Rubor Dolor Calor Tumor

I sometimes get asked what: what does the patient have.

Sometimes I get asked how: how to treat the patient. That was todays patients. The patient had a fever the day after he has his laparoscopic mesenteric biopsy and three days later his blood cultures popped positive for Candida glabrata of all things.

They asked be about the best antibiotic to use (I picked caspofungin).

But the interesting question is why.

Preop, he had no symptoms.

Past medical history diabetes, pacemaker dependent, obesity with chronic ‘diaper rash’ in his skin folds. His pacer is three years old.

His exam is negative.

The classic risk factors for Candida in their blood are central lines, hyperal, broad spectrum antibiotics, neutropenia and a major surgery.

He had none of the above.

The only reason he could have positive blood cultures is if he had seeded his pacer system from his intermittently oozy groin Candida, and, unfortunately his TEE today showed infection on the wires.

Crap.

Can’t cure it medically and if the pacer system comes out, he has no rhythm. He has no rhythm, Who could ask for anything more? Me. It is why I am glad I am not a cardiologist.

There is exactly one case of C. glabrata pacer infection in the lit-tra-chure and a smattering of a handful of a smidgin of other Candida species on pacers. Like all infections of pacers, the system absolutely, positively has to be removed.   Unlike prosthetic valve endocarditis, the literature suggests you are as likely to cure a pacer infection medically as you are to get an accounting of money spent to bail out Fanny Mae.

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J Infect. 2000 Sep;41(2):176-8.   Medical treatment of a pacemaker endocarditis due to Candida albicans and to Candida glabrata.

  We describe a case of pacemaker infection due to two fungal species: Candida albicans and C. glabrata. Transthoracic echocardiography showed a large vegetation on the intraventricular wires. Because of severe underlying diseases, surgery was believed to be contraindicated. The patient was treated using high dose of fluconazole, resulting in clinical improvement and negative blood cultures. However, 2 months later, the patient underwent a fatal stroke. At autopsy, a large vegetation was found only all along the wires. Postmortem culture of the infected material was positive for both C. albicans and C. glabrata. Copyright 2000 The British Infection Society.

   PMID: 11023765

mcrislip Eitiology, Fungi

Busy busy busy.

Sometimes life keeps me away from the computer. There are things to be done away from the interwebs, at least until I become one with matrix.

I spent a chunk of my day teaching residents as one of my hospitals has an internal medicine residency program. The problem is I often do not know here my ideas come from. Like today.

I was asked to see a patient with a hematologic malignancy and fevers for five days despite ceftriaxone and azithromycin for the not really there pneumonia.

I know from a quick chart review that is white cells have gone form 6 to 1.7, his platelets from 230k to 90, and his hgb has dropped 2 points. Rest of his labs are ok

So the patient tells me he has teeth chattering rigors (which he has during the interview), fevers, severe myalgias, and abdominal pain. Otherwise no localizing symptoms

Hmmmm.

PMH: Waldenstrom, but no treatment for a year.

Animals? Dogs.

Travel outside Portland?

We were at out cabin in Eastern Oregon, near Bend, at 4900 feet.

Why he mentioned the elevation, I do not know, but my ears perk up.

So, any ticks?

Yeah. 4 tick bites, and his wife volunteers that they are swarmed with ticks this time of years.

And like a bubble floating up out of the bath and popping, I could smell what he had. But I do not know where the thought came from. The diagnosis was made far below conscious thought, then I need to do a rapid song and dance to justify the diagnosis.

I should mention that I have yet to confirm the diagnosis, and like many great diagnoses I make, reality often contradicts me. Pesky labs.

My motto: Saepius in Erroris, Nunquam in Nuto.

Frequently in Error, Never in Doubt.

I will probably report in a few weeks I was wrong.

But for now I am calling it Colorado Tick Fever.

====

From http://www.oregon.gov/DHS/ph/acd/diseases/ctf/facts.shtml#more

What is Tick-borne Colorado Tick Fever (CTF)?

Colorado tick fever (CTF) is a tick-borne viral illness of humans in the United States. This disease is caused by infection with the Colorado tick fever virus, a member of the Coltivirus genera. In the past, it has been named Mountain fever or American mountain fever. CTF virus was first isolated from human blood in 1944.

