(I'm not providing you with medical advice. Clinical correlation and professional interpretation required)
Tuesday, December 16, 2008
Day #159 - Fever of Unknown Origin - The Return
Due to fun rounds time constraints -- will point you to my previous blogs on FUO -- here.
Wednesday, December 10, 2008
Day #153 - Pneumocystis (PCP) Redux
Today we heard a case of PCP pneumonia with a classic presentation. For those of you who will end up doing medical education -- you should start saving up cases during your residency that you can use as exemplars of diagnoses, management, or approaches -- especially if they have key teaching points or interesting imaging. This will also help you for when you are suddenly called upon to provide impromptu teaching.
I have previously blogged in detail about PCP here. This blog links to a number of other blogs and articles that are also useful.
I have previously blogged in detail about PCP here. This blog links to a number of other blogs and articles that are also useful.
Wednesday, December 3, 2008
Day# 146 - Two cases
We talked about a case of stroke in a young patient. An approach to stroke in a young patient is outlined briefly here.
The case turned out to be meningovascular syphilis.
Here is an interesting article on the history of syphilis and another which talks about whether or not Shakespeare himself was infected.
The second case was that of massive liver enzyme elevation with synthetic dysfunction. I have previously blogged about hepatitis here.
The case turned out to be meningovascular syphilis.
Here is an interesting article on the history of syphilis and another which talks about whether or not Shakespeare himself was infected.
The second case was that of massive liver enzyme elevation with synthetic dysfunction. I have previously blogged about hepatitis here.
Tuesday, December 2, 2008
Day #145 - Pyogenic Liver Abscess
Today we heard about a great case of pyogenic liver abscess. I wanted to clarify a few points of discussion.
Pathogenesis (most common in blue):
Pathogens
Treatment:
Pyogenic - use emperic coverage that will cover most pathogens above - I.e. Pip/tazo or ceftriaxone/metronidazole. Narrow spectrum to culture results not forgetting anaerobes
Drainage - either IR or surgical -- "Never let the sun set on undrained pus"
Amoebic - metronidazole 750po TID x 10 days followed by luminocidal agent
Hydadid - Specialized surgical care.
Pathogenesis (most common in blue):
- Ascention of pathogens up biliary tree
- Ascention of pathogens through portal circulation. Often in the context of an intraabdominal nidus of infection like diverticulitis. May be in context of septic portal thrombophlebitis
- Cyptogenic
- Direct innoculation from trauma or iatrogenic
- Hematogenous spread from systemic infection
- Direct spread from gallbladder infection
Pathogens
- Gpc - strep milleri and other alpha haemolytic strep.
- Gnr - ecoli and klebsiella. Anaerobes (which often won't grow in culture)
Treatment:
Pyogenic - use emperic coverage that will cover most pathogens above - I.e. Pip/tazo or ceftriaxone/metronidazole. Narrow spectrum to culture results not forgetting anaerobes
Drainage - either IR or surgical -- "Never let the sun set on undrained pus"
Amoebic - metronidazole 750po TID x 10 days followed by luminocidal agent
Hydadid - Specialized surgical care.
Wednesday, November 12, 2008
Day #126 - Hepatitis B
Today we discussed a patient with acute hepatitis on the backgroud of hepatitis B chronic infection. I have previously discussed acute hepatitis, cirrhosis and complications thereof.
I wanted to talk about hepatitis B -- Firstly, this is a great review article and so is this.
Secondly - Serologies:
A natural, but cleared infection will have positive HepB surface antibody and core antibody and no surface antigen
A patient with chronic active hepatitis will have core antibody and in most cases hepatitis B surface antigen. They may also have E antigen (or E antibody). They will not have surface antibody.
For chronic carriers treatment depends on a number of factors -- this table provides an excellent summary:
Note that I link to a lot of NEJM articles. This is my preferred journal. Those of you with a U of T library account have NEJM access via e-journal search in the gerstein library website. We pay for an institutional license @ U of T which you can access at home and there is a licence here at the hospital.
Those of you who would like their own subscription (b/c above don't work) can obtain one here ($~60/year for electronic only ~ $150 for print copy too)
I wanted to talk about hepatitis B -- Firstly, this is a great review article and so is this.
Secondly - Serologies:
- Early in infection you have the production of Hepatitis B Surface Antigen and Hepatitis B Envelope Antigen which represents active infection
- The you develop hepatitis B core IgM then core IgG. These antibodies are not protective
- If you are going to clear your infection you will next develop anti-hepatitis B-EAg antibodies, clear your E antigen and then start to clear your S-Antigen
- You then make hepatitis B surface antibodies
- There can be a window period in between clearing the S-Ag and developing the anti-HepB surface antibody where the only way you will know if they are infected is by the core antibody.
A natural, but cleared infection will have positive HepB surface antibody and core antibody and no surface antigen
A patient with chronic active hepatitis will have core antibody and in most cases hepatitis B surface antigen. They may also have E antigen (or E antibody). They will not have surface antibody.
For chronic carriers treatment depends on a number of factors -- this table provides an excellent summary:
Note that I link to a lot of NEJM articles. This is my preferred journal. Those of you with a U of T library account have NEJM access via e-journal search in the gerstein library website. We pay for an institutional license @ U of T which you can access at home and there is a licence here at the hospital.
Those of you who would like their own subscription (b/c above don't work) can obtain one here ($~60/year for electronic only ~ $150 for print copy too)
Tuesday, November 11, 2008
Day #124 - Pretibial Septic Bursitis
Today's case was of a painter, who did a lot of work on his hands and knees, presenting with acute onset knee pain. We discussed the differential diagnosis in detail and then focused on septic arthritis. I have previously blogged about this here and had linked to an excellent article that I recommend you reading.
In this case, the diagnosis was pretibial septic bursitis, which can mimic septic arthritis and is commonly seen in people who do labor on their hands and knees and is associated with minor traumas. The most common infectious aetiology is stapylococcus aureus.
In this case, the diagnosis was pretibial septic bursitis, which can mimic septic arthritis and is commonly seen in people who do labor on their hands and knees and is associated with minor traumas. The most common infectious aetiology is stapylococcus aureus.
Thursday, November 6, 2008
Day #119 - Adult Onset Still's Disease
This was a great case which the discussant enjoyed taking us through. I have previously blogged about fever of unknown origin here, here and here.
There was a previous special guest blog about FUO here.
Here are articles suggested by the discussant on rheumatologic causes of FUO, Adult Onset Still's Disease, and the use of IL-1 antagonists in the treatment of Still's.
Here is another review on Stills.
There was a previous special guest blog about FUO here.
Here are articles suggested by the discussant on rheumatologic causes of FUO, Adult Onset Still's Disease, and the use of IL-1 antagonists in the treatment of Still's.
