention. There is only this question: Does renal artery angioplasty cure, or even ameliorate, hypertension? (I leave aside the more difficult question as to whether renal artery angioplasty preserves, or ameliorates, GFR). Undoubtedly, angioplasty of the renal artery yields a lovely radiologic image. But what does it do for blood pressure?

I'm treating a patient in his mid-50s with baseline hyperlipidemia (elevated: TG, VLDL, LDL, total cholesterol, low HDL.) He's responded well to high dose statins (fenofibrate 145 mg qd, simvastatin 40 mg bid), niacin (1 gm po qd)and lovaza (4 gm po qd). He can't exercise because of an open venous stasis ulcer and compression fx of T12 and L1. On meds, LDL, VLDL, TG and total choesterol are under excellent control but still low HDL. Additionally, his cardiac CRP and homocysteine levels are elevated in spite of high dose statins and folate supplementation. Cardiac risk factors: former smoker- 30 pk/yrs, quit 2 years ago. Formerly obese (+ metabolic syndrome), lost 45 pounds and is now close to ideal body weight with BMI in the upper 20s). No HTN, no DM, no significant family hx of early CVD. Recovering alcoholic (10+ years sober). Suggestions to increase HDL and decrease cardiac CRP and homocysteine levels?

65 yr old well controlled DM with OSA presents with 2 months recent memory loss, truncal ataxia, personality change (apathy, outbursts of anger) and myoclonus. He has recently discovered thrombocytopenia, etiology presumed to be splenomegaly and "incidentally" diagnosed portal hypertension without liver synthetic or transaminase anomolies and no thrombosis of the portal or hepatic vein. On PE, afebrile, normal BP P and sat. Myoclonic jerks upper extremity. No nystagmus. Alert, Affect is agitated. Attends infrequently to commands. Otherwise no findings He has not eaten in days and has to be reminded to urinate but is continent. Ammonia is normal. LFT, BUN, Cr normal. PLT stable at 120, Htct 49, WBC 8 normal diff. INR albumin, bili normal.

I have this 72 year old patient who I started seeing earlier this year, inherited from a colleague who left the practice. Has had abnormal mammogram, USG and MRI of breast. i recommened biopsy, initially refused, later agreed to go after I saw her in the clinic and explained the possible consequences of not intervening to her, referral done but she refused to take the reminder call the day before appt from the surgeon's office. I have had my office manager call her, have had 2 nurses call, she doesn't want to have anything to do with my office or me which is ok with me. Now let me explain another side of the story, she has been on meds including Darvocet for 'chronic shoulder spasms for years' - will not tell me exactly how she is taking it, Xanax - 1mg tid (doesn't want to talk about SSRIs), and soma, all these medications high addiction potential. When I asked her to sign a medication management contract, she refused and walked out of my office raising hell, asking the receptionist to make copies of her records so she can transfer her care to another provider. It is besides the point the support I get from my office manager, I took this patient's chart to her telling her never to schedule the patient with me again after she walked out of the office last time. Her response was that she is going to call the patient, make sure she got what she needed ( records & all ) and see if she wants to see another provider in my clinic ( rest of which is all NPs). My question here is of course she has a good chance of having breast cancer give all those abnormal studies, have I done enough to not be blamed of that. I have made appropriate referral, reminder calls, sat down with her and talked the consequences with her. is this enough ?

I had a 23 year old caucasian female present as a new patient yesterday complaining of some anxiety symptoms, but she said the main reason she had come was at her FP's request to get "cleared" to be given ultram. She had a history of heroin and cocaine abuse from the age of 15 but had been clean for at least the last year. She tried and did not like NA but is heavily involved in her Church. She had a spinal fusion for scoliosis when she was 15 and had two rods placed, and she said that over the last few months pain from the site where the rods had been inserted had gotten somewhat worse. She denied any neurologic symptoms. She has had some significant psychosocial stressors recently. When I queried the referring doctor as to how we could help her she said that she did not feel comfortable prescribing ultram to a patient with a history of substance abuse but was willing to do so if and only if the patient was being followed by a psychiatrist on a regular basis who could "screen her to see if she was resuming a chemical dependency cycle" at any point. The patient called the FP's office yesterday after the appointment requesting to know the status of her rx request and the FP's office forwarded the message to me, where it's still sitting on my computer desktop. Has anyone dealt with a similar situation before?