How do people get CTF?

The organism that causes CTF is transmitted by the bite of an infected tick. The Rocky Mountain wood tick (Dermacentor andersoni) is the principal carrier of CTF in the United States. Some cases have been associated with exposures to the virus in laboratory settings and one case followed transfusion of blood from a person infected with CTF virus within 4 months of donation.

What are the symptoms of CTF?

Patients infected with CTF virus often develop a two-staged fever and illness following an average incubation period of 4 days (range of 1-19 days) after a tick bite. The early signs of CTF are often nonspecific and may resemble many other infectious and non-infectious diseases. Initial symptoms may include sudden onset of fever, chills, headache, pain behind the eyes, light sensitivity, muscle pain, and generalized malaise. Abdominal pain, nausea and vomiting may occur during the course of the illness in addition to a rash. Flat or pimply rashes may occur in 5% to 12% of cases. The acute illness lasts 5 to 10 days, and in half of the cases, a first phase, with fever lasting 2 to 3 days is followed by a period without fever of 24 to 72 hours with anorexia and malaise. A second phase consisting of a return of fever and an increase in symptoms lasts for about 48 hours. Two important symptoms are fever (two-staged in 50% of cases) and a recent tick bite. CTF can be a severe illness, especially in children under 10 and older adults. Hospitalization may occur in 20% of CTF cases.

(BTW: it leads to pancytopenia)

Where do the most cases of CTF occur in the United States?

CTF is a seasonal disease, and occurs in mountain forest habitats at altitudes from 4,000 to 10,000 feet in the Rocky Mountain region of the United States during the months of February through October. Approximately 90% of cases occur between April and July. Half of all cases are reported from Colorado and Idaho. An assessment of reported cases 1980 and 1988 revealed that of the 1,432 cases reported, the highest number (256) was from Colorado. Although no asymptomatic infections are known to occur, the disease is easily confused with other infections and is extensively underreported. Here in Oregon, 296 cases of CTF were reported from 1950 through 1983 with 82 (28%) residing in Harney County and 77 (26%) residing in Deschutes County (where Bend is).

mcrislip Eitiology, Virus

I no long remember why I became a doctor, it was too long ago and I barely remember yesterday anymore.

But I do remember why I remain one, and its because it is so cool.

It is nice to make people better and talk with them and help them, don’t get me wrong. But the fun, what really bakes my potato, is figuring out the diagnosis before the cultures pop positive.

Like the patient today. Old heart transplant, as an outpatient he has a new temporal headache, and, despite the negative biopsy (which are known to have a high false negative rate) he is put on high dose prednisone for temporal arteritis.

He declines, has hemoptysis, a nodular upper lobe infiltrate on CT and develops petechiae on his legs.

He is admitted, his blood cultures grow a yeast and he is transfered to my hospital.

I am far more often wrong than I am right, and it is always annoying how often reality gets in the way of a good diagnosis. I wish I were a CAM provider and did not have to worry about that.

I said that it will be Cryptococcus, that it is the ONLY diagnosis possible, and by golly his serum cryptococcal antigen is > 1:2048. CNS evaluation is in process.

It always impresses people when you hit one out the ballpark.

In my mind there are two take homes.

One. And I can’t prove this by any data that I can find, but my local rheumatologist agrees. If you are on transplant medications, you cannot develop a vasculitis. I wonder if the temporal arteritis was, in fact, early cryptococcal disease.

B. Disseminated cryptococcus causes petechiae. I didn’t know that. Red bumps and molluscum contagiosum are the most common manifestations. Ulcers and cellulitis less so, and while I cannot find it on pubmed, doing the google on the interwebs finds all sorts of references.

III. 3 out of 2 people do not understand arithmetic, but everyone seemed to worry it might be Candida. Candida does not get in the blood stream unless there is a intravascular catheter, which he does not have. Just because he has a heart transplant doesn’t mean he is equally at risk for all fungi. Candida just ain’t on the list.

Thats now four cases of cryptococcus, three in less than a month.

This will be the year of cryptococcus and west nile in Oregon.

Something wicked this way comes.

Cue up the music from Jaws.