Here is another review on Stills.
Tuesday, November 4, 2008
Day #118 - Probable Leptospirosis
Today we heard a case of a returning traveller who suffered complete cardiorespiratory collapse as part of a sepsis syndrome. In this syndrome the patient was hypotensive requiring inopressors, hypoxemic/hypercapnic requiring ventillation, coagulopathic with a microangiopathic hemolytic anemia (see TTP blog and previous anemia/thrombocytopenia blogs) from DIC, and in acute renal failure. In the context of this illness he suffered either myocarditis or a myocardial infarction related to hypoperfusion.
This was as sick as anyone can be and survive and it is a testiment to our critical care system that he did indeed survive.
We spent time discussing the approach to diarrhea, which was his initial presenting symptom.
We then defined sepsis
SIRS Criteria:
Severe sepsis includes sepsis with end organ dysfunction or lactate >4
Septic shock includes severe sepsis with refractory hypotension requiring inopressors
We then talked about the approach to early goal directed therapy in sepsis.
In this case, I believe early appropriate antibiotic therapy would include:
The etiology in this case is unclear but I wonder about leptospirosis. I didn't really want to talk about leptospirosis in detail during the case presentation.... This is the case of leptospirosis in NEJM that I elluded to.
I have provided you with a copy of a talk I once gave on leptospirosis here.
Free tidbits:
Here is an article on fever in the returning traveller
A good review of typhoid fever is here.
This was as sick as anyone can be and survive and it is a testiment to our critical care system that he did indeed survive.
We spent time discussing the approach to diarrhea, which was his initial presenting symptom.
We then defined sepsis
SIRS Criteria:
- Fever or hypothermia
- WBC >12,000 or less than 4,000
- HR >90
- RR >20
Severe sepsis includes sepsis with end organ dysfunction or lactate >4
Septic shock includes severe sepsis with refractory hypotension requiring inopressors
We then talked about the approach to early goal directed therapy in sepsis.
In this case, I believe early appropriate antibiotic therapy would include:
- Vancomycin (in case of community associated MRSA in a young man)
- Meropenem (to cover streptococcus, gram negatives including ESBL/drug resistant)
- Doxycycline to cover leptospirosis
The etiology in this case is unclear but I wonder about leptospirosis. I didn't really want to talk about leptospirosis in detail during the case presentation.... This is the case of leptospirosis in NEJM that I elluded to.
I have provided you with a copy of a talk I once gave on leptospirosis here.
Free tidbits:
Here is an article on fever in the returning traveller
A good review of typhoid fever is here.
Thursday, October 23, 2008
Day #113 - Fever of Unknown Origin (FUO)
Today we talked about a case of true FUO. The discussant is published on the issue and I have linked to that article in previous blogs.
FUO blog #1
FUO blog #2
FUO blog #1
FUO blog #2
Tuesday, October 21, 2008
Day #111 - TB Pleuritis
Today we talked about a great case.
There is a *great* free resource called the Canadian Tuberculosis Standards available here.
First we talked about the diagnosis and treatment of latent tuberculosis infection.
Diagnosis:
Diagnosis:
Acute to subacute illness (2/3 present less than 1 month) with fever, pleuritic chest pain, minimally productive cough. Unilateral effusion.
There is a *great* free resource called the Canadian Tuberculosis Standards available here.
First we talked about the diagnosis and treatment of latent tuberculosis infection.
Diagnosis:
- Positive mantoux test
- Interpret in context of patient's history
- less than 5mm - negative (or false negative in immunosuppressed or very ill patient)
- 5mm-10mm - HIV, close contact with known case, chest xray evidence of old TB as fibronodular disease, children, immunosuppression (chemo, TNF alpha, high dose steroids)
- Greater than 10 - positive for all others
- Increase in 6 from previous known positive.
- BCG -- only consider BCG as the cause of a TST if it was given after 12 months of age to a patient from a low risk country and does not have radiographic evidence of old TB
- Interpret in context of patient's history
- Can consider inferferon based assay, though this is not the standard
- Evidence of prior tuberculosis on imaging
- No evidence of active disease
- Tend to treat people who are at the highest risk of re-activating or those with the lowest risk of drug side-effects
- High risk includes: HIV, organ transplant, TNF alpha inhibitors and other immunosuppression
- Risk in health normal person is ~ 5% in first 2 years and 10% over the lifetime
- Immigration and reactivation risk
- INH 300mg PO OD x 9 months with Vitamin B6 25mg po OD
- Alternative (not as good): RIFAMPIN 600mg po OD x 4 months
Diagnosis:
Acute to subacute illness (2/3 present less than 1 month) with fever, pleuritic chest pain, minimally productive cough. Unilateral effusion.
- Exudative effusion
- pH usually ~ 7.4
- Glucose usually normal
- Lymphocytic pleocytosis (though can be neutrophils early)
- Usually less than 5% mesothelial cells
- AFB stain less than 10%
- Culture ~ 30% (yield may improve by inoculating into special culture media)
- PCR positive in 90-100% of culture positive but only 30-60% of culture negative
- Sputum positive in ~ 50%
- Pleural biopsy shows either granulomas or AFB or is culture positive in up to 95%
- INH, RIF, ETH (add PZA if sputum positive, sick, bilateral effusions, other extrapulmonary disease) x 2 months then if INF/RIF sensitive INF/RIF to complete 6 months
- Adjuvant steroids are not clearly indicated
- Effusion may take up to 6 months post treatment to resolve.
Friday, October 10, 2008
Day #101 - Eosinophilia
Today we discussed a case of hypereosinophilia.
We discussed the differential diagnosis of eosinophilia including:
We discussed the differential diagnosis of eosinophilia including:
- Idiopathic Hypereosinophilic Syndrome (HES)
- Eosinophilic malignancies
- Systemic mastocytosis
- Associated with lymphoma (IL5 production)
- Infections
- Parasitic (during tissue invasion): strongyloidiasis, ascariasis, hook worm, angiostronyliasis, liver flukes (fasciolysis, chlonorcis), trichenosis, filariases, paragonamiasis.
- Viral: HIV
- Fungal: Aspergillosis (especially ABPA), coccidiomycosis
- Parasitic (during tissue invasion): strongyloidiasis, ascariasis, hook worm, angiostronyliasis, liver flukes (fasciolysis, chlonorcis), trichenosis, filariases, paragonamiasis.