The following case is part of the Sermo Case Conference Series. This case will unfold over several days - feel free to ask for additional data, test results, or supporting materials you think would be most appropriate. The patient is a 42 -year-old Caucasian female with history of HIV, presents with right breast swelling. She started to notice right breast tenderness and swelling 10 days ago, but decided to seek medical attention after her right breast almost doubled in size within one week. PAST MEDICAL HISTORY: HIV for 5 years. She has been followed at HIV Clinic for HAART. PAST SURGICAL HISTORY: None. MEDICATIONS: Atripla once a day. SOCIAL HISTORY: The patient reports smoking marijuana. She otherwise denies any illicit drugs, smoking and alcohol use. FAMILY HISTORY: Her mother died of Breast cancer at the age of 78. Father is healthy. REVIEW OF SYSTEMS: She denies any trauma to the breast; no rashes, no ulcers; no furuncles, carbuncles. This swelling started spontaneously and was progressively getting worse. The patient denies any fevers, chills, nausea, vomiting, diarrhea, abdominal pain, chest pain, shortness of breath, bright red blood per rectum, hematochezia or any other symptoms. She also denies headaches or any neck stiffness or any neurological changes. PHYSICAL EXAMINATION: BREASTS: Right breast enlarged, swollen and erythematous, almost twice as big as the left breast. Very firm and tender on palpation. The swelling and the firmness occupy about 15 cm around the nipple area with no active discharge. Left breast has tenderness on palpation around the left nipple; otherwise normal. There are shotty lymph nodes in right axilla. No lymphadenopathy in the neck or inguinal area. LUNGS: Clear bilaterally to auscultation. CARDIOVASCULAR: No murmurs, rubs or gallops. ABDOMEN: Soft, nontender, nondistended. Normal bowel sounds and no hepato-spleenomegaly.

Is it necessary to load patients with Dilantin after a one time seizure, with a normal metabolic workup? Is there a concern for possible suppression of abnormal brain activity with use of Dilantin on EEG, for evaluating these first time seizures? Not to mention the toxicity of the meds to the patient, some CMDT states that the recurrence of another seizure within 1 year is only 40%. I did have one patient in the ED that had a seizure was brought in then had another seizure an hour and a half later. Is that a common occurene, or an unusual circumstance?

I an one of the two medical directors at a large SNF. I was recently asked to take over care for a long term resident who had a brainstem infarct 2 years ago that left the patient unable to speak and swallow. The patient now has contractions and a healing bed soar. She is only responsive to painful stimuli. When this patient had her CVA she was given a poor prognosis of recovery. It was recommended that she be made DNR. The patients husband refused in spite of the patient having a living will. The attending physician at that time proceeded to have a PEG tube placed at the husbands request. The patients children (from her first marriage) did not want heroic measures and wanted the living will to be enforced. The attending of record at that time did not deem the patient to be terminal and did not enforce the living will. There is not record that the patient herself at that time indicated one way or the other what her treatment should be. The patient was discharged from the hospital to the SNF where her care has been taken over by another physician. She has been there for the last 2 years. Two weeks ago the patients husband died of some illness. In his will, he has relinquished the POA of this patient to a non family member conservator (lawyer). The patients children contacted the SNF and requested the patients care be changed to me since the attending of record refuses to stop the tube feeding. The POA authorized the change. An ethics consult was asked for by the POA. The end results of the ethics consult was the tube feeding should be discontinued and the patient should be placed on hospice since this would be following the last documented patients wishes. I agree with that treatment plan as does the family. At this facility, a signature by the POA is required to change the code status of the patient. This patient is currently full code. Though the POA agrees with the plan, he refuses to sign the DNR without this matter being presented in court and having a judge sign off on it. I told the lawyer that I believed that this is necessary only if the patient had not expressed their preferences in advance. In this case the patient has a current living will. He disagrees and he requests the patient be a full code until the issue is resolved. I do believe that I could discontinue the tube feeds now, since I have a living will and the patient does have a terminal irreversible state, but I will not because it would need to get my own lawyer and it would cost me. It would go to the state board and who knows what they will say. BUT what do I do in the next 6-8 months for this issue to be worked out in the courts if this patient decompensates and needs to be sent to the hospital?