=====

Arch Dermatol. 1996 May;132(5):545-8.

Cutaneous Cryptococcus infection and AIDS. Report of 12 cases and review of the literature.

BACKGROUND: Cryptococcal infections occur in 6% to 13% of patients with acquired immunodeficiency syndrome (AIDS), most commonly infecting the central nervous system. Cutaneous lesions have been described morphologically as umbilicated papules, nodules, and violaceous plaques and can mimic molluscum contagiosum and Kaposi’s sarcoma. Cutaneous lesions can present months prior to other signs of systemic infection.

OBSERVATIONS: Cases of infection with cutaneous Cryptococcus and AIDS were reviewed and compared with cases reported in the literature. Among patients with Cryptococcus infection and AIDS seen at our institutions, 5.9% had skin lesions. All patients with cutaneous lesions had systemic involvement. Women were less commonly infected than men. There was no apparent predisposition associated with age, race, or human immunodeficiency virus infection risk factors. The median CD4 helper T-cell count was 0.024 X 10(9)/L (24/microL), and 44% (16/36) of the patients had previous opportunistic infections. Lesions were most commonly seen on the head and neck (78% [36/46]) and often mimicked molluscum contagiosum (54% [25/46]). The median serum and cerebrospinal fluid cryptococcal antigen titers were 1:32,768 and 1:512, respectively. Patients in our group did well with therapy (one death at 6 weeks, compared with 38% [13/34] mortality in the literature). There was no correlation between onset of lesions, number of lesions, CD4 helper T-cell count, or histopathologic characteristics. CONCLUSIONS: Disseminated Cryptococcus infection in AIDS presents with cutaneous lesions in up to 6% of cases. Clinicians need to be aware of the varied morphologic characteristics, since cutaneous lesions may present well in advance of other signs of systemic infection.

   PMID: 8624151

mcrislip Eitiology, Fungi

There is an ongoing ‘discussion’ in my family of what is better: rice or potatoes. I am a rice fan, my wife prefers potatoes. Mashed, fried, boiled or baked, she like her hot potatoes.

And that brings us to the clinical sign of the hot potato voice.

What is it about old time Doctors and their urge to descrbie everythung after one food or another? Makes eating less enjoyable.

Todays patient had fever, bad sore throat, was toxic appearing with a marked left shift. There was also a soft, deeper than usual, whispery voice, the hot potato voice, so called because it sounds as if the patient talks as if there is a hot potato in their mouth.

This is a sign of peritonsillar abscess or cellulitis.

And sure enough the CT showed two early tonsil abscesses and peritonsillar inflammation, and, though the magic of antibiotics, the patient is getting better.

However. Let’s see a show of hands: everyone who has listen to someone talk with their mouth full of hot potato. I thought so. Nobody.

And is the peculiar way of talking with a peritonsillar abscess really like talking with a hot potato in your mouth? There is no question in medicine that is not worth a study. Dr MF Bhutta compared the talking of people with tonsillitis to them what had a hot potato in their mouth and the sounds were different:

“The study, Hot Potato Voice in Peritonsillitis: A Misnomer, appeared in the Journal of Voice. “Voice changes are a well-recognised symptom in patients suffering from peritonsillitis,” it says. “The voice is said to be thick and muffled, and is described as a ‘hot potato voice’, because it is believed to resemble the voice of someone with a hot potato in [their] mouth. There have been few studies analysing … the voice changes in tonsillitis or peritonsillitis and none that have compared these changes with those that occur with a hot potato in the oral cavity.”

To remedy this lack of knowledge, the three doctors recruited two sets of volunteers. The first group comprised 10 hospital patients whose suffering related to their tonsils. Each volunteer pronounced three particular vowel sounds, which the doctors recorded and subsequently analysed using special software.

The second group were 10 healthy hospital staffers, “with each of these participants placing a British new potato of approximately 50 grams in their oral cavity, warmed by microwave to a ‘hot’, but not uncomfortable, temperature”.

The doctors detected unmistakable differences. The unique sound of someone burdened with an actual potato, they explain, “is related to interference with the anterior tongue function from the physical presence of the potato.”