- Allergy including asthma
- Medications
- NSAIDS, allopurinol, phenytoid, semisynthetic penicillins, ASA
- NSAIDS, allopurinol, phenytoid, semisynthetic penicillins, ASA
- Autoimmune disease
- Addison's disease (usually low level)
- Cholesterol embolism
Thursday, October 9, 2008
Day #100 - Pleural Effusion/Empyema
Today we talked about the approach to pleural effusions:
1) How to do a thoracentesis
Pleural fluid can be mainly water (transudate) or exudative: blood (hemothorax), pus (empyema/complicated parapneumonic effusion), inflammatory, or chyle (chlothorax)
2) Light's Criteria for transudate vs. exudate
One of:
This article discusses liklihood ratios for each value of these measurements and can be really helpful.
3) Management of complicated pleural effusion/empyema (great article here)
Shameless self plug: here is my talk on the epidemiology of pneumococcal empyema.
1) How to do a thoracentesis
Pleural fluid can be mainly water (transudate) or exudative: blood (hemothorax), pus (empyema/complicated parapneumonic effusion), inflammatory, or chyle (chlothorax)
2) Light's Criteria for transudate vs. exudate
One of:
- Protein in pleural fluid >0.5 plasma
- LDH in pleural fluid >0.6 plasma
- LDH in pleural fluid >2/3 upper limit of normal in serum
This article discusses liklihood ratios for each value of these measurements and can be really helpful.
3) Management of complicated pleural effusion/empyema (great article here)
- "The Sun Should Never Set of An Undrainded [Unsampled] Parapneumonic Effusion"
- Sample the fluid at least
- If >50% of lung has effusion, loculated, air-fluid levels, pleural thickening or pleural enhancement on CT highly suggestive that you will need drainage
- Aspiration of frank pus, anaerobic smell, positive gram stain/culture, pH below 7.2, LDH >1000 imply you will need drainage
- Drainage options include:
- repeated thoracentesis
- pig tail catheter (probably safer than surgical chest tube, less morbidity, but more likely to become clogged if frank pus. can also be inserted by seldinger technique with initial thoracentesis)
- surgical chest tube (probably required for very thick, poorly flowing purulent material. higher morbidity than pig-tail)
- VATS drainage: for failure of above, for patients with chronic empyema, ongoing sepsis, if need for decortication of "trapped lung"
- "The Sun Should Never Set of An Undrainded [Unsampled] Parapneumonic Effusion"
Shameless self plug: here is my talk on the epidemiology of pneumococcal empyema.
Wednesday, October 8, 2008
Day #99 - PCP Pneumonia
Today we talked about a classic case of PCP pneumonia as a presenting illness for HIV.
Classically PCP presents with progressive dyspnea, usually initially with exertion then at rest, with dry hacking cough and fever. Classically the respiratory exam is relatively normal (sometimes there is a pleural rub) despite often remarkably abnormal chest x-ray. The classic x-ray, shown here, is of bilateral perihilar infiltrates.
LDH is usually elevated but can be normal in up to 10%. LDH can also be elvated in a number of other infections and malignancies.
Exercise induced desaturation is classic and one can do walking oximetry on their patients to see this effect.
The diagnosis is confirmed by direct calciflor stain or silver stain for organisms in the sputum, induced sputum, or BAL fluid.
There is some evidence that high resolution CT can be helpful in excluding the diagnosis and perhaps saving a bronchoscopy.
Treatment is ideally TMP/SMX (dosed 15mg/kg TMP component divided TID/QID) either IV or PO depending on status. Adjunctive steroids should be considered in patients who are hypoxemic on presentation (PaO2 <70,>35), who are in severe respiratory distress, or who have poor cardiopulmonary reserve. Ironically, this Toronto study showed that steroids did not influence outcome but did reduce septra intolerance. However, a cochrane metanalysis showed a NNT of 9 to prevent one death.
The use of HAART in acute PCP remains contraversial. You shouldn't stop someone's HAART if they are on it already (unless it is clearly failing); however, initiation of new HAART is unclear. Some studies show survival benefit, others mortality.
There have been many studies looking at prognostication. Obviously more severe disease at presentation is related to more adverse outcomes. This study found that age, previous history of PCP, treatment other than TMP/SMX, CMV PCR+ in the BAL, and previous use of PCP prophylaxis when diagnosed were all highly associated with mortality.
This simple prognostic score seemed to identify survivors from those who died.
I have previously written about HIV and cryptococcal meningitis here and here. These blogs link to the HIV treatment guidelines as well as the guidelines for the management of opportunistic infections.
Classically PCP presents with progressive dyspnea, usually initially with exertion then at rest, with dry hacking cough and fever. Classically the respiratory exam is relatively normal (sometimes there is a pleural rub) despite often remarkably abnormal chest x-ray. The classic x-ray, shown here, is of bilateral perihilar infiltrates.
LDH is usually elevated but can be normal in up to 10%. LDH can also be elvated in a number of other infections and malignancies.
Exercise induced desaturation is classic and one can do walking oximetry on their patients to see this effect.
The diagnosis is confirmed by direct calciflor stain or silver stain for organisms in the sputum, induced sputum, or BAL fluid.
There is some evidence that high resolution CT can be helpful in excluding the diagnosis and perhaps saving a bronchoscopy.
Treatment is ideally TMP/SMX (dosed 15mg/kg TMP component divided TID/QID) either IV or PO depending on status. Adjunctive steroids should be considered in patients who are hypoxemic on presentation (PaO2 <70,>35), who are in severe respiratory distress, or who have poor cardiopulmonary reserve. Ironically, this Toronto study showed that steroids did not influence outcome but did reduce septra intolerance. However, a cochrane metanalysis showed a NNT of 9 to prevent one death.
The use of HAART in acute PCP remains contraversial. You shouldn't stop someone's HAART if they are on it already (unless it is clearly failing); however, initiation of new HAART is unclear. Some studies show survival benefit, others mortality.
There have been many studies looking at prognostication. Obviously more severe disease at presentation is related to more adverse outcomes. This study found that age, previous history of PCP, treatment other than TMP/SMX, CMV PCR+ in the BAL, and previous use of PCP prophylaxis when diagnosed were all highly associated with mortality.
This simple prognostic score seemed to identify survivors from those who died.
I have previously written about HIV and cryptococcal meningitis here and here. These blogs link to the HIV treatment guidelines as well as the guidelines for the management of opportunistic infections.
Tuesday, October 7, 2008
Day #98 - Pneumonia
Today we talked about a case of pneumonia. I previously presented a case of pneumonia in "case of the week" back in July.
We stressed the management which includes:
We stressed the management which includes:
Stabilize the patient:
- IV fluids, pressors if required, oxygen, mechanical ventilation if required. Early goal directed therapy.
Obtain microbiological specimens:
- sputum, blood culture, legionella urinary antigen if appropriate, other special tests as appropriatge
- pathogens most likely: streptococcus pneumoniae, haemophilus influenza, moraxella catarrhalis, staphylococcus aureus (including MRSA if risk factors), legionella, mycoplasma pneumoniae, chlamydia pneumoniae
Empiric antibiotic therapy (within 4h)
- Cover the most likely pathogens
- IDSA/ATS joint guidelines (are being revised to make more use of beta-lactams -- my suggestions include these guidelines and some new evidence)
- Healthy young person: macrolide (like azithromycin 500mg po x1 then 250mg po OD x 4d), beta-lactam like amoxicillin (1g po TID)
- Older, more ill:
- respiratory fluoroquinolone (like levofloxacin -- 750mg po Q24h x 5days)
- beta-lactam (ceftriaxone 1g IV q24, amoxicillin - high dose) plus macrolide
- MRSA: vancomycin (1g IV q12, renal dosed)
- Pseudomonas or other hospital acquired: Piperacillin-Tazobactam (4.5g IV q8h infuse over 4 hours) or Meropenem (1g IV q8h infuse over 4 hours)
Decision re: admission
Decision re: sending home
- Eating, drinking, mobilizing
- Off oxygen
- Ideally afebrile
- tolerating PO antibiotics
- Reliable follow up
Wednesday, October 1, 2008
Day #93 - Staphylococcus Aureus Bacteremia
Today we talked about a patient who presented with a febrile gastrointestinal illness who happened to have two diagnoses. First, a probable viral gastroenteritis acquired from his daycare aged son. Second, a concomitant staphylococcus aureus bacteremia.
I wanted to talk about the management of Staphylococcus Aureus Bacteremia. There is a good article here on the management of MRSA bacteremia.
Treatment:
In medicine we often attempt to find one unifying diagnosis that explains all symptoms -- in satisfying what is known as Occam's Razor.
The important teaching point in a complicated case like this is that the patient may have multiple diagnoses and that we must keep an open mind. In response to Occam's Razor, Hickam's Dictum states that "[the patient] can have as many diseases as the damn well please".
I wanted to talk about the management of Staphylococcus Aureus Bacteremia. There is a good article here on the management of MRSA bacteremia.
- Never treat staphylococcus aureus in the blood as a contaminant. Like fungus in the blood, this always needs to be treated!
- The *minimum* treatment duration is 14 days (intravenous). This is for uncomplicated infections only.
- Risk factors for complication:
- Longer duration of illness
- Community acquired infection
- Persistent fever at 72h (OR 2)
- Persistent positive blood culture at 96h (OR 5)
- Hemodialysis patients
- Indwelling lines or other prosthetic material
- MRSA
- No identifiable source for the bacteremia (i.e. no skin or line focus)
- Blood cultures positive within 14 hours of drawing them
- Risk factors for complication:
- You need to exclude bacterial endocarditis. Present in 10-13% of cases...
- TEE is much more sensitive than TTE for making this diagnosis (103 patients with SA -- TEE dx endocarditis in 25%, TTE only found 7%). In patients for whom you are planning 14d therapy (particularly those who have risk factors for complication) you should probably not rely on a TTE to exclude IE.
- Can also cause pacemaker and AICD infections
- Vertebral osteomyelitis
- Septic arthritis
- Splenic abscess (persistant fever, LUQ pain)
- Septic thrombophlebitis (particularly with lines)
- Septic pulmonary emboli
- Brain abscess/meningitis/mycotic aneurysms
- Skin/soft tissue abscesses
Treatment:
- Ideal treatment for MSSA is with a beta-lactam like cloxacillin or cefazolin. These are superior head to head with vancomycin for the treatment of MSSA.
- Removable foci should be removed if feasible and practical to do so
- Duration depends on complications. IE 4-6 weeks. Osteo ~6 weeks.
- 20 to 40%!
- Age
- MRSA (OR 9.3)
- Blood cultures positive less than 12 hours (OR 7)
- Complication (OR 9)
In medicine we often attempt to find one unifying diagnosis that explains all symptoms -- in satisfying what is known as Occam's Razor.
The important teaching point in a complicated case like this is that the patient may have multiple diagnoses and that we must keep an open mind. In response to Occam's Razor, Hickam's Dictum states that "[the patient] can have as many diseases as the damn well please".
Tuesday, September 30, 2008
Day #92 - "I don't know"
Wow. What a great case. It isn't often that I truly throw my hands up and say that "I don't know" but this was one of them.
But I hope the exercise in reasoning was useful for you. I think we demonstrated an approach that was safe, cost-effective, and broad in going through the history and physical exam.
Dr. Gold previously spoke about meningitis (bacterial) and that talk is available here.
In approaching a patient with multiple infarcts we need to consider the following differential:
I would confirm whether or not he has had a mantoux. He should have one prior to immunosuppression anyways and should be treated for latent TB if this does not represent CNS TB.
I would probably scan his chest/abdomen/pelvis to look for evidence of malignancy, lymphoma or TB disease -- or something safer than the brain to biopsy and make a diagnosis.
Ultimately he may require a stereotactic brain biopsy to exclude TB and make a diagnosis. In a young man, with progressive infarcts and no other cause, I would discuss this with the patient.
TB is treatable, thrombophilia and emboli preventable, and lymphoma may be cured but CADASIL can not so we had better be sure!
But I hope the exercise in reasoning was useful for you. I think we demonstrated an approach that was safe, cost-effective, and broad in going through the history and physical exam.
Dr. Gold previously spoke about meningitis (bacterial) and that talk is available here.
In approaching a patient with multiple infarcts we need to consider the following differential:
- Emboli - Arising from the heart or great vessels. One possibility is subacute bacterial endocarditis, particularly given the history of night sweats. I think this patient needs blood cultures drawn with blind subculturing (endocarditis blood cultures) to look for unusual pathogens like brucella. I also think he needs a trans-esophogeal echo looking for a cardiac source including a bubble study to exclude PFO. This can also look at the aortic arch.
- Ischemia -- Either bad luck from uncontrolled risk factors, or genetic stroke syndrome like CADASIL, Fabry's or MELAS, or thrombophilia like antiphospholipid antibody syndrome, ATIII deficiency or hyperhomocysteinemia. I would exclude thrombophilia. As a last resort I would look into genetic testing. Night sweats don't fit with ischemia.
- Vasculitis (Night Sweats would fit with this too)
- Primary:
- Primary CNS angiitis
- GCA/Takayatsu, polyarteritis nodosa (patient has Hep B!)
- Secondary due to:
- Infection:
- Syphilis always needs to be considered in young patients who present with stroke like syndromes.
- HIV can do this -- though he is suppressed.
- CNS TB can cause this also (usually have CNS pleocytosis).
- Fungal infections like cryptococcus can do this too.
- Malignancy -- Angioinvasive lymphoma or lymphovascular lymphamatosis
- Infection:
- Primary:
- Other
I would confirm whether or not he has had a mantoux. He should have one prior to immunosuppression anyways and should be treated for latent TB if this does not represent CNS TB.
I would probably scan his chest/abdomen/pelvis to look for evidence of malignancy, lymphoma or TB disease -- or something safer than the brain to biopsy and make a diagnosis.
Ultimately he may require a stereotactic brain biopsy to exclude TB and make a diagnosis. In a young man, with progressive infarcts and no other cause, I would discuss this with the patient.
TB is treatable, thrombophilia and emboli preventable, and lymphoma may be cured but CADASIL can not so we had better be sure!
Thursday, September 25, 2008
Day #87 - Post Influenza Sepsis
This was one of my most memorable cases I presented to the discussant today. The article he asked me to send you is here.
Teaching Points:
In this case, the patient likely had a secondary bacterial infection with lobar pneumonia, sepsis and eventually multiorgan failure. Early recognition and treatment of sepsis is important. The principle is called "Early Goal Directed Therapy". This is a protocol of interventions designed to maximize tissue perfusion and interventions in a rational way.
Essentially this means:
Notable people affected by the 1918 pandemic:
Teaching Points:
- Influenza presents year-round but with a predominantly seasonal distribution. It is a highly transmissible virus with droplet (and possibly airborne particle) spread. Patients present with fever, malaise, lassitude, cough, myalgias, arthralgias and headache. The illness is usually self-limiting lasting approximately 1 week.
- Patients with underlying cardiac disease, respiratory disease, diabetes, or immunosuppression are at high risk of developing severe disease. Pregnant women, in the third trimester are also at risk compared to age-matched controls.
- Vaccines have been shown to have mortality and morbidity benefit, particularly amongst high risk groups. But vaccination of healthy individuals is proposed to have indirect benefit to these high-risk groups as well.
- A study done here in Toronto has shown that admitted patients with influenza, particularly those who are critically ill should be treated with oseltamivir. There is a reduction in mortality.
- Other notable sequelae:
- Primary viral pneumonia or bacterial superinfection -- Most commonly streptococcus pneumoniae or staphylococcus aureus (including community acquired MRSA). This can be severe.
- Viral myocarditis (rare)
- myositis with possible rhabdomyolysis
- Guillain-Barre syndrome, Influenza meningoencephalitis, Transverse myelitis
- Primary viral pneumonia or bacterial superinfection -- Most commonly streptococcus pneumoniae or staphylococcus aureus (including community acquired MRSA). This can be severe.
In this case, the patient likely had a secondary bacterial infection with lobar pneumonia, sepsis and eventually multiorgan failure. Early recognition and treatment of sepsis is important. The principle is called "Early Goal Directed Therapy". This is a protocol of interventions designed to maximize tissue perfusion and interventions in a rational way.
Essentially this means:
- IV crystalloids to maintain central venous pressure of 8-12 (JVP 3-7cm is about that if you don't have a CVP line), normal blood pressure (MAP >=65) and mixed venous oxygen saturation of >=70%
- If still not at goal with crystalloids add vasopressors (i.e. norepinephrine)
- If still not at goal with this and hematocrit <30%,>
- If still not at goal with this, add positive inotrope dobutamine.
- Early appropriate antibiotic therapy
- Source control -- removal of septic focus, drainage of pus, etc --> this is often the neglected step....
- NB: pentastarch may be harmful and so I don't use it. The use of albumin is also contraversial -- an ongoing clinical trial hopes to solve this.
Notable people affected by the 1918 pandemic:
- Woodrow Wilson -- allegedly had meningoencephalitis while signing the treaty of Versailles
- Harvey Cushing -- developed Guillain-Barre post-influenza
- William Osler -- died of empyema (post influenza superinfection)
Wednesday, September 24, 2008
Day 85 - "That sounds bad"
Back pain is one of the most frequent complaints in medicine. Today's case highlighted why it always needs to be taken seriously.
Back Pain:
In the case today the patient had progressive, severe back pain in the context of 2 months of B-symptoms. He presented with cord compression.
Differential:
Back Pain:
- Mechanical: Classically worsens with movement, better with rest. Can be referred down to bilateral hips, thighs.
- Patterns:
- Radiculopathy (classically sciatica): pain radiates in dermatome of nerve root impingement. May be associated with neurologic symptoms (weakness or numbness) in the affected area
- Spinal Stenosis: pain radiates to legs. Worse with activity. Predictably improves with leaning forward, rest
- RED FLAGS:
- Night pain
- B-Symptoms (fever, sweats, weight loss)
- Neurological symptoms including numbness, weakness, bladder incontinence (overflow), fecal incontinence (loss of sphincter tone)
- Known history of malignancy
- Patterns:
- Inflammatory: associated with morning stiffness, aggravated by rest, possibly extra-axial symptoms of connective tissue disease.
- Referred pain
In the case today the patient had progressive, severe back pain in the context of 2 months of B-symptoms. He presented with cord compression.
Differential:
- Malignancy:
- Most commonly prostate, breast, lung. Then RCC, lymphoma and myeloma
- Pain (present in 95%) is often the first symptom, usually preceeding neurologic symptoms by several weeks
- Weakness (up to 85%) and sensory losses follow. Can also have bowel/bladder dysfunction and gait ataxia.
- Patients should get steroids (dexamethasone 10mg IV x 1 then 16mg/day in divided doses tapered over 2 weeks), intravenous pamidronate, and either neurosurgery or radiation.
- This trial showed that for metastatic disease in a single area, surgery +RT was superior to RT alone for solid tumors.
- Infection:
- Other:
- Traumatic, vertebral compression fracture
Friday, September 19, 2008
Day #77 - Malaria
Today we talked about a case of a new immigrant to Canada who presented with cyclical fever and anemia. She had emigrated from a malaria endemic country and had had plasmodium malariae.
JAMA has a great article on malaria available here.
NEJM has a great article on malaria prevention available here.
Also, see my previous approach to anemia and thrombocytopenia.
JAMA has a great article on malaria available here.
NEJM has a great article on malaria prevention available here.
Also, see my previous approach to anemia and thrombocytopenia.
Day #80 - Diarrhea
Today we talked about a case of acute diarrhea. The discussant took us through an excellent approach to acute diarrhea. Some highlights below:
Etiology:
Etiology:
- Infection (great article -- also IDSA diarrhea guidelines)
- Viral: rotavirus, enterovirus, norovirus, etc. (CMV in immunocomprimized)
- Bacterial: shigella, yersinia, e. coli, salmonella, campylobacter, C. difficile, TB (usually chronic), atypical mycobacterial (immunocomprimised)
- Protozoal/Parasitic: Giardia, amebiasis, etc.
- Viral: rotavirus, enterovirus, norovirus, etc. (CMV in immunocomprimized)
- Inflammatory
- UC/Crohn's
- Ischemic
- Small bowel -- pain out of proportion, post prandial pain
- Large bowel -- bloody stool, colitis
- Osmotic
- Laxatives, chewing gum diarrhea (xylulose), sorbitol, sucrose, post-surgical "dumping"
- Laxatives, chewing gum diarrhea (xylulose), sorbitol, sucrose, post-surgical "dumping"
- Endocrine
- Hyperthyroidism, carcinoid syndrome, VIPoma
Wednesday, September 10, 2008
Day #72 - Acute Cognitive Decline
We had actually discussed this case before in early August. At that time there were no myoclonic jerks, mri abnormalities, or eeg triphasic spikes suggestive of the diagnosis (now presumed) of CJD (from nejm or here from CID).
The previous discussion points on acute confusion, aphasia, and neurosyphilis are available here.
The previous discussion points on acute confusion, aphasia, and neurosyphilis are available here.
Tuesday, September 9, 2008
Day #70 - Fever of Unknown Origin III
I missed the rounds -- but have discussed pyrexia of unknown origin twice before. #1 and #2. Probably not as good as the discussant, but I referenced the article they were referring to.
"Special Guest Blog" by the discussant:
"Special Guest Blog" by the discussant:
- Even in the "modern era", up to 1/3 of cases may go undiagnosed -these cases carry a good prognosis.
- Infections only account for 1/4 of all diagnoses.
- In certain cases without diagnosis, the benefits of liver biopsy outweigh the risks.
- Bone marrow cultures are of low diagnostic yield. Bone marrows should be performed only when there are other indications to do so ie unexplained cytopenias.
- I recently cared for a patient with FUO whose Hodgkin's disease was diagnosed on liver biopsy alone. Patients with FUO are challenging to investigate, are rewarding by virtue of the enigmatic causes that are may be found and reinforce the importance of basic principles like the careful history and physical examination.
Wednesday, September 3, 2008
Day #65 - Endocarditis
A confession -- today's case was "recycled" for your benefit -- and so is today's blog.
I have previously blogged on endocarditis, renal failure, and hyperkalemia and direct you to those sections.
I have previously blogged on endocarditis, renal failure, and hyperkalemia and direct you to those sections.
Monday, August 25, 2008
Day #56 - Acute Monoarthritis Redux
We again approached this issue today.
The differential diagnosis of subacute-acute monoarthritis includes:
The differential diagnosis of subacute-acute monoarthritis includes:
- Septic arthritis (gonococcal, non-gonnococcal bacterial, tuberculosis, fungal)
- Crystal (gout, pseudogout AKA CPPD, hydroxyapatate)
- Osteoarthritis flare
More rarely an acute monoarthritis can be a presentation of
- Seropositive and seronegative arthridities including reactive arthritis and post-streptococcal arthritis
- Hemarthrosis (in hemophilia and acquired hemophilia)
We use the history and physical to help us form an opinion on the etiology, but ultimately because septic arthritis is so damaging if missed, a synovial fluid analysis is required if there is suspicion of septic arthritis.
A previous blog discussed septic arthtiris and synovial fluid analysis.
Thursday, August 21, 2008
Day #52 - Multiple possibilities...
Today we heard a very complicated case of a patient with known hematologic malignancy and a previous bone marrow transplant who presented with acute dyspnea, fever, and hypoxemia. The clinical exam was suspicious for congestive heart failure, in particular with RV overload/dysfunction.
We cast an appropriately wide net, thinking about a differential diagnosis that was most consistent with one/multiple of:
In medicine we often attempt to find one unifying diagnosis that explains all symptoms -- in satisfying what is known as Occam's Razor.
The important teaching point in a complicated case like this is that the patient may have multiple diagnoses and that we must keep an open mind. In response to Occam's Razor, Hickam's Dictum states that "[the patient] can have as many diseases as the damn well please".
Another important point is that while inelligant, in significantly ill patients who are awaiting a diagnosis empiric therapy for multiple conditions may be considered. In this case emperic broad-spectrum antibiotics (for example ceftriaxone + quinolone), treatment of CHF (lasix, nitrates as tolerated, ideally IV) , and empiric treatment for PE (based on our clinical suspicion, the high likelihood that a secondary event would be fatal, and the delay in being able to get a diagnostic test) were all appropriate. In this case, with unclear renal function, IV heparin is probably safer.
I alluded to the fact that the date of the allogeneic bone marrow transplant may be relevant to the differential diagnosis. The following figure from uptodate illustrates this point.
Early infections (pre-engraftment of the donor marrow) tend to occur with usual bacterial pathogens (gram positive and negative including pseudomonas), invasive candidiasis and aspergillosis, and herpes simplex and respiratory viruses.
Once the donor marrow has engrafted, the risk of non-encapsulated bacterial infections and decreases. However, the risk of encapsulated organisms and aspergillosis persists and the risk of more unusual opportunistic infections increases. These include CMV and other herpes viruses, toxoplasmosis, and PCP.
Later on, while the risk of VZV and EBV increases as well.
We cast an appropriately wide net, thinking about a differential diagnosis that was most consistent with one/multiple of:
In medicine we often attempt to find one unifying diagnosis that explains all symptoms -- in satisfying what is known as Occam's Razor.
The important teaching point in a complicated case like this is that the patient may have multiple diagnoses and that we must keep an open mind. In response to Occam's Razor, Hickam's Dictum states that "[the patient] can have as many diseases as the damn well please".
Another important point is that while inelligant, in significantly ill patients who are awaiting a diagnosis empiric therapy for multiple conditions may be considered. In this case emperic broad-spectrum antibiotics (for example ceftriaxone + quinolone), treatment of CHF (lasix, nitrates as tolerated, ideally IV) , and empiric treatment for PE (based on our clinical suspicion, the high likelihood that a secondary event would be fatal, and the delay in being able to get a diagnostic test) were all appropriate. In this case, with unclear renal function, IV heparin is probably safer.
I alluded to the fact that the date of the allogeneic bone marrow transplant may be relevant to the differential diagnosis. The following figure from uptodate illustrates this point.
Early infections (pre-engraftment of the donor marrow) tend to occur with usual bacterial pathogens (gram positive and negative including pseudomonas), invasive candidiasis and aspergillosis, and herpes simplex and respiratory viruses.
Once the donor marrow has engrafted, the risk of non-encapsulated bacterial infections and decreases. However, the risk of encapsulated organisms and aspergillosis persists and the risk of more unusual opportunistic infections increases. These include CMV and other herpes viruses, toxoplasmosis, and PCP.
Later on, while the risk of VZV and EBV increases as well.
Monday, August 18, 2008
Day #49 - Cryptococcus and HIV Redux
2 cases of cryptococcal meningitis admitted in 1 week. This is somewhat unusual.
We have previously discussed HIV+Cryptococcus here.
We talked again about the management including:
(a) effective anti-fungal therapy (amphotericin B 0.7mg/kg) induction (14d +/- flucytosine) followed by consolidation with fluconazole 400mg x 10 weeks followed by maintenance with fluconazole 200mg until CD4 >200 x 6 months and
(b) effective management of increased ICP.
If OP >320mmH20 -- they should have aggressive management of ICP (serial LP to <200) or VP shunt
If OP >180 and symptomatic -- they should also have aggressive management
The OP should also be measured at the end of the 14d induction therapy.
FYI -- The US HIV guidelines are available here and here.
For the CC4s we will be discussing HIV again in seminar later this month.
Thursday, August 14, 2008
Day #45 - Fever of Unknown Origin Redux
Today we discussed a very complicated (perhaps too complicated) case of a patient with fever of unknown origin, pancytopenia with granulomas in the bone marrow, probable disseminated intravascular coagulation, altered mental status and abnormal liver function.
The consultant, an infectious diseases specialist, went through a very broad differential diagnosis which I will attempt to re-create for you.
Non-infectious:
Unusual bacterial causes
Some of these were discussed today:
The consultant, an infectious diseases specialist, went through a very broad differential diagnosis which I will attempt to re-create for you.
Non-infectious:
- Hematologic malignancy
- Non-hematologic malignancy (i.e. renal cell carcinoma)
- Venous thromboembolism
- Inflammatory:
- Vasculitis -- i.e. temporal arteritis
- Collagen Vascular Disease -- i.e. SLE
- Endocrine -- i.e. hyperthyroidism
- Periodic Fever Syndromes
- Factitious fever
- Viral:
- HIV, EBV, CMV, influenza, measles/mumps, other.
- Bacterial:
- Endocarditis, occult abscess, osteomyelitis from various pathogens
- Unusual bacterial causes (see below)
- Fungal:
- Endemic fungi such as:
- Histoplasmosis (Ohio river valley, St. Laurence River Valley, Montreal in 1960s, Caves w/bats)
- Blastomycosis (Northwestern Ontario)
- Coccidiomycosis (Southwestern US)
- Endemic fungi such as:
- Mycobacterial
- Parasitic -- i.e. malaria (usually non-falciparum), babesiosis
Unusual bacterial causes
Some of these were discussed today:
- Rat-bite fever
- Meilodosis (travel to Australia, Southeast Asia)
- Plague
- Brucellosis (travel, exposure to sheep, cattle, goats, unpasturized cheese)
- Bartonella Henselae (Cat Scratch Disease)
- Q-Fever (Sheep, Pregnant Cats, high rates in Nova Scotia)
Wednesday, August 13, 2008
Day #44 - HIV
Today's case was a patient with HIV who presented with fever, confusion, headache, anorexia and malaise. His CD4 count was less than 100.
We discussed, based on the clinical features that the patient probably had a CNS infection of a indolent nature. The differential included toxoplasmosis, cryptococcosis, TB meningitis, syphilis, viral encephalitis or non-infectious causes like primary CNS lymphoma. The normal CT scan left cryptococcosus, TB meningitis, syphilis or viral encephalitis. The CSF studies confirmed cryptococcal meningitis, of which this was a fairly classic case.
The IDSA has guidelines for the management of cryptococcal meningitis, and this RCT in NEJM is probably the landmark study.
Remember in HIV there is a marked increase in the risk of certain infections:
We discussed the "AIDS" defining criteria (CD4 less than 200 or specific conditions - see list). Guidelines for the management of HIV and opportunistic infections are available here.
We discussed, based on the clinical features that the patient probably had a CNS infection of a indolent nature. The differential included toxoplasmosis, cryptococcosis, TB meningitis, syphilis, viral encephalitis or non-infectious causes like primary CNS lymphoma. The normal CT scan left cryptococcosus, TB meningitis, syphilis or viral encephalitis. The CSF studies confirmed cryptococcal meningitis, of which this was a fairly classic case.
The IDSA has guidelines for the management of cryptococcal meningitis, and this RCT in NEJM is probably the landmark study.
Remember in HIV there is a marked increase in the risk of certain infections:
- Any CD4 count: TB, pneumococcus, herpes simplex, varicella zoster
- CD4 less than 200 Pneumocystis Carini
- CD4 less than 100 Toxoplasmosis, Cryptococcus
- CD4 less than 50: CMV, Mycobacterium Avium Complex
- The patient is ready to take the medication
- AIDS defining event OR
- CD4 >350 with rapidly decreasing CD4 and very high viral load
- CD4 less than 350 stongly consider starting
- CD4 less than 200 start
- Viral fusion inhibitors (T20)
- Chemokine inhibitors CCR5 (miraviroc)
- Reverse transcriptase inhibitors (NRTI -- eg tenofovir, ermtrictabine/lamivudine, abacavir) and (NNRTI -- effavirenz)
- Protease inhibitors (lopinavir/ritonavir, atazanavir/ritonavir)
- Integrase inhibitors (raltegravir)
We discussed the "AIDS" defining criteria (CD4 less than 200 or specific conditions - see list). Guidelines for the management of HIV and opportunistic infections are available here.
Tuesday, August 12, 2008
Day #43 - Endocarditis
Today we discussed a great case of subacute bacterial endocarditis which presented as renal failure, uremia, and life threatening hyperkalemia. We discussed the approaches to altered level of consciousness and hyperkalemia. We also briefly discussed the approach to renal failure.
I wanted to touch upon the diagnosis of endocarditis. Endocarditis is a clinical and microbiological diagnosis which is established using epidemiologic criteria. The criteria are called the Modified Duke Criteria. They include:
Major Criteria
Microbiologic:
Positive blood cultures (>=2) with an organism that classically causes endocarditis (viridans group streptococci, staphylococcus aureus, enterococcus, HACEK organisms)
OR
Persistantly positive (>=3 or >=2 12h apart) for another organism
Echocardiologic:
Vegetation on valve not otherwise explainable or dehiscence of mechanical valve or abscess
OR
Clinical: *NEW* (not worsening) regurgitant murmur
Minor Criteria
The ACC has updated guidelines on the management of valvular heart disease including endocarditis and endocarditis prophylaxis. These address the diagnostic algorithm and treatment in more detail.