I'm treating a patient in his mid-50s with baseline hyperlipidemia (elevated: TG, VLDL, LDL, total cholesterol, low HDL.) He's responded well to high dose statins (fenofibrate 145 mg qd, simvastatin 40 mg bid), niacin (1 gm po qd)and lovaza (4 gm po qd). He can't exercise because of an open venous stasis ulcer and compression fx of T12 and L1. On meds, LDL, VLDL, TG and total choesterol are under excellent control but still low HDL. Additionally, his cardiac CRP and homocysteine levels are elevated in spite of high dose statins and folate supplementation. Cardiac risk factors: former smoker- 30 pk/yrs, quit 2 years ago. Formerly obese (+ metabolic syndrome), lost 45 pounds and is now close to ideal body weight with BMI in the upper 20s). No HTN, no DM, no significant family hx of early CVD. Recovering alcoholic (10+ years sober). Suggestions to increase HDL and decrease cardiac CRP and homocysteine levels?

i treat a 42 y.o. bipolar male with earlier (13 years ago) history of significant alcohol, heroine, cocaine usage. he reported paranoid hallucinations during usage -- specifically, hearing sounds and voices in his house with concern about being threatened by police or intruders. he has been sober for 13 years, active in AA -- sponsors two, non-psychotic now. Yet he continues frequently to experience same disturbing hallucination at home alone at night only which occur both when manic as well as depressed as well as euthymic. Has severe sleep apnea/uses cpap. Meds include Depakote 500, Lithium 300, Zonegran 400, Lunesta 2 mg, Rozerem 8 mg, Seroquel 200 mg. Has any one else seen persistence of this heroine/cocaine-related hallucinating long after ceasing usage?

This is a case I was curbsided on. 29 year old G1 P0 with no other medical problems presented 2 months ago with pelvic pain, irregular periods. Got an U/S showing right ovarian cyst with homogenous internal echoes and increased peripheral doppler signal with possible through transmission, 2.5 cm in greatest diameter. Repeat U/S 1 wk ago shows 11 wk singleton pregnancy, ovarian cyst unchanged. CA 125 was 211 (not sure when it was drawn). Pt has no personal or family hx that suggests increased risk for ovarian cancer. I found a case series that shows CA 125 typically is elevated in pregnancy to around 30-40, but apparently at least one normal patient with a CA125 of 250 in the first trimester. Generally the 2nd trimester levels were lower. There is a repeat level from this week pending. Pt was given the option by her primary OB to have cyst removed at 15-16 wk range, but no later. The pregnancy is desired.

7 year old previously healthy female presents to the Pediatric ER with 1 week history of productive cough, fever (Tm104), and chest discomfort. Patient had visited another ER 3 days before where an Chest Xray revealed a Pneumonia for which she was prescribed Azithromycin. Past Medical History, Allergies, Medications all negative. Immunizations up to date. Family History significant for WPW syndrome (Father). Physical Exam revealed: Temp 103, normal RR, BP and O2 sats. HEENT negative. Heart: 3/6 Harsh Holosystolic murmur, loudest along the entire left sternal border and apex, noticeably louder on sitting and squatting positions. Lungs Clear. Abdomen normal with no hepatosplenomegaly. Neuro normal. Pulses Normal. Derm Normal. Initial Investigation: CBC normal, Chem normal, LFT normal, LDH elevated (337), CRP Elevated (3.48), TSH normal. CXR: Enlarged cardiomegaly, prominent left atrium and left ventricle. EKG: Consistent with Left atrial and left ventricular hypertrophy, normal QTc., UA-15-25 WBC Pending Tests: ASO titers, Bartonella Titers, Blood and Urine Cultures, 2D-Echo

I would really appreciate your input on this challenging patient. Very pleasant 70 yo woman was referred to me by her gynecologist for "leg pain." Turns out there's more to the story... Just to set the scene, she can't read, can't write, doesn't trust doctors and is afraid of medicine. The patient was hospitalized in February with vaginal and rectal bleeding which required blood transfusion. She had an endometrial biopsy which showed benign hyperplasia. She refused colonoscopy. Her current complaints are of weight loss, abdominal pain, brown vaginal discharge, and calf pain when walking to the mailbox. Her labs included WBC 12.1 and elevated ESR of 31. Urine cx grew E coli which I treated. She reluctantly agreed to a CT abdomen/pelvis which showed: 1. elongation and tortuosity of the colon and cecal redundancy 2. cecum, ascending, transverse and part of descending colon dilated 3. sigmoid and rectum not distended 4. 7cm parapelvic cyst of the left kidney (she had a 6cm cyst in 4/2006) Any suggestions regarding workup, treatment? She's refusing barium enema or scope.

This question was asked about 9 months ago for a very low risk patient, but I would like to ask it again for a higher risk patient. I have a 30 yo wf Type 1 Diabetic patient, hx of Type 1 diabetes for about 5 years. She smokes 1 ppd, she is about 25 pounds overweight (she was grossly underweight prior to her dx of JOD). She has a family hx of ASHD. Her Total Cholesterol is only 167, but her LDL direct is about 110. Her HgbA1C is about 7.3 on an insulin pump. With her risk factors, ie smoking, type 1 diabetes, family history, overweight, would you put her on a statin to try to get her LDL under 70? My concern is that over the long run, she is going to have an event. I have tried to get her to quit smoking without success....she won't quit because when she tries she gains more weight. She won't even try until she loses 30 pounds and that does not look like it is going to happen. Her endocrinologist is strongly objecting to the of a statin....he says it is too risky and unnecessary. What would you do if this patient were your daughter?

Patient had labor epidural one week ago. The day after delivery she described subjective weakness of left leg, and numbness. On evaluation she had decreased touch/temp sensation of entire left leg. Patellar reflex present but diminished. I could discern no motor deficit. Voiding normally. No back pain. I reassured her and told her to let me know if things got worse or did not get better. Today she had her one week follow-up, and the left leg is still numb. Numbness is circumferential, and goes from about mid-thigh to mid-calf. Patellar reflex is still diminished. No subjective or objective weakness. No back pain. She is not terribly concerned, but I'm starting to be... Would you refer this woman for a neurologic evaluation?

Today, I saw a 31 y.o. woman with a recent diagnosis of left breast cancer, just had her first dose of chemotherapy 3 days ago, came in because of fever to 100.9 and nausea/vomiting. She had swelling, warmth, and erythema to her left breast with an ultrasound demonstrating likely abscess. WBC is 34K, other labs normal, vitals normal. Our on call surgeon says, "This is not a life-threatening issue. She does not need to be admitted. Give her pain medications and antibiotics and discharge her and tell her to follow up with her primary doctor or surgeon in the morning." I'm now trying our internist to see if maybe he can admit for IV antibiotics and to have IR drain the abscess under U/S guidance. I figure draining it myself and potentially spilling or seeding cancerous cells in different areas is clearly not the thing to do. She meets septic criteria and there's no way in hell that I'm going to discharge her. I really think it's my surgeon that should handle it. What about you?

Give me input please--just saw this lady with Type 1 Dm who has been on NPH 15 in am and regular unclear doses. Came to hospital after fall and "hypoglycemia" Has known hypothyroid. On synthroid 112. TSH in 1/08 was .25. TSH now 96. In hospital getting a fairly standard SSI and NPH 15 am and D5 at 100 cc/hr had lab glucose of 33-but was asx per nurse. Then during the day is over 300 at lunch and dinner dinner then 200 range by bedtime. I stopped the NPH last dose 48 hours ago, give Lantus 15 at night-started last night and order novolog with meals to start today-has not happened yet. Today glucose on 0500 labs is 28! Again per nurse aymptomatic. I think it is related to profound hypothyroid-which is a cause of hypoglycemia. Question-why is she asymtomatic? Why only low in am even if no insulin given in >12 hours on D5 in a Type 1 diabetic. I am stopping the D5 the hospitalist started. I plan on calling her pharmacy when it opens to find out what happened with her synthroid since January.

I have a 10 year-old girl in my practice who has history of complex partial seizures, and also rather severe ongoing ge reflux. Growth and development have been normal, but she has always struggled at school with visual problems and some learning difficulty, mild social skills issues. Ophthalmology felt no muscle weakness problems. She has had deterioration in her behaviors over past few months, and presented with pseudoseizures that were quite refractory to treatment for a few months. She was on Depakote already, but moods were fluctuating and behavior worse so I placed her on Prozac also. This helped a little but still a lot of violent outbursts and behavior problems. She saw peds psychiatry and was put on Risperdal. This improved her behavior but she seemed to have increased tremor and more pseudoseizures. I consulted a new neurologist and he felt very likely Asperger's ( I had never entertained this dx and this was confirmed by psychology a week later). She got to point of being physically violent and mom couldn't control her anymore, and had inpatient psychiatry admission. She has been unable to attend school, her behavior is very hard to predict but tends toward mainly negative and agressive. Her moods don't fluctuate enough to suggest bipolar, but it has been a possible differential diagnosis. This child has hoped that a day treatment program wil help her, but it has been weeks to get her in, and she is getting discouraged. Mom is concerned that the program may use a lot of punitive discipline which might backfire given her autistic diagnosis. Mom wonders if the program would be good for her dx, as the center hasn't had a great deal of autistic children in it, and mom's insurance has limited coverage for all of this, so she doesn't want to have her enter a program that will lead to inpatient if she doesn't behave. Mom is wondering if anxiety issues are causing her to become agressive, as her daughetr is very unhappy and unsure of her behaviors, feeling she will lose control. The parents are recently divorced and there may be some stressors related to that, but I do feel mom has tried to follow through with the behavior program counseling outlined and nothing has worked so far. I am at a loss as every day there is some new problem mom has had to deal with and she is getting exhausted. My questions are several-fold, but my main question is has anyone ever had a patient with autism present in crisis such as this, with recent dx of autism, and what has the experience been with getting needed services promptly. I am also interested in whether anxiety or panic can present with agression like this, in autistic children.

Settle a debate between my partner and I. A lady recently came in through ER with complaints of pain and drainage from a midline incision. Three weeks prior, she had had an open ventral hernia repair with mesh at some hospital in North Carolina. She also has a history of multiple cutaneous infections with MRSA. A CT in the ER showed a large fluid collection abobe the fascia/mesh but no air bubbles. On exam, her abdominal wall was erythematous, warm, and tender around the entire length of the incision. The wound had epithelialized but there were a couple of pinpoint openings in the skin draining serous, foul smelling fluid. Her WBC was 16k. She had low grade fevers and appeared pretty ill. She was started on Vancomycin and brought to the OR by my partner. The wound was opened and a large amount of murky fluid was evacuated and cultured (grew out MRSA). He says that the mesh (composix, he thought)appeared to be well incorporated into the fascia and excising it would have required a major abdominal wall whack. So he left it in, lavaged the bed, and placed a wound VAC. I was puzzled. MRSA and infected, exposed mesh.... does this plan of his have any chance of working? I saw her today and there seems to be a wider area of erythematous skin and tenderness around the VAC apparatus. Is this a set-up for fasciitis? Should I more strongly push that he slices the damn thing out? Or is it reasonable to continue vanco/VAC for a few days to see if she improves?

AB is a 64 year old white male who just started seeing me for the last month or so. Came in on 5 antihypertensive medications (diltiazem 240 mg qhs, hctz 25 mg qd, terazosin 10 mg qhs, losartan 100 mg qd, and labetolol 200 mg qd) and STILL had BP 154/74. After looking through his old records, I ordered 24 urine for cat/met and MRA of renal arteries. All normal. Then ordered plasma renin activity and aldosterone: PRA was 0.3, aldosterone 4 (presumably sitting, at 8 a.m.), for ratio of 13.3. He was diagnosed with DM2, but has A1C of 6.6% with MNT only. Dyslipidemic with TC 165, LDL 104, HDL 38, triglycerides 129, and Lp(a) of 1 on lovastatin 80 mg qd. I just got results back from ambulatory blood pressure monitoring... yes, his pressure is consistently high (daytime average 162/83, noc 165/79 mmHg). So... if PRA is already lower, would aliskiren do anything? He's already on a centrally acting alpha blocker... would adding peripherally acting alpha blocker (clonidine) do anything? Suggestions...?

I hate to post two cases back to back, but that's how it goies sometimes. 68 year old diabetic/PVD male presented with septicemia (WBC 28k, hypotension). He had a perianal abscess drained in the ER which grew out MSSA. 12 hours later I was called to evaluate. He had ecchymotic skin changes and crepitus of his perineum and he was still septic and shocky. I took him emergently to the OR and ended up essentially debriding literally pounds of dead flesh from his buttocks, perineum and genitalia. Basically he had a giant horseshoe abscess that tracked through the tissue planes. One of the worst cases I've seen. I had to remove a testicle and decided to divert stool with a loop sigmoid colostomy. Currently he's doing ok. Off pressors. Extubated. Tube feeds at goal. Question: His wound care now is wet to dry kerlix gauze twice a day. I had a plastic surgeon take a look but he said he wouldn't do anything until things have a chance to granulate a bit. This is a gruesomely large wound. No chance for a wound VAC. Any ideas on coverage? Whirl pools? Send to tertiary care center?