There are obvious flaws in the study. The potato should have been an Idaho baker, not a new potato Wrong thermodynamics. Part of the reason people with tonsillitis talk that way is to decrease the pain they have when talking. The potato should have been HOT, not hot. It should hurt.

They need to repeat the study, or use hot pizza instead.

Baboon butts and hot potatoes, this blog has it all.

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http://www.guardian.co.uk/education/2009/jan/13/improbable-research-mahmood-bhutta

J Voice. 2006 Dec;20(4):616-22. Epub 2005 Dec 19.

“Hot potato voice” in peritonsillitis: a misnomer.

Bhutta MF, Worley GA, Harries ML.

Department of Ear Nose and Throat, The Royal Sussex County Hospital, Brighton, UK.

The “hot potato voice” is widely recognized as a symptom of peritonsillar cellulitis or abscess; yet there have been no studies assessing the resonance characteristics of the vocal tract in peritonsillitis. Analysis was undertaken of formant frequencies in the articulation of the vowels /i:/. /a:/ and /u:/ in six subjects with peritonsillitis and compared with articulation once the peritonsillitis had settled. Significant variation was found in F1 when articulating /i:/ and in F2 when articulating /a:/, which are explainable by dyskinesis of the peritonsillar musculature. These findings were compared with six subjects articulating the same vowels with and without a hot potato in their mouth. Variation was found in both F1 and F2 when articulating /i:/, which can be related to interference of the potato with movement of the anterior tongue. The changes in the vocal tract differ in these two cases and the title “hot potato voice” in peritonsillitis is a misnomer.

PMID: 16360301

mcrislip Eitiology

Oregon is the best place to live on earth. Period. But don’t tell anyone. One of the delights are the strawberries, which are not the fibrous only slightly sweet posers that come from California. Oregon strawberries are luscious, but do not travel, going bad in less than 48 hours after picking.

The season usually doesn’t begin to June, but for me the season started early.

Fevers, hypotension, acute renal failure, altered mental status, a diffuse erythroderma that included the palms and sole, red conjunctiva and the tongue. The tongue was cool. It looked like a strawberry. Not the best I have seen, that being in a case of post partum toxic shock syndrome (yes, it’s a case of Staphylococcal toxic shock syndrome) where it looked like a big Hood River strawberry. Didn’t taste like it, though. (Just joking).

Strawberry tongue has a limited differential: Toxic shock syndrome, both Staph and strep, scarlet fever, and Kawasaki’s.

There is also, evidently, a recurrent familial form. And there can be a white strawberry and a red strawberry, but not a chocolate covered, strawberry tongue.

Here are some links (to not violate copyright):

http://th03.deviantart.com/fs37/300W/i/2008/249/a/d/Strawberry_Tongue_by_DragonInk7.jpg

http://static.desktopnexus.com/wallpapers/43540-bigthumbnail.jpg

as well as a more legitimate example:

http://www.nature.com/bdj/journal/v186/n6/thumbs/4800085-f1.jpg

Google images is full of example.

I cannot find why TSS causes a strawberry tongue and cannot find reports of a tongue biopsy, as well as why Kawasaki’s cause the same physical finding. What does Kawasakis have in common with TSS? Got me.

But I did find Baboon syndrome, where you get a rash that looks like a baboon butt. Cool. It can be due to the same toxin that causes scarlet fever, so there is a link.

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Clin Exp Dermatol. 2009 Apr;34(3):355-7. Epub 2008 Aug 9.   SDRIFE (baboon syndrome) induced by penicillin.

We report a patient who developed a drug rash after systemic administration of amoxicillin. After oral re-exposure to the alternative beta-lactam antibiotic phenoxymethylpenicillin, the patient developed a sharply demarcated V-shaped erythema of the inguinal region, the thighs, and the gluteal area, resembling the buttocks of baboons. Historically, the condition coined ‘baboon syndrome’ was described as a special entity of a mild systemic cutaneous erythema after oral exposure to type IV allergens, such as nickel, mercury or drugs. Recently, it has been proposed to replace this term by the acronym SDRIFE (symmetrical drug-related intertriginous and flexural exanthema) for those reactions occurring after exposure to systemic drugs. PMID: 18699835

J Dermatol. 2003 Jan;30(1):69-71. A case of baboon syndrome associated with group a streptococcal infection.

We described a 21-year-old Japanese patient with sore throat, fever, and diffuse erythema on the neck, trunk, and limbs. Erythema markedly appeared on the neck, axillary, antecubital, and popliteal fossae. However, other skin signs of scarlet fever such as red strawberry tongue and linear petechial eruption did not appear. Before his visit to our clinic, he had been diagnosed as pharyngitis and treated with cefaclor 750 mg daily for six days. However, the symptoms did not improve. Oral prednisolone of 20 mg daily rapidly improved all the symptoms. Pharyngeal culture grew Streptococcus pyogenes that was sensitive to cefaclor. Laboratory findings showed elevated serum levels of antibody against streptolysin O. Together with the distribution of erythema, culture of Streptococcal pyogenes, and elevated anti-streptolysin O titer, the diagnosis of baboon syndrome associated with streptococcal infection was made. This seems to be the first report of baboon syndrome due to streptococcal infection.

PMID: 12598713

mcrislip Eitiology

Technology becomes increasingly available. I heard that there is now a ultrasound probe that uses your iPhone as the screen. I am sitting in the parking lot at the mall, with my netbook in my lap as my children look for a mothers day present.

And the anesthesiologists have transesophageal echocardiograms and they can check out cardiac function any time they please, and this time they pleased.

Patient has a chronic foot infection that needs debridement and in the OR the anesthesiaologists slip that old probe down the esophagus and there is the heart, beating away nicely and there is that aortic valve and, hey, what the…

A vegetation.

Really. I looked at the ECHO and it sure looks like a veggy to me, a 6 mm clot on the tip on the aortic valve, flopping in and out.

Once I get to talk to him and examine him he has no consitutional symptoms, no murmer, no emboli, no lab findings of IE. Nothng to suggest endocarditis but a really abnormal TEE.

Blood cultures are negative, but he is on antibiotics for the foot infection.

Classically, an incidentaloma is an adrenal mass found in CT when you were not expecting it.

It does not typically refer to a vegetation on a valve, but I have been called twice this year about unexpected clots on valves. The other was a 1.4 cm aortic vegetation that was found on a routine ECHO obtained for other reasons.

So what is it? Treated endocarditis? Partially treated endocarditis? Culture negative endocarditis? Murantic endocarditis? A really really really odd tumor on the valve? I don’t know. Only way to know is to cut it out, and that hardly seems worth it. The heart is one of the few place I can’t get my interventional cardiologists to biopsy. Go figure.

If the cultures remain negative I will send of all the serologies that in 20 years have yet to strike pay dirt. In the end they have to be treated for culture negative endocarditis, safe is better than sorry.

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Ann Cardiol Angeiol (Paris). 2001 Oct;50(6):316-8.

We describe a case of lipomatous hypertrophy of the atrial septum mimicking a tumor of the right atrium. The association of echocardiography and radiology for the detection of this disease is illustrated in this report.

PMID: 12555622

Medicine (Baltimore). 2005 May;84(3):162-73.   Blood culture-negative endocarditis in a reference center: etiologic diagnosis of 348 cases.

To identify the current etiologies of blood culture-negative infective endocarditis and to describe the epidemiologic, clinical, laboratory, and echocardiographic characteristics associated with each etiology, as well as with unexplained cases, we tested samples from 348 patients suspected of having blood culture-negative infective endocarditis in our diagnostic center, the French National Reference Center for Rickettsial Diseases, between 1983 and 2001. Serology tests for Coxiella burnettii, Bartonella species, Chlamydia species, Legionella species, and Aspergillus species; blood culture on shell vial; and, when available, analysis of valve specimens through culture, microscopic examination, and direct PCR amplification were performed. Physicians were asked to complete a questionnaire, which was computerized. Only cases of definite infective endocarditis, as defined by the modified Duke criteria, were included. A total of 348 cases were recorded-to our knowledge, the largest series reported to date. Of those, 167 cases (48%) were associated with C. burnetii, 99 (28%) with Bartonella species, and 5 (1%) with rare, fastidious bacterial agents of endocarditis (Tropheryma whipplei, Abiotrophia elegans, Mycoplasma hominis, Legionella pneumophila). Among 73 cases without etiology, 58 received antibiotic drugs before the blood cultures. Six cases were right-sided endocarditis and 4 occurred in patients who had a permanent pacemaker. Finally, no explanatory factor was found for 5 remaining cases (1%), despite all investigations.Q fever endocarditis affected males in 75% of cases, between 40 and 70 years of age. Ninety-one percent of patients had a previous valvulopathy, 32% were immunocompromised, and 70% had been exposed to animals. Our study confirms the improved clinical presentation and prognosis of the disease observed during the last decades. Such an evolution could be related to earlier diagnosis due to better physician awareness and more sensitive diagnostic techniques. As for Bartonella species, B. quintana was recorded more frequently than B. henselae (53 vs 17 cases). For 18 patients with Bartonella endocarditis, the responsible species was not identified. Species determination was achieved through culture and/or PCR in 49 cases and through Western immunoblotting in 22. Comparison of B. quintana and B. henselae endocarditis revealed distinct epidemiologic patterns. The 2 cases due to T. whipplei reflect the emerging role of this agent as a cause of infective endocarditis. Because identification of the bacterium was possible only through analysis of excised valves by histologic examination, PCR, and culture on shell vial, the prevalence of the disease might be underestimated. Among patients who received antibiotic drugs before blood cultures, 4 cases (7%) were found to be associated with Streptococcus species (2 S. bovis and 2 S. mutans) through 16S rDNA gene amplification directly from the valve, which shows the usefulness of this technique in overcoming the limitations of previous antibiotic treatment. Right-sided endocarditis occurred classically in young patients (mean age, 36 yr), intravenous drug users in 50% of cases, and suffering more often from embolic complications. Finally, 5 cases without etiology or explaining factors were all immunocompetent male patients with previous aortic valvular lesions, and 3 of the 5 presented with an aortic abscess. Further investigations should be focused on this group to identify new agents of infective endocarditis.

PMID: 15879906

mcrislip Eitiology

Hepatocellular carcinomas are bad. Often you can’t cut them out and they are not particularly responsive to chemotherapy. They are preventable, as many are due to chronic hepatitis B. The consult todays is an elderly female from SE Asia with a life time of chronic hepatitis B and now a mass in her liver.

What they do to kill these tumors is cut off its blood supply and they do that mechanically: stuff the hepatic artery that feeds the tumor with beads and gelfoam and the artery clots off and the tumor dies. It works, but is not without its potential problems. Like pockets of pus.

She had several days of fevers, chills, fatigue and, after admission, E. coli in the blood. A CT looking for the source of the E. coli demonstrated that the tumor, which was embolized about a month ago, now has a pocket of gas in it.

Only way to get gas in there is if something is making gas, and, as my 12 year old likes to demonstrate loudly, to be alive is to make gas. While one worries about gas gangrene, the end by product of all metabolism is gas, and every organism, from anaerobes to E. coli to Candida can make gas. The worst gas forming infection I have ever seen, at least in term of quantity of gas made, was a S. aureus infection that looked like a seltzer bottle had been released in his muscles.

Infected infarctions are also problematic to treat as the dead tissue is a huge foreign body with no antibiotic penetration, so they tend to respond poorly to drainage and antibiotics. I am not optimistic that I can cure the infection.

======

Br J Surg. 2005 Oct;92(10):1248-54.Adverse effects of radiofrequency ablation of liver tumours in the Netherlands.

BACKGROUND: Radiofrequency ablation (RFA) is a new treatment for liver tumours. Complications encountered after RFA in the Netherlands were evaluated in the present study. METHODS: Between June 1999 and November 2003 patients undergoing RFA of irresectable liver tumours in eight medical centres were registered prospectively. RESULTS: One hundred and forty-three RFA procedures were performed in 122 patients. RFA was combined with partial hepatectomy in 37 instances. Death occurred after two procedures (1.4 per cent), and was mainly due to concomitant partial hepatectomy. A total of 19 major complications occurred after ten procedures, including biliary tract damage (seven patients), liver failure (four), hepatic abscess (three), peritoneal infection (two), intrahepatic haematoma (one), hepatic artery aneurysm (one) and pulmonary embolism (one). Twenty-four minor complications were related to concomitant partial hepatectomy or laparotomy. The overall complication rate was 20.3 per cent and the rate of complications related directly to RFA was 9.8 per cent. CONCLUSION: The procedure-specific complication rate was almost 10 per cent and it is recommended that RFA should be performed only by an experienced team comprising a hepatobiliary surgeon, gastroenterologist, hepatologist and interventional radiologist. Biliary stricture, hepatic vascular damage and hepatic abscesses were the most common major complications.

   PMID: 15997440

mcrislip Bacteria, Eitiology

Patient has S. aureus bacteremia from heroin use. No surprise. Has a vegetation on the mitral valve, so the diagnosis is not in doubt.

(I once, years ago in another city, got called from a surgeon who had a price of broccoli fall out of her mask and on the the heart. Biggest vegetation I have ever seen.)

So she is sent to the nursing home for treatment of endocarditis and comes in three weeks later with Candida albicans in her blood. Presumptively from her line, so we pull the line, wait a day, and repeat the blood cultures. At day 3 they pop positive. Repeat echo show no new or changed vegetation, but how she has clot in her jugular vein.

Fungal septic thrombophlebitis. Crap. Evidently there are less than 20 cases ever reported on pubmed.

The take home is that sustained positive blood cultures over time means some sort of endovascular infection, usually endocarditis or a catheter infection, but the vascular tree is big and sometimes you have to look around to find the source.

Some coumadin and antifungals and, one hopes, no more heroin, and the patient will get better.

====

Intern Med J. 2009 Jan;39(1):61-3.   Thrombolytic therapy for management of complicated catheter-related Candida albicans thrombophlebitis.

In immunocompromised patients, endovascular infection due to Candida albicans is associated with significant morbidity and mortality. Recommended management includes removal of any existing central venous catheter. Rarely, complications of endocarditis or infected mural thrombi may arise, with poorer clinical outcomes. For large endoluminal lesions, particularly of the great vessels or those that are intra-atrial, thrombolysis has been used in paediatric populations or before surgery for dissolution of infected thrombus. We describe the case of an adult patient with lung carcinoma who developed persisting candidaemia with a large endovascular fungal lesion adherent to the tip of a peripherally inserted central venous catheter. Local urokinase infusion enabled safe removal of the catheter without embolization. As an adjunct to antifungal therapy, local thrombolysis may play a contributory role in the management of central venous catheter-related candidal septic thrombosis.

PMID: 19290985

Clin Infect Dis. 1998 Feb;26(2):393-7.Links

Management of candidal thrombophlebitis of the central veins: case report and review.

Candidemia and major organ candidiasis are problems that emerged in the past 2 decades and that are partially due to medical progress. Catheter-related thrombosis of the central veins is known to be a frequent but mostly subclinical complication of central venous lines. Although candidemia and catheter-related thrombosis are frequent, candida thrombophlebitis of the central veins is rarely reported. We recently successfully treated a 19-year-old polytrauma patient with candidal thrombophlebitis of the innominate vein. Despite catheter removal and therapy with amphotericin B, recurrent candidemia and signs of infection persisted, and a complete resection of the involved vein had to be performed. Only 16 well-documented cases of candidal thrombophlebitis of the central veins in adults have been reported over the past 20 years. An analysis of these 16 patients, together with our patient, is made in relation to risk factors, clinical features, diagnosis, therapy, and mortality.

PMID: 9502461

mcrislip Eitiology, Fungi

Been very busy the last few weeks. We have a French exchange student staying with us, so my evenings are spent showing him the different variations of rain that are available in Portland. It is said, incorrectly, that Eskimo’s have 4 million words for snow, or some such number. In the Pac NW we have far more words for rain, starting with God Damn rain, and moving down. But the bottom line is sometimes there is little time for blogging.

I have a case of something I have not seen in years: PJP. One never says PJP pneumonia, since the second P stands for pneumonia. It is like saying ATM machine. He is an AID’s patient who has not been on HAART for reasons I cannot yet discover, but his immune system has been destroyed to the point where he has PJP.

PJP is short for peanut butter and jelly, no, sorry, Pneumocystis jirovecii Pneumonia, a disease that, thanks to prophylaxis and HAART is almost a disease of historical interest in AIDS. I do not think I have seen an AIDS related case this century, although, thanks to anti-TNF antibodies and other immunosuppressive agents, I have seen PJP in many patients being treated for Lupus, rheumatoid arthritis, and other such diseases.

Back in day, when nickels had bumble bees and the style was to wear an onion on your belt, there were always a few PJP patients in the hospital. Now, residents can go an entire career and not see one.

Another triumph of modern medicine. I really don;t want it to come back.

====

Chest. 2009 Mar 2.    Trends in Hospitalizations for AIDS-Associated Pneumocystis jirovecii Pneumonia in the United States (1986-2005).

Background Although hospitalizations for AIDS-associated Pneumocystis jirovecii pneumonia (PCP) in the United States have decreased since the introduction of chemoprophylaxis and potent combination antiretroviral therapy (ART), PCP remains an important cause of illness and death among AIDS patients.

Methods We analyzed trends in AIDS-associated PCP hospital discharges using the National Hospital Discharge surveys between 1986 and 2005.

Results An estimated 539 million patients were discharged from hospitals between 1986 and 2005, of which an estimated 312,411 had AIDS-associated PCP. The proportion of AIDS-associated PCP discharges decreased from 31% before the introduction of chemoprophylaxis (1986 - 1989) to 17% with chemoprophylaxis (1990 - 1995) and subsequently to 9% after the introduction of ART in 1996 (p < 0.001). Mortality from AIDS-associated PCP decreased from 21% to 16% and subsequently to 7% between these three time periods (p < 0.001). Among those who received mechanical ventilation, mortality decreased from 79% in the prechemoprophylaxis era to 31% in the ART era (p < 0.001) alongside a two-fold increase in the use of mechanical ventilation. We also observed a shift in the population at-risk for PCP over time: a greater proportion of blacks, women, and people from Southern states were affected (all p < 0.001).

Conclusions While there have been significant reductions in hospitalizations and hospital mortality for AIDS-associated PCP over the last twenty years, these reductions have not been homogenous across demographic subpopulations and geographic regions and point to new at-risk populations. Furthermore, mortality in severe cases of PCP that require mechanical ventilation has improved substantially.

   PMID: 19255292

mcrislip Eitiology

I took my Echinacea, I took my vitamin C, I took my airborne, I took my zinc, and I boosted by immune system with Dannon. And I still got a cold today. Stuffy, runny, scratchy, I am a living Niquil commercial. So I spent my day wearing a mask. Everyone said I looked better.

As usual, lots of cases that I have not yet, and maybe never will, figure out.

Like the 45 year old with a history of asthma, maybe acute pneumonia on CXR (but CT has some nodules), febrile, and a creatinine of 5.

The weird thing is the proptosis. Both of her eyes are bugging out. It will probably be Graves disease common things commonly being common.

But.

If it turns out she does have an hepatorenal syndrome, then maybe the proptosis is a manifestations of Wegener’s. As I learned today thanks to the magic of Pubmed. It would tie it all together nicely.

Ask me in a week, I will let you know if the ANCA is positive.

===

Am J Med. 1977 Jul;63(1):131-41. The ocular manifestations of Wegener’s granulomatosis. Fifteen years experience and review of the literature.

Ocular manifestations of Wegener’s granulomatosis may occur secondary to contiguous granulomatous sinusitis or as a result of focal vasculitis. Contiguous granulomatous sinus disease causes nasolacrimal duct obstruction, proptosis and ocular muscle or optic nerve involvement. Focal vasculitis unrelated to contiguous upper respiratory tract disease is manifested by conjunctivitis, episcleritis, scleritis, corneoscleral ulceration, uveitis, and granulomatous vasculitis of the retina and optic nerve. A review of 29 cases of Wegener’s granulomatosis and three cases of lymphomatoid granulomatosis studied over the past 15 years at the National Institute of Allergy and Infectious Diseases (NIAID) disclosed single or multiple ocular manifestations of disease in 15 patients (47 per cent). The pattern of ocular disease, its relationship to systemic involvement, diagnostic methods and the response to therapy are discussed.

PMID: 327802

mcrislip Eitiology