I wanted to touch upon the diagnosis of endocarditis. Endocarditis is a clinical and microbiological diagnosis which is established using epidemiologic criteria. The criteria are called the Modified Duke Criteria. They include:
Major Criteria
Microbiologic:
Positive blood cultures (>=2) with an organism that classically causes endocarditis (viridans group streptococci, staphylococcus aureus, enterococcus, HACEK organisms)
OR
Persistantly positive (>=3 or >=2 12h apart) for another organism
Echocardiologic:
Vegetation on valve not otherwise explainable or dehiscence of mechanical valve or abscess
OR
Clinical: *NEW* (not worsening) regurgitant murmur
Minor Criteria
- Predisposition -- known pre-existing valvular disease or IVDU
- Fever
- Evidence of vascular phenomenon -- septic emboli, mycotic aneurysm, Janeway lesions,
- Immunologic: glomerulonephritis (like this case), positive RF, roth spots, Osler nodes,
- Microbiologic: Blood culture not meeting major
- Echocardiographic not meeting major
The ACC has updated guidelines on the management of valvular heart disease including endocarditis and endocarditis prophylaxis. These address the diagnostic algorithm and treatment in more detail.
Monday, August 11, 2008
Day #42 - Herpes Zoster (Shingles)
This morning we discussed a case of dermatomal vessiculobullous lesions in an immunosuppressed patient.
Differential diagnosis of vessiculobullous lesions::
Treatment of herpes zoster (shingles):
Should be given to:
Treatment options:
Disseminated Zoster (multiple non-contiguous dermatomes) or visceral/end organ involvement should probably be initially treated with IV.
Acyclovir 10mg/kg iv q8h (needs to be renal dosed, is nephrotoxic - need to keep extremely
well hydrated to prevent acyclovir crystals causing ATN)
Acyclovir 800mg po FIVE TIMES DAILY
Famciclovir 500mg po TID
Valacyclovir 1000mg po TID
Duration depends on clinical context. Non-immunosuppressed uncomplicated zoster - 7 days
The article on the zoster vaccine is here.
Differential diagnosis of vessiculobullous lesions::
- Herpes zoster
- Herpes simplex
- Bullous impetigo (staph/strep)
- Ecthyma gangenosum (gram neg esp pseudomonas)
- Hemorhagic bullous cellulitis (nec fasc, clostridial myonecrosis, vibrio
- vulnificus)
- Dermatitis herpeteformis
- Bullous skin diseases (eg bullous pemphigoid)
Treatment of herpes zoster (shingles):
Should be given to:
- Immunocomprimised patients
- V1 Zoster (Zoster Opthalmicus)
- Ramsey hunt syndrome
- Pregnant patients
- Age over 50 (decreases incidence of zoster associated pain)
Treatment options:
Disseminated Zoster (multiple non-contiguous dermatomes) or visceral/end organ involvement should probably be initially treated with IV.
Acyclovir 10mg/kg iv q8h (needs to be renal dosed, is nephrotoxic - need to keep extremely
well hydrated to prevent acyclovir crystals causing ATN)
Acyclovir 800mg po FIVE TIMES DAILY
Famciclovir 500mg po TID
Valacyclovir 1000mg po TID
Duration depends on clinical context. Non-immunosuppressed uncomplicated zoster - 7 days
The article on the zoster vaccine is here.
Thursday, August 7, 2008
Day #38 - Invasive Pulmonary Aspergillosis
Today we talked about a case of a patient with acute myelogenous leukemia on chemotherapy who is presenting with febrile neutropenia.
In this case, the patient had a CT scan which had numerous pulmonary nodules with the so-called CT Halo sign (which is a nodule with ground glass haziness surrounding it). This led to the suspicion for an invasive fungal infection, the most commonly encountered in this population is invasive pulmonary aspergillosis.
If you are interested, you can email me and I will send you a copy of a talk I have given on IPA diagnosis and management.
The key to successful treatment is appropriate antifungal therapy and, if possible, recovery of the neutrophil count and reduction of immunosuppression. Treatment is "usually" for ~12 weeks or complete resolution of the clinical syndrome/lesions, whichever is longer.
In this case, the patient had a CT scan which had numerous pulmonary nodules with the so-called CT Halo sign (which is a nodule with ground glass haziness surrounding it). This led to the suspicion for an invasive fungal infection, the most commonly encountered in this population is invasive pulmonary aspergillosis.
If you are interested, you can email me and I will send you a copy of a talk I have given on IPA diagnosis and management.
The key to successful treatment is appropriate antifungal therapy and, if possible, recovery of the neutrophil count and reduction of immunosuppression. Treatment is "usually" for ~12 weeks or complete resolution of the clinical syndrome/lesions, whichever is longer.
Tuesday, August 5, 2008
Day #36 - Acute Confusion
Today we talked about a case of an elderly woman with an acute confusion. In approaching this problem, the history is important to exclude dementia which was sub-clinical for a long period but subsequently becomes obvious to the family.
We looked at a differential for an acute change in level of consciousness and the following general framework is helpful:
We then talked a bit about aphasias because the patient had anomia with a non-fluent aphasia and inability to understand.
Aphasias
1-naming-if normal - no aphasia
2-command-
DON'T UNDERSTAND
non fluent, no repeat - global aphasia
non fl - can repeat mixed transcortical
fluent - no repeating - wernikes
- can repeat - trans cortical sensory aphasia
UNDERSTAND
non fl--no repeat - brocas
non fl - can repeat - transcortical motor
fl - no repeat - conductive
fl - repeat - no name - nominal
We then entertained the possibility of neurosyphilis or a paraneoplastic syndrome such as paraneoplastic limbic encephalitis.
Neurosyphilis can present with a variable presentation.
"Early" <>
CSF should:
We looked at a differential for an acute change in level of consciousness and the following general framework is helpful:
- Drugs/Iatrogenic
- Infection
- Meningitis (bacterial, viral, TB, other -- e.g. cryptococcal, neurosyphilis)
- Encephalitis (HSV1/2, HIV, CMV, WNV, Eastern Equine encephalitis, other)
- Non-CNS infection with delerium
- Metabolic
- Electrolytes (hyper Ca, hypo/hyper Na, hypoglycemia)
- hypothyroidism. B12/folate not usually acute.
- Structural
- Tumour
- Bleed (SDH, SAH, ICH)
- Other mass lesion
- Epileptogenic focus (post ictal)
- Stroke syndrome
- Vasculitis
- End-organ Failure
- Cirrhosis (encephalopathy)
- CHF
- Respiratory -- Hypoxemia/Hypercarbia
- Renal - Uremia
We then talked a bit about aphasias because the patient had anomia with a non-fluent aphasia and inability to understand.
Aphasias
1-naming-if normal - no aphasia
2-command-
DON'T UNDERