Postings for April 2008
I have a patient with remote history of grand-mal seizures, last was 5 years ago. 3 days ago she had another seizure after 4 days of ciprofloxacin for a UTI. She was on Tegretol when she was treated (5 years ago) without complications from Tegretol.
What would you do at this point? Put her back on Tegretol? Simply avoid Cipro and observe? Put her on something else?
Thanks for your time and feedback. I am a family practice doc, and can't reach my neurologist....he's on vacation in Napa Valley.
I hate to overtreat my head and neck patients, so I would appreciate your opinion, here.
56 yo former smoker (quit over 20 years ago) but still dips tobacco, who presented with an advanced cancer of the right posterior, lower gumline. The tumor was about 3cm, but invaded the lower mandible.
His post-op result was good, and they were able to reconstruct his R lower mandible with hardware. He expects to be fitted with dentures later and is able to eat soft foods, now. No PEG, so far ...
He has been otherwise healthy, works full time and has had no weight loss. Only drinks alcoholic beverages rarely (and I believe him!). No significant medical history.
Physical exam and later PET scan reveal no other worrisome findings.
The tumor was resected en bloc and final path was of a T4 (bone invasion) N0 (0/25 nodes). Only concern were close margins - 0.2cm but no frankly (+) margins.
He will definitely receive post-op radiation therapy. The question is, should he receive combined modality therapy - ie chemo & XRT? Cetuximab??
If you would add systemic therapy, which regimen?
Please add your votes to the right --->
Thanks!
I had a patient last week, a 2 year old with a bad RML pneumonia and an effusion to ~25% of the R lung field. The decision was made not to drain the effusion and to watchfully wait as, at this particular hospital (not my usual home institution) they cannot manage chest tubes on the floor and so the patient would have been transferred. She improved (white count from 30 down to 18 and no more fevers) without drainage on ceftriaxone and clindamycin, but on hospital day 5 spiked new fevers, bumped her white count, and an x-ray now showed an effusion to 75-80% of the R lung. Throughout this time she was not overly tachypneic and had a very minimal intermittent O2 requirement (blow-by mostly). Needless to say, at that point we transferred her for drainage, likely via a VATS, at a nearby institution.
Have any of you had similar situations and if so, how have you managed them? Should we have transferred her for drainage sooner, despite her initial improvement? How do you manage children with parapneumonic effusions?
According to a recently published nested case control study from the Netherlands antipsychotic use among elderly patients was associated with an almost 60% increase in the risk of pneumonia (adjusted OR=1.6, 95% CI=1.3-2.1). The risk was highest during the first week after initiation of an antipsychotic (adjusted OR=4.5, 95% CI=2.8-7.3). Current users of atypical agents showed a higher risk of pneumonia (adjusted OR=3.1, 95% CI=1.9-5.1) than users of conventional agents (adjusted OR=1.5, 95% CI=1.2-1.9). There was no clear dose-response relationship.
Here is the link to the abstract
Wilma Knol MD, Rob J. van Marum MD, PhD, Paul A. F. Jansen MD, PhD, Patrick C. Souverein PhD, Alfred F. A. M. Schobben PharmD, PhD, Antoine C. G. Egberts PharmD, PhD (2008) Antipsychotic Drug Use and Risk of Pneumonia in Elderly People
Journal of the American Geriatrics Society 56 (4) , 661-666 doi:10.1111/j.1532-5415.2007.01625.x
http://www.blackwell-synerg...
Do you agree that antipsychotics may possibly increase the risk of pneumonia among the elderly?
I've been a Sermo member for several months but I haven't posted before. The patient I'm discussing is aware that I'm posting her information because after several specialists, we have no good answers.
The Mrs. N.C. is a 52 yo Caucasion female that I've been seeing for about 7 months (I assumed her care when I joined the practice). For the past 3-4 years, she's been suffering from spastic muscles as well as severe tremors. Her symptoms initially started in the left hand and eventually involved both the left and right hand. The hand tremor was initially at rest, but eventually progressed to being both a resting and intentional tremor. She also had "twitching" of larger muscles in the arms and legs that eventually involved to complete inability to control her left thigh and leg muscles. Around the same time she initially presented to a neurologists, she developed a rash on her legs and had occasional short term memory loss. Since her initial symptoms, the "twitching" that occurred in her left thigh and leg has evolved into a foot drop, she has lost enough of her motor skills that she is no longer working. For the past year, she has developed ocular symptoms in both eyes which were described as blepherospasms and inability to completely open the eye.
Her other past history includes Meniere's disease, Celiac Disease, Diabetes, Hypertension and migraine headaches. Because of the rash she had at presentation, she was diagnosed with Discoid Lupus.
Her relevant lab and diagnostic studies include negative MRI's (brain and spine), positive ANA (titer 1:1080); a skin biopsy done on her initial rash showed discoid lupus; she had a muscle biopsy done during her intial presentation that showed perfasciular inflammation; ESR and CRP are usually elevated.
She has seen several neurologists. There has been some thought that her worsening symtpoms were possible psychogenic (malingering) and the patient is a registered nurse. I sent her to a psychiatrists, who believes she is not malingering. I also sent her to a rheumatologists.
Her twitching and spasciticy improved with prednisone; She was treated with immunoglobulin with no response. SHe also recieved methotrexate with no response.
Most recently, the spasticity has involved her arms, legs, abdominal muscles, and likely her perianal area (she is now fecally incontinent). Her blepherospasms don't allow her to open her eyes completely, and she is now using a cane because of foot drop on the left.
Any ideas would be much appreciated. Needless to say, this poor woman is suffering. Thank you.
I've had two patients in the past 6 months with what appeared at first to me rather mild midfoot injuries. After not improving for a month or so in a boot and with limited weightbearing I obtained an MRI. Both showed the cuboid lighting up like a christmas tree but no other ligament injuries. I treated them as presumed fx with a month or so of casting followed by boots. After 3 months I tried a bone stimulator too. I wound up sending both out for second opinions to "foot experts" but have really not been sure why these are so slow to heal. I even sent the one for a block in case RSD was part of the picture....no luck. Lidocaine patches help a little. Any ideas????
[Click here for information on this opportunity.]
Don't show me this again
37 y.o. very obese female with 15 year history of prolactin secreting pituitary adenoma treated until 2007 with bromocriptine. Had transphenoidal debulking in 10/2007. Postop MRI showed residual 2.5x1.5 cm mass invading left cavernous sinus and clivus. Referred for postoperative XRT, Treated 1/2008 with IMRT to 50.4 Gy. /28 fractions. (1.8 Gy. daily) Had recurrent MRSA sinus infections before and during XRT treated with multiple courses of different antibiotics. (No Zyvox) Approximately 8 weeks post XRT developed severe right eye pain followed by almost complete visual loss. MRI scan showed no edema, hemorrhage or significant change in pituitary mass from pre-XRT scan. MRI of orbits showed minimal (extremely subtle) enhancement of right optic nerve relative to left. No pallor or hemorrhage fundiscopically. Spinal tap done and CSF shows elevated protein and presence of oligoclonal bands.
Review of radiation dosimetry shows 60% of right optic nerve received less than 40 Gy., and only 20% received between 45-50Gy. No part of nerve received more than 50 Gy.
Neuro-opthalmologist feels this is XRT related and has started patient on steroids and hyperbaric oxygen.
Review of literature indicates XRT optic neuropathy generally occurs after 1-3 year latent period, is painless, and usually there is significant MRI enhancement. No cases have been reported at this dose level with this fractionation, with most cases seen with doses in excess of 63 Gy.
She also had an incidental finding of a Chiari 1 malformation.
In light of the infections, the oligoclonal bands, etc. is XRT related optic neuropathy at the top of the differential? If it truly is related to XRT is HBO the treatment of choice or would it be better to treat with intravitreal Avastin?
I have a 40 something y/o female who reportedly was "living the vida loda" in her heyday many years ago. She was wanting to get tested for STD's so I ordered the usual tests. HIV, GC, NG all came back normal. RPR came back pos with 1:2 titers. I ordered a FTA-Abs test which also came back positive. The pt is rather elusive when I interviewed her and stated she was told she had an infection in her blood in the past. I am not sure whether she has ever been treated and doubt the pt would know the answer to that question. My question is if there are there any further tests I can order to confirm she has an active infection since I know that FTA-Abs can remain positive even after tx. She had a normal exam except some diffuse pigmented patches on skin of neck and abdomen that had the appearance to acanthosis nigircans although her glucose was normal. Should I just tx this pt as if she has syphilis?
I tried to post this earlier but I don't see it appearing so here goes, again.
What do you all out there think of using trazodone as a hypnotic in bipolar patients? Where I have seen this most is on inpatient units where a patient may be admitted with a manic or mixed picture and needs a sleep prn. Sure, trazodone is a poor antidepressant but still, it bothers me. I can't understand how it would not add a destabilzing effect.
I use a sedating SGA, a non-benzo hypnotic or sometimes a benzo, unless there is some reason I can't use something in these groups. But, others seem to use trazodone on a reflex basis for insomnia, no matter the diagnosis.
Is anyone aware of published work or opinions on this issue? What has been your practical experience? Do you think you could tell if an illness episode were prolonged or required higher doses of stabilizing agents when trazodone is used?
I'm looking for some positive news out there. I have a 6 yo female, known history of Neurofibramatosis I who is pretty new to our clinic. I first saw her several months ago for URI--noticed the NF mentioned in her chart and asked when she last saw neurology. Turns out, they'd moved here releatively recently, had seen neuro in previous place, at a Children's Hospital, but had not been seen in several years. Had been referred to our local peds neuro a few months back, but had not yet made an appt. Had never had MRI. I reinforced need for Neuro eval.
Saw her again last week for WCC. She has had a drastic vision change in last few months (20/200 in clinic and had new glasses <1 month ago). She had seen neurologist the week before, who recommended an opthomologist, MRI of brain and spine, none of which had been done yet, though she saw the optho 2 days or so after I saw her. I expedite the MRI brain and spine, given this new vision problem, which happened yesterday.
Results: 4x3x3cm mass in hypothalmus, likely astrocytoma, causing an obstructive hydrocephalus. PLUS, bilateral optic gliomas extending to the optic chiasm. PLUS, possible neurofibroma of second branch of CN V. PLUS, possible metastatic disease in the pons. PLUS, possible "drop metastases" along the thoracic spinal cord.
I met with the parents this morning to discuss the results, and they are getting set up to see the Neurosurgeon in a few days. Can anyone offer any hope of a less-than-dismal prognosis?
had a middle aged female undergo a routine right and left heart cath for admission diagnosis of dyspnea and atypical CP.. questionable anterior wall defect on stress .... pt was on Coumadin for a history of Afib, INR was 1.9 when we took her to Cath...
LHC was normal.... clean cors
Upon performing the RHC, we found normal right heart pressures... We advanced the catheter to wedge position and obtained nl pressures...after deflating the balloon, the catheter was noted to jump distally briefly, and was pulled back quickly... Within minutes, however, the patient began to cough, and soon after , hemoptysis was noted...
A diagnosis of pulmonary artery rupture was quickly made, .. the patient was put on 100 fio2, anesthesia was called, protamine was given to reverse intial heparin bolus during time of LHC, and balloon tamponade of the PA was performed... Luckily the patient survived, but I have seen cases like this where the outcome is horrible with rapid demise, and there is not a lot that can be done...
It bothers me when a routine diagnostic procedure that may not have significant benefit for the patient can result in possible disastrous outcomes....I am curious, are any of the cardiologists holding off on obtaining wedge pressures in patients with elevated INR?
I have tried to ponder this question about whether it's beneficial to combine Abilify with other antipsychotics in refractory schizophrenia or psychotic symptoms or not. It seems to me like there are 2 camps so far..the one who said this is a No-no because of Abilify is a strong D2 binding so other antipsychotics wouldn't work at all, vs. the clinical ones who feel that they have seen benefit from their experience. The only article I have seen about this is for the Clozapine which showed additional benefit from the combination than Clozapine alone. So I would love to hear your comments about this and please share your experiences with me about this good but somewhat tricky to use medications. Thank you
NOW I am confused. One of my 14 year old patients, who is a very active young lady, went to the ER (where she's a frequent flyer) for back pain. She was promptly told that "she had fibromyalgia", gave her three shots (on her upper back, apparently in one of the intercostal muscles) and said she "needed an MRI to diagnose fibromyalgia". The mom is a nurse, and she is convinced that is what this is, and has a ton of articles to back it up. I hate to say this but I sent her to a pediatric rheumatologist, to sort this out.
She and her siblings are in my office really, really often for nonspecific things: viral illnesses, sore throats, knee pains, etc. Her growth patterns are normal. She has good grades and has no history of depression. She does, however, act very dramatically when going through minor illnesses; she tends to act in a childish way and whine a lot.
Phisical exam seemed normal. All joints were full ROM, there was no pain anywhere ("but she's on Lortab, that's why she feels better"). There was no joint swelling.
My questions are:
1. How common is this diagnosis in an active teenager who is not depressed?
2. Why was an MRI suggested?
I have a 55 y/o RN with severe cervical myofascial pain which has not responded to stretching, PT, soft tissue therapy, spasmolytics, etc. I would like to incorporate trigger point injections with Lidocaine. She tells me she is allergic to Lidocaine. She reports that she went into cardiac arrest after she had Lidocaine for another procedure many years ago. She however states that she did well with Marcaine for a bier block prior to shoulder surgery before. I am not carzy about doing dry needling for trigger point injections. Has anybody else ever used Marcaine for trigger point injections? What were your experiences? Thank you!
37 yo otherwise healthy female has c-section delivery of normal full term child but develps severe post op pneumonia and ARDS. Recovery complicated by massive PE. She makes full recovery. Hypercoagulable workup completely negative. Because of persistent elevation of D-dimer and evidence of "old clot" in peroneal vein at 6 months, I continued her coumadin for one year. She is now over one year out from PE and is completely asymptomatic. D-dimer off coumadin is minimally elevated (less than is was 6 months ago) but still has evidence of "old clot" in peroneal vein on ultrasound.
A patient presented to my office with a firm left submental mass about the size of a lima bean. He had a history of melanoma of the forearm, Clark's Level 2, which was resected. It then caused left axillary adenopathy which was positive.
This melanoma was first discovered about 4 years ago. Wide local excision was followed by repeat wide local excision for local recurrence, and then followed by the axillary lymph node dissection.
The submental mass is positive for metastatic melanoma, also.
What next for treatment? Interferon?
22 year old male comes in: "doc I woke up yesterday am with a tremendous pain in my eye, blurred vision and swollen eyelids. I didn't have any problem when I went to bed."
Exam: leathery, brownishly discolored, blistered looking upper eyelid skin, smaller blisters on the lateral canthus and lower eyelid, 3+ conjunctival hyperemia, 7 by 6 mm inferonasal corneal abrasion"
What do you want to know and what is your diagnosis?
A patient presented to my office with a firm left submental mass about the size of a lima bean. He had a history of melanoma of the forearm, Clark's Level 2, which was resected. It then caused left axillary adenopathy which was positive.
This melanoma was first discovered about 4 years ago. Wide local excision was followed by repeat wide local excision for local recurrence, and then followed by the axillary lymph node dissection.
The submental mass is positive for metastatic melanoma, also.
What next for treatment? Interferon?
55 year old female with only minimal smoking history (less than 5 pack history over 3o years ago) presented with headaches. MRI of head revealed hydrocephalus with enlarged first, second and third ventricles but no mass lesions. VP shunt placed with relief of headaches. CT of body revealed 3 RUL lung nodules, largest measuring 1.5 cm. Cytology from lung mass and CSF both c/w lung adenocarcinoma. Patient's headaches only mild, has 30 pound weight loss and c/o fatigue, but otherwise asymptomatic. Good Performance Status (KPS of 70.) No breast masses.
Would you recommend further work up?
Assuming further work up is negative, what treatment would you recommend?
54 y/o male (non-smoker) TCC dx'd in October 2007 was Multifocal papillary grade II with no involvment of lamina propria Ta. FISH was negative at the time of initial cystoscopy. Five months later there was recurrent papillary tumor X 2 which were of the same stage and grade. What is routine management at this point? I'm an ER doc and this is a family friend who is asking what I think. Any input from ONC or Urology would be appreciated. Thanks
We had a long discussion today about this where I work. This seems to be a well-done study of patients with lumbar spinal stenosis that argues that surgical therapy is clearly more effective at reducing pain severity and improving function than non-surgical approaches.
Is this news?
I'm not sure. In our practice, we agreed that a trial of conservative management was first-line, surgical referral if refractory if necessary later.
Does this finding change anyone's mind? In other words, assuming someone was a good candidate for surgery, etc.? Given the findings of this study, how likely are you to change your practice?
I recently saw a 90 y/o female with a T2N1M0 SCCA of the R lateral soft palate. No evidence of bone invasion, no evidence of deep soft tisue invasion both clinically and by CT. PET positive for tumor and neck. The patient is very functional at 90. She lives by herself, cares for herself, etc. No major problems other than well controlled HTN. She is edentulous and wears dentures.She was sent by the oral surgeon for RT however the family wanted me to see her also. My question is how many of you would consider operating the patient for cure? I will probably need to resect about half of the soft palate and do a modified neck dissection. The question will be wheather she will need post op RT. If that is what we are trying to avoid(6 weeks of RT), then I may be willing to forgo it, given her age, even if she has minimal critera (ie. angio/nerve invasion, ECS, NOT pos. margins).. Your thoughts? She can easily be rehabed with a denture obtruator.
We've had 3 recent cases of routine spinal anesthetics which were completely normal in their courses until they resolved suddenly and completely at about 45 minutes. Otherwise unremarkable complete recovery.
Trays were Braun and all different lots. Bupivicaine .75% in 8.25% dextrose from Hospira.
In light of Chinese heparin tragedy and scandal, has us wondering....
( We are using separate vials from another manufacture now just to be safe)
Anyone with similar experiences?
75 yo male developed recurrent transient episodes of right eye monocular vision loss. Was evaluated by his opthamologist and was diagnosed with idiopathic retinal vasculitis, and was thought to have a possible embolic etiology. Underwent a surface echo, which revealed Aortic insufficiency, and was referred to our practice for TEE and further eval to rule out cardioembolic source...
TEE was done, LAA was clean, no spontaneous echo contrast, LV fx was normal, LA size was normal, moderate AI due to AV sclerotic changes (PHT 390ms). Aortic root is 4.2cm. upon inspection of the aortic arch, there was found the presence of moderate atherosclerotic debris, with a significant mobile component, approx. 0.96cm in width. This atheroma appeared proximal to the take off of the great vessels.
LDL is 66 on statin therapy.
What is the next step in management for large atheroma (9mm) in the arch with possible recurrent TIAs?
Recommendations in the literature are all over the board from 10-20, while research indicates that the higher numbers are directly associated with increased long term and disease free survival, based in part on the concept that the nodes left behind are resevoirs for cancer cells and in part on the idea that the more nodes examined pathologically the more likely a patient is to receive adjuvant therapy. One study actually tripled the average number of nodes found in a given specimen by bench treatment of the specimen. What do you view as the minimum number of acceptable nodes?
I have a 50 male who has DM type2 with microalbuminuria of 104 on spot urine. He is on Diovan HCT 320/25 and Coreg XR 40mg qd for his HTN. His HTN has been erratic and was 150/80 at last visit. He is poorly controlled in his diabetes with HgA1c of 8.2 and diabetic retinopathy and neuropathy.
My question is what would you add or do next to control his microalbuminuria? Would you add an ACE inhibitor to the regimen to further control his microalbuminuria? If so, would you keep upping the ACE inhibitor to stop the microalbuminuria assuming his BP supports it and his renal function doesn't worsen by more than 30% and his K level is stable? Is it just as important to use any agent to lower his blood pressure? I am obviously trying to get his blood sugars under better control. His latest Bun/Cr is 26/1.5. with a GFR of 50's. Thanks.
This is one of those weird ones where you shake your head and realize how interesting, challenging and difficult doctor's jobs can be.
Clinical History:
83 yo male HTN/DM presents to the ED for headache and fatigue. Recent travel to a foreign country. English is okay, but not great. Presents with his son. On history patient complains of a severe headache and cough. He presses the magic button when he says "worst headache of life" like none he has had before. He has positional neck pain. Otherwise he just feels tired. No chest pain, no shortness of breath. Non-smoker. On exam HR 80s BP 170/80 RR 18 SPO2 96%. Exam is fairly unremarkable. Neuro exam is normal. No meningmus or reproducible pain. Mild wheezing on the right base.
EKG shows some non-specific flattening of t waves in the lateral leads. Not that different from 2 years ago. No white count, no anemic. Glucose is 177, Cr 2.1 (baseline). Otherwise unremarkable.
CT head shows old non-specific changes. LP shows glucose of 100. 1 RBC, otherwise negative. CXR shows a small RLL infiltrate. I hang my hat on that. I treat him. Tylenol and 6mg of morphine. He feels better. I walk him (functional assessment). Nurse notes something "funny" on telemetry.
Repeat EKG shows ST elevation in AVL and V1 with deep ST depressions. Uh oh. Right sided EKG shows borderline elevation RV4. I call the cardiologist and fax him the EKGs (no cardiology in house). Give aspiring and send enzymes. Vital signs still stable BP is now 130/80. Patient has no other symptoms. I am keeping him now. Cardiologist calls back. Doesn't think it's an MI, not real interested in him, asks us to keep him unless something else pops up. Headache and neck pain get a little worse when patient sits up or moves around. Troponin is 0.36. CK 86, MB 4.0. Add Lovenox call the cardiologist and ship.
Going off shift a few hours later. Cardiologist calls me. "Good thing you sent this guy. He started complaining of right arm pain. Took him to cath. He has severe three vessel disease. RAD completely collateralized. 95% LAD. He's now on a ballon pump, we are going to try to 'cool him down overnight' but he's going for a CABG today or tomorrow."
Holy crap. I guess I need to broaden my differential for headaches (although positional neck pain was now clearly his anginal equivalent). Just though I'd share.
This job if nothing else keeps you on your toes. I was thinking about sending this guy home! That probably wouldn't have worked out so good.
32 year old anxious woman with a history of systemic scleroderma, rheumatoid arthritis, and fibromyalgia. On short courses of prednisone in the past. Presents last month to my office with questioned adrenal insufficiency following a few syncopal attacks. her (?am) cortisol prior to seeing me was 0.7 mcg/dl.
Follow up testing in my office revealed an am baseline cortisol of 2.7 mcg/dl which spiked to 20.6 mcg/dl one hour after stim with 250 mcg ACTH. Other pituitary indices are as follows: TSH=0.6 with a fT4 of 0.66 (0.8-1.8 ng/dl) and a T3 of 132 (60-181 ng/dl), prolactin=12.8 ng/ml, FSH=5.8, LH<0.5, IGF-1=177 ng/ml, ACTH=6 pg/ml.
Subsequent pituitary MRI revealed a "doming of the gland which is mildly greater on the right than the left... there is a very subtle suggesting of a mass lesion present this measures 4.1 mm in height x 5.9 mm in transverse dimension and 7.1 mm in anterior to posterior dimension. this is a soft finding. That is this is not definitively a true abnormality but is suspicious for the presence of a microadenoma."
What is your next step?
I saw 20 y/o female with VB x 2weeks (time of menses, but longer duration), some break through than regular VB heavy at times with clots, no bleeding from other sites or passing out. I put her on provera 10mg QD x 5d, explained how it should slow VB and then she would have wirthdarawal bleed and to then re start comb. OCP instead of yasmin after withdrawal bleed. She is back today, as VB slowed, but family wants CBC checked since she felt a little faint in shower 3 days ago, but no syncope. Provera last day yesterday and waiting for withdrawl. Her exam last time(last week) was normal. Her vitals are normal.
Is anyone skipping provera and just using the comb. OCP, also do most people find provera stops VB altogether or just slows it? She had regular menses before trying to take yasmin continuously. Thanks-
i am working on a case report for an interesting case that i was not personally involved in. pt is a 54 year old male with pmhx of allergic rhinitis and likely undiagnosed hypertension who presented for endoscopic sinus surgery. the general anesthetic was uneventful and lead II was exclusively monitored throughout the case. upon arrival to pacu, pt was complaining of chest and left arm pain. a twelve-lead ekg revealed significant st elevation in all lateral leads with reciprocal changes in III and aVF, but not lead II. was wondering about other's practices as far as lead monitoring......
A horrible situation has come up tonight that I have never experienced in quite this way. I wondered if others had seen anything like this and what they did about it. A man in his 70's had an emergency right hemicolectomy, resection of two infarcted segments of small bowel, and cholecystectomy a week ago when he presented with bowel perforation. He had a general anesthetic with an arterial line placed and was kept ventilated overnight, but actually went home.
We got called today because he was back with a massively distended abdomen and shock. He came to the OR with a 20 guage IV in, BP in the 60's, HR in 130's. I easily got in a subclavian line, but the CRNA and I tried for almost an hour to get an arterial line. There were absolutely no radial pulses and blind attempts failed. I was able to get pulsatile blood from brachial, axillary and femoral arteries, but could not cannulate the vessels, even with a guide wire. We decided that we had to proceed with noninvasive pressures.
The surgeon found multiple areas of infarcted bowel and suctioned several liters of fecal-smelling liquid from the abdomen, and we got another couple from the NG. The surgeon said that the blood vessels all felt as hard as a rock, which explained our problems with the arterial line. He asked for consultation with the family because the man had pretty much infarcted his entire small bowel and most of the colon. The family understood the situation and only wanted pain control for him.
The horrible part of this for me is that the one organ that was being perfused pretty well was his brain. This man was quite awake and alert when I visited him preoperatively, and had pain. We were trying to keep him alive with massive infusions of fluid and blood and a wide-open epinephrine drip, but the CRNA and I did not feel he would tolerate any anesthetic at all. The CRNA loaded him with as much Versed as he would tolerate.
So, we have a man receiving maximum cardiovascular support, who may have awareness but tolerates no anesthetic agent, who is having his abdomen closed after the situation is deemed surgically hopeless. Other than slowly titrating in as much narcotic as possible, what is one supposed to do now? I know what will happen. He will be kept on the ventilator and continue to receive vasopressors until his body finally gives up. I have seen similar situations many times over the years, but not in someone who seems so likely to have awareness. Is this the best we can do? How are we supposed to sleep at night after dealing with something like this?
I've been revising my guidelines for anticoagulated patients receiving interventional pain management procedures under fluoroscopic guidance.
I am not performing regional anesthesia.
I've taken the most conservative guidelines I can find from various regional anesthesia societies.
I used the following AWESOME document which compares the recommendations of all the major anesthesiology societies for the data:
http://forums.studentdoctor...
I'd appreciate your thoughts on the below document. If you like it, feel free to use it:
PAIN MANAGEMENT PROCEDURE INSTRUCTIONS FOR PATIENTS USING "BLOOD THINNERS"
Certain drugs MUST be discontinued prior to pain management procedures, as they cause abnormal bleeding and clotting. It is your responsibility to check with the prescribing physician of the below medications whether it is OK for you to stop these medications temporarily. DO NOT STOP THESE MEDICATIONS WITHOUT CONSULTING THE PRESCRIBING DOCTOR FIRST!
54 yo female with anemia undergoes colonoscopy which shows a big fungating tumor in the cecum. I board the patient for my regular OR time 48 hours later, and while waiting get a CT to determine the status of the liver for mets. CT comes back with 'thickening of the cecum', no surprise, but also read out as 'prominent lymph nodes medial to the cecum, recommend PET/CT? Now, the radiologists knows that I've found a colon tumor not resectable through the scope in this anemic patient, and still talks about doing a PET in this patient to 'see if the nodes are metabolically active'?!? To me, this is just nuts. I want to know the status of liver mets, as it plays a major role in determining how hard I have to work for a liver biopsy for pathologic evaluation concerning future chemo/rad treatment. But what is a PET scan possibly going to add in this situation?
I have an interesting and confusing case of a 28 yo F with no prior medical history who was referred to me for 2 months of chronic watery diarrhea, constant sharp epigastric and right sided abdominal pain which radiates to the back, with occasional flares, and about 50 lbs weight loss. She was not using alcohol, medications, drugs, OTC's or herbal preparations. Review of systems is otherwise negative.
Extensive workup has been unrevealing. The only abnormalities have been a mildly increased indirect bili (probably Gilberts), mildly increased platelets, intermittent mild inc in WBC, intermittent eosinophilia (up to 15%), and very mildly low B12...
Generally healthy 68 y/o WF went to an orthopod with a painful hip. After evaluation, he recommended an intra-articular injection of steroid, which he performed under fluoroscopic control. 24 hours later, she developed worse pain, and within another 24 was unable to walk. She was advised this was "not unusual" and to wait for improvement. After another two days, her husband and an RN neighbor sent her by ambulance to the hosiptal, where it was determined she had septic arthritis which required open drainage and prolonged IV Abiox.
An infectous disease consultant told her the infection was the result of a fall she had suffered a week (+/-) before the injection, and not the result of the injection ittself.
To me, this seems like a preposterous covering of your friend's asterix, which is akin to "I did not have sex with that woman", in which the cover-up is worse than a truthful admission.
A 68-year-old white gentleman is referred for evaluation of anemia. He complains of increasing fatigue, dizziness, and swelling in his feet. He has no history of fever or weight loss. His past medical history is notable for hypertension, hyperlipidemia, GERD, obstructive sleep apnea, DVT, hypothyroidism, and renal cell carcinoma 9 years ago for which he is status post nephrectomy, chemotherapy, and most recently-biotherapy and radiofrequency ablation. He had a recurrence of the renal cell carcinoma in the opposite preserved kidney 4 years ago, and pulmonary metastasis 3 years ago, currently resolved.
The pertinent findings on physical exam are: mild pallor, no icterus, no peripheral lymphadenopathy, no hepatomegaly, and mild splenomegaly. He has pedal edema 2+ and mildly dilated veins.
Available Labs from 2005 indicate a hemoglobin value of 10.5g/dL.
Current Labs: hemoglobin: 9.9g/dL hematocrit: 28%; WBC 12.5x103/µL; Platelet count 221x103/µL.
Additional lab data to follow questions and as case proceeds.
I've got a woman newly diagnosed with colon cancer. She needs a colectomy. Unfortunately, drug eluting stent placed a couple months ago.
I understand the importance of plavix with these stents. I also understand that many surgeons are uneasy operating during plavix use (other than emergency surgery, which can't be helped.)
What would you do in this case? It's neither emergent nor an elective problem that can be put off 6 months. I already know the cardiologists don't want to stop it.
Would you operate without stopping it? If so, would you still do a laparoscopic colectomy, or proceed open? Platelet transfusion immediately before surgery, or just do it?
I wanted to see what my colleagues in pain managment and anesthesia thought about this.
I have a colleague who routinely does radiofrequency facet denervations of the lumbar and cervical medial branch nerves, as we all often do. However, he does not do any sensory or motor nerve stimulation before lesioning. I was always taught to do 50Hz (sensory) and 2 Hz (motor) stimulation to ensure that the medial branch was being treated, as opposed to the spinal nerve segment.
We do use flouroscopy as well, but I don't fell comfortable lesioning without doing some form of stimulation.
What do others think of this?
54 yo female with anemia undergoes colonoscopy which shows a big fungating tumor in the cecum. I board the patient for my regular OR time 48 hours later, and while waiting get a CT to determine the status of the liver for mets. CT comes back with 'thickening of the cecum', no surprise, but also read out as 'prominent lymph nodes medial to the cecum, recommend PET/CT? Now, the radiologists knows that I've found a colon tumor not resectable through the scope in this anemic patient, and still talks about doing a PET in this patient to 'see if the nodes are metabolically active'?!? To me, this is just nuts. I want to know the status of liver mets, as it plays a major role in determining how hard I have to work for a liver biopsy for pathologic evaluation concerning future chemo/rad treatment. But what is a PET scan possibly going to add in this situation?
I had an interesting case recently: 42 yo man in for a physical. No significant history. He usually runs - sometimes marathons or shorter races - and swims and bikes when he does not run but not nearly at the same intensity. Recently he has curtailed his running due to left sided hip pain. The ROS is normal except for the hip pain and the PE is normal. His labs showed a sodium of 130. What would you check? I do have the dx - it is not polydipsia or simply related to the running (especially since he has not been running much lately). He is not taking any OTC/herbal supplements.
Two nights ago, I saw a guy in his mid-20's with no prior medical history who came in with epigastric abdominal pain with nausea. No fever, no vomiting. Worsened with eating, tender to palpation of the epigastric region. No radiation, non-tender anywhere else.
At some point, the nurse came and told me that while the patient had good relief with the GI cocktail, the pain was coming back. Another GI cocktail, not so much relief. WBC 16.6. Everything else normal. Vitals... mild tachycardia in the low 100's, otherwise normal.
Re-evaluation of his abdomen, tender in the epigastric region, nowhere else. Something didn't strike me as right about him and I ordered a CT. CT result: a 13 mm appendix with periappendiceal fat stranding consistent with acute appendicitis. Re-evaluation: still only tender in the epigastric region, absolutely no tenderness in the RLQ (where the appendix was in the normal location on the CT). And I mashed on his abdomen quite hard.
Second case: my memory is fuzzy 'cause this was about 1.5 years ago. Guy in his late 20's or mid 30's. Said he had an abdominal wall hernia in the upper abdomen and that it was hurting. He was concerned about incarceration. Examination: tender around the epigastrium, no hernial defect palpated. Short of it is: I CT'd him to help rule out an incarcerated hernia given his stated history. It showed acute appy. I recall being very surprised... I'm pretty sure his vitals and labs were all normal. I re-examined him and nothing except epigastric tenderness.
My question for the rest of you is, WTF???? And, do you have any other stories to share? Appy is not supposed to present this way. We all know of the early periumbilical pain but typically people are usually tender over the appendix.
44 y/o weightlifter, mildly elevated cholesterol on Lipitor, only other meds are Andro and creatine, presents with acute left arm and leg clumsiness, dysphagia and right gaze preference on 4/14. CT showed acute left cerebellar stroke with significant edema and hydrocephalus, and a smaller right occipital stroke. Partial craniotomy and EVD put in on 4/15. MRA had motion artifact, but shows minimal flow in left vertebral and CTA also had motion artifact, and showed probable left vertebral dissection with no flow in the left PICA and normal flow in the right vert, basilar, both PCAs, and the anterior circulation.
He remains alert and able to use his right arm and leg well, left arm and leg very clumsy and slightly weak. Due to the craniotomy and EVD I have been hesitant to start any anticoagulants, and there does not seem to be much agreement in the literature about the best treatment for a vertebral dissection. A repeat MRA will be done on 4/21 to get a clearer look at the left vertebral and basilar.
Especially with the complete loss of function in the left PICA distribution, would there be any benefit to reopening the vert?
Is he at risk for further distal embolization from the vert to the occipital lobes (given the visibile small right occipital stroke)?
Would you start heparin/Coumadin, or just continue aspirin, as I have done so far?
I need some sermoan input. I have a pleasant and unfortunate patient with newly diagnosed lung CA eroding into his ribs. I have been talking with pulmonary and heme-onc and no one seems to be able to come to a consensus on what stage he is in the work-up thus far. I need some heme-onc help! I was told by pulmonary that this was stage IV and then was stuck trying to explain treatment/prognosis to the patient when i didn't agree w/ them.
Pulm cancelled PET--said not indicated. CT abd/pelvis pending.
Bone Scan: Left 5th, 6th, 7th ribs posteriorly suggestive of metastatic disease most likely secondary erosion of the ribs by underlying tumor.
CT Chest: 3.4 cm soft tissue mass in left peripheral upper chest with extension into adjacent rib most likely represents malignancy. Prominent Lymph nodes in mediastinum and hilar areas. Also adjacent pneumoitis changes noted in left upper lobe.
BX Lung Mass: UNDIFFERENTIATED LARGE CELL CARCINOMA
Had a 78 yo gentleman with history of DM, CML, otherwise healthy and active, who suffered a CVA with resolving sxs.... Carotids were normal. echo and TEE confirmed a PFO with moderate right to left shunting by bubble..... He was determined by neurology to have had a "cryptogenic'stroke:...Pt had been on ASA therapy at this time. We were consulted to consider PFO closure.
Given the recent data on PFO in the elderly, would anybody consider closing this PFO, or do we think that making a diagnosis of true "cryptogenic stroke" is ridiculous
A good patient of mine,a frail 81 y.o M with h/o recent IMI and p recent Dx of presumptive IPF(started on steriods 6 weeks ago) was reported acting strange per his wife: confused and emotionally labile. With her concern she brought him into the EW, and besides his baseline tachypnea he was actually alert/oriented/appropriately interactive with otherwise stable VS.
His hospitalization progressed as such: the full dMS w/u was initiated; noted leukocytosis without bandemia(on steroids), clean U/A, neg BCx, stable CXR, but head CT with small focus ? R temporal SDH. MRI revealed what was suspicious for tiny chronic SDH. During this workup the patient's MS was noted degrade quickly so much so that over 24 hrs he failed to interact with anyone, and was in this bradykinetic, anorectic daze. Neurology and neurosurg were c/s'd to weigh in, in regards to the contribution of the SHD which they felt was too small to cause this dMS and it remained stable on imaging in-house.
His dMS labs remained nonremark, clear U/A's/BCXs/TFTs/NH3 and recent neg underlying dementia labs(B12/folic/RPR). His VS remained stable but his interactivey was shot. EEG showed classic slowing c/w toxic metabolic. As a last ditch effort, we trialed an ativan trial for suspected catatonia, and after an injection of 1 mg he was arisen ... he didn't tolerate transition to clonopin but did well with ECT
Anyways, no one could explain why this happened .. any clues ????
Just got this biopsy back today, and am not sure what to do next. Patient is a 43 year old G2 P2 S/P TAH LSO in 1988 (with previous RSO) with documented dysgerminoma at that time. The cancer was limited to the ovary. She has done well for the last 20 years. She came in for her pap smear, and had LGSIL.
Colpo revealed white areas where the suture line was at the TAH, and some white epithelium at 6-7:00 This was biopsied. Pathology report today shows "1...nonspecific findings. Squamous epithelium is attenuated without evidence of atypia. The subepithelial fibrovascular stroma discloses mild edema and vague hyalinization. 2. Findings are suggestive of early lichen sclerosus, however, nondiagnostic."
OK, guys and gals, I need help. Do I
1. watch?
2. Treat with clobetasol?
3. Refer back to GYN ONC?
4. Watch my hair get greyer and greyer?
43 yo wm had a pT2N0 biphasic tumor of lung origin resected 9/07 with clean margins, negative mediastinal staging (by a good thoracic oncologist). Original path report reads:
"Poorly differentiated squamous cell with sarcomatoid features (Carcinosarcoma)".
Patient was referred to another Med Onc but did not follow up. Now found with single hepatic met about 3 cm. Core biopsy "High Grade Sarcoma". This is felt by the pathologists to represent/appears similar to the sarcomatous elements of the original biphasic tumor.
Obviously a rare tumor. My understanding is that this is treated like any other NSCLC, and that the sarcoma portion of the slides essentially represents a metaplasia which looks like sarcoma with spindle cells, IHC staining etc. Interstingly to me, the core of the met has absolutely no epithelial tumor features in any slide.
Questions for the esteemed panel:
I was wondering if I may get some insight from some of the nephrologists on Sermo.
I saw a patient several night ago, looked well, afebrile, other vitals normal, had symptoms of pyelonephritis with dysuria, flank pain. She also noted a rash to her legs but she thought it was a sunburn. Her CBC, CMP, PT/PTT were normal, urine dip was consistent with a UTI with leuks, nitrites, and I believe there was either moderate or large blood on the dip but no gross hematuria.
The rash on the legs was not a sunburn, but rather like a mild ecchymosis -- erythematous, non-blanching, non-palpable, kind of dithering out at the edges. She had a burning sensation over these areas which consisted of the lower legs over the anterior shins with some progression up the right lateral thigh.
I decided to ultrasound her legs, since she'd had a very long car ride previous to presentation and had some pain and tenderness in her calves as well. This was negative bilaterally. She said that she'd done "a lot" of dancing on the trip that she'd just returned from and figured that's why her calves were hurting.
My question is, would you consider this consistent with glomerulonephritis and treat with steroids? Her symptoms were very typical for a mild pyelonephritis, but I can't say I've ever had a patient with that kind of rash with pyelo. I know that with glomerulonephritis, there can be a rash, however, from what I understand, it's usually palpable.
Any input would be appreciated.
A 56 yo WF was sent to see me for fairly typical increasing biliary colic and gallstones by ultrasound. PMH was significant for ulcerative colitis for many years, (clinically stable on sulfasalazine), HTN, NIDDM, and elevated lipids. At the time of surgery, she had fairly typical moderate local inflammation and a large (over 2 cm) lymph node at the neck of the gallbladder, as well as whitish, flat nodular areas over the surface of the liver. The cholecystectomy and IOC went uneventfully, and I did a liver biopsy of a representative lesion. Both the lymph node and the liver parenchyma showed granulomas (granulomata?) with caseation necrosis. AFB and fungal stains were all negative. The patient works as a school teacher and her yearly PPD's have always been negative. Any ideas as to what this could be?
I have a 53 yo man with GERD and a small sliding hiatal hernia who became more symptomatic recently. He is overweight, drinks diet Coke all day, has a stressful job and unwinds at night with a couple of gin and tonics. I did an upper endoscopy recently and, not unexpectedly, he had severe distal erosive esophagitis, a small hiatal hernia and mild diffuse gastritis. He is negative for h. pylori. He has no visual or biopsy evidence of Barrett's.
My question is this...Biopsies of his distal esophagus show evidence of acute inflammation with greater than 21 eosinophils per HPF. The rest of his esophagus appears grossly normal. He has no specific "allergic" history. Is this truly eosinophilic esophagitis? Or, is it part of the spectrum of acute reflux esophagitis? In addition to standard treatment for reflux...dietary changes, elevation of HOB, no late meals, avoid alcohol, lose weight, and PPI therapy, would anyone add Singulair or consider referral to an allergist? Or, would you get the acute problem under control and rescope him in several months with biopsies of multiple levels of the esophagus?
Thank you for any thoughts!
24 yr old female with lupus, s/p postpartum developed blurry vision, headaches, High BP , Seizure on admission, and memory loss, pt had neuro w/u , MRI brain s/o parietal , occipital lobes bilaterally, findings s/o lupus vasculitis, mild stenosis of anterior and middle cerebral artery, mild narrowing of basilar and vertebral artery.
pt was not able to recall her family members name or about her delivery and birth of the baby. was not able to see things in front of her. echo shows mild Mitral regurgitation.
pt on prednisone and chloroquine for lupus.
pt does not have any psychiatric care, reports feeling stressed out in the second trimester of pregnancy. no neurovegetative symptoms. no drug or alcohol history.
now pt able to remember family members names, and the baby and few details of her pregnancy but not to full extent.
no psychosis observed or informed by the staff. no reports of any hallucinations by the pt or chart. pt reports she was feeling confused for first few days, not now. pt able to spell world backwards correctly, memory 3/3 immediate recall, at 3 minutes, 1/3 and with cues 2/3.
what is it? amnestic d/o NOS? WAS SHE Delirious for first few days.? how will you manage this pt for memory loss?
27 year old male playing basketball went for a dunk and planted both feet. Legs went out from under him and he felt sharp pains in both knees. Presented to the ER with bilateral swollen knees and inability to stand. No known previous history of knee problems. Played safety for Div. I university, 6' and 200 lbs. MRI's showed bilateral traumatic separation of bipartite patella. Only other MRI finding was extensive tear of the retinaculum. Plan is to take him to OR and take down fibrous tissue between fragments and fix with screws and fiberwire. Any other suggestions? Review of the literature shows only one reported case which was unilateral.
The following case is part of the Sermo Case Conference Series. This will unfold over several days - feel free to ask for additional data, test results, or supporting materials you think would be most appropriate.
This is a 71 year old African American female with DM, 20 pack year smoker, anemia of chronic disease presented to our emergency room with complaints of left sided abdominal pain. Pt also complained of worsening chronic sob, nonproductive cough, early satiety and weight loss that she was unable to quantify. A chest xray in the ED demonstrated a left lower lob chest mass 8x10 cm confirmed on follow up ct scanning. This mass was unknown prior to this admission and an cxr one year prior was unremarkable.
PMH: As Above, reflux, asthma, hypertension, osteoarthritis, and morbid obesity.
PSH Left total knee replacement, left carpal tunnel release, a right breast biopsy in 2005, and a tubal ligation several years ago.
Social History: Previous 20 pack year smoker quit 10 years ago. Denies alcohol or illicit drug use. Widowed. G6P6 all normal spontaneous vaginal deliveries with one daughter and five sons. Has worked several different odd jobs over the years - most recently in a box factory. Denies any history of blood transfusions or toxic exposure. No travel history outside the united states. She underwent menopause at age 57 and has never been on hormone replacement therapy or oral contraceptives.
Health Maintenance: screening mamm 05/2007 with "possible nodule in left breast" Egd many years ago to evaluate reflux. A colonoscopy in may 2005 showed scattered diverticulum.
Family History: Brother died of mets lung cancer. Mother died of unknown cancer. Maternal uncle, grandmother and grandfather all passed away from Mis.
Allergies: NKDA
MEDS: Singulair, Zetia, Asa, Cardizem, Advair, Pravachol, Iron, Lasix, Aspart 70/30, Diovan, HCTZ
ROS: chronic sob, pain symptoms as described, nonproductive cough, early satiety.
PE (pertinent positives): 259lb (280 lb in 11/2007) pulse ox 96%, respiratory rate 18, left lung with decreased breath sounds with the exception of the apex. Rest of exam is otherwise unremarkable.
Please share your insight and again feel free to request more information as we formulate a differential diagnosis. .
I have done thousands of TFESI's without complication. I recently performed an L1 and L2 right TFESI on a patient which has has many others from me. Usual protocol, negative aspiration, good flow of contrast into the epidural space, etc...
Immediately after the injection she had numbness in both legs and pelvic region.
Initially, I assumed she had a spinal injection, but when the numbness did not regress as expected, it was worrisome. She was sent for CT, which showed medulary changes in the spinal cord indicating spinal infarct.
She still has unfortunately had little recovery.
I have since changed from DepoMedrol to Betamethasone for my TFESI's The exact cause of infarction in these cases is still not known, but a Depot steroid could be a cause. Just wanted to warn others of this rare but devastating complication
This is a 50 y/o caucasion male who recently had a ventral hernia repair done 1 month ago. He previous had 3 liver lesions seen on a previous CT of abdomen, so I got this repeat CT scan done to check stability of the lesions. The new CT report reads:
History: FU CT SCAN for 3 LOW DENSITY LIVER MASSES
FINDINGS:
Two small right hepatic hypodense lesions are seen, unchanged in size.
The third lesion is not well seen on this examination. There has been
replacement of a majority of the spleen with low-attenuation, which may
represent infarction. The splenic vein appears somewhat attenuated
compared to the prior examination. The portal vein is patent. The
gallbladder and right adrenal gland are normal.
The left adrenal gland is thickened. There is a small hypodensity in the right kidney, too small to be characterized and several nonobstructing left renal calculi are present. There has been interval repair of a large ventral hernia.
There is a fluid collection in the subcutaneous tissues at the repair
site measuring approximately 7.0 x 2.9 cm. The visualized abdominal
aorta is normal. The lung bases are unremarkable.
IMPRESSION:
1. Stable right hepatic low-density lesions.
2. Interval replacement of majority of the spleen with
low-attenuation material, which likely represents infarcts. The
splenic vein appears somewhat attenuated compared to the prior
examination.
3. Unchanged thickened left adrenal gland.
4. Interval repair of ventral hernia with residual fluid collection
measuring 7.0 x 2.9 cm, which likely represents a seroma.
Underlying abscess cannot be entirely excluded.
5. Nonobstructing left renal calculi.
I would appreciate any advise or suggestions on further diagnostic options,
my plan is to repeat a CT in 3 months.
Not sure what to think about this one.
67 year old man with no ongoing chronic medical problems. A year ago he was
He saw his primary doctor who ordered and MRI of his knee. The MRI showed some medial compartment arthritis and a tear of the posterior horn of the medial meniscus. By my exam and history, the MRI findings are irrelevant. He has only minimal arthritic symptoms and I have explained to him why scoping the knee to "pretty-up the cartilage" wouldn't help his symptoms. Lately he has been wearing a neoprene pull-on knee sleeve because it makes his knee feel more secure.
Repeated exams have shown a consistent area of decreased skin sensation of the anterior right leg, from approximately mid-patella to the ankle and mid- medial to mid-lateral leg. Motor exam and reflexes are normal.
Finding no ready explanation for his numbness, I sent him to one of two local neurologists. The neurologist's initial consult DDx was lumbar radiculopathy, posterior tibial nerve entrapment, peroneal nerve entrapment.
The neurologist proceded with EMG/NCV and found no evidence of peripheral neuropathy, peroneal or posterior tibial nerve impingement; did note "slight irritation to the right L5 radical". His impression: "local tendonitis that would not have been picked up by the MRI of the knee, causing a chemical mononeuropathy" (HUH??)
It's a year later and I saw him last week. Numbness is the same. Knee exam is consistent with mild DJD and he has only mild intermittent symptoms from the arthritis. Motor and reflexes normal. Skin is unremarkable. I did note very slight pitting edema of the right ankle last week. Measurement of the circumference of the calves showed a 2 cm difference, right larger. Calf is nontender. He notes buying a new neoprene knee sleeve recently and that it is a bit tight (might explain the trace edema?)
I'm stumped. The distribution of his numbness is not radicular nor is it in the distribution of a single peripheral sensory nerve.
Ideas, anyone?
The recent JCO article "Should Randomized Clinical Trials (RCT) Be Required for Proton Radiotherapy?" brings up an interesting question (below).
http://jco.ascopubs.org/cgi...
My mentors told stories how they justified the transition from orthovoltage to cobalt, cobalt to conventional linacs based on improved dose distribution rather than RCT. They said "You don't need a RCT to see if extra dose to normal tissue harms patients." They also told stories about the resistance to change by those who didn't have access to the newer technologies.
Interestingly, I see history repeating itself with transition form conventional linacs to IMRT/tomotherapy/accuray/rapid arc based linacs .
So the question is: do we need a RTC to see if a beam that stops is an improvement over a beam that doesn't?
I am at a complete loss to explain what I thought was a spegelian hernia. I know, the pre-op diagnosis of these is uncommon, but the story was pretty convincing.
Of interest, the patient is a 41 yo white male, HIV positive via both lifestyle and substance abuse issues, who was drug-treated with minimal viral load for a number of years, then stopped his meds about 5 years ago and now is seeing his viral load creep up again. For the past 3-4 years, he describes a mass lesion in his lateral left mid-abdomen, which would be relieved and disappear with gentle pressure, and was worse with prolonged standing. The symptoms became more frequent and severe over the last 3-4 months, and he came to see me.
His abdominal exam, with no previous surgeries, was normal. His point of maximal (historical) tenderness was at the expected site of a spegelian hernia, but was not reproducible in the office. He describes the "mass" as extending superiorly from that point for a few cms before dissipating. There was no history of local trauma.
Not knowing what else to do, I took him to the OR and put in a laparoscope, and found absolutely nothing- no defects, no palpable masses in the abdominal wall, nothing. I took out my single 5 mm trocar and quit. Now one week post op, he reports the same symptoms, and still has nothing reproducible on exam.
Any Ideas? I am stumped.
A 46yo married, female originally from Croatia had been employed as a nurse for many years, before getting injured on the job. She suffered a L5-S1 HNP, underwent discectomy/ laminectomy x 2 ( secondary to reherniation). She developed chronic radiculopathy, CRPS Type 1,right LLE, extreme fatigue and depression. Her weight gradually increased by about 60lbs within a year. She was diagnosed with fibromyalgia, interstitial cystitis (retained failed medtronic implant sacral stim), insomnia and IBS.
Her PMH is significant for thyroid goiter @ 15yo and transient treatment with thyroid replacement. Her diet was deficient in iodine/iodide as a child. She delivered 2 premature sons in her 20's. She has had and has multiple ovarian cysts, severe PMDS, fibroids, menorrhagia, chronic anemia (Hbg 8-9), and multiple drug sensitivities.
Her mother has a h/o thyroid , breast, and cervical cancers.
Within 4 years of her work injury she presents with these pertinent positives: (1) goiter with dysphagia and follicular CA thyroid; (2) CT shows mass on upper pole of kidney; (3) clinically hypothyroid; (4) adrenal insufficiency; (5) uterus size of 5 month gestation ; (6) monthly dysfunctional bleeding requires 19 super tampons with pads; (7) diverticulosis; (8) chronic painful breasts (fibrocystic) with h/o solitary palpable cyst inferior mid border L breast by chest wall; (9) umbilical and bilateral inguinal hernias; and (10) extreme exhaustion and chronic pain.
Her medications include: Lyrica, Tramadol, Celexa, Trazadone, Ambien, and IV iron.
One of the docs in my group had a great case this week. A thirty year old male with 8 hours of severe right axilla pain. Absolutely no risk factors. EKG was consistent with an acute ant MI. Now the cool part. He happened to order a stat CT scan for possible dissection. The radiologists only saw the order as CT for dissection. But the radiologist made note that there was no dissection but that there were changes in the ant wall of the left ventricle on CT scan that was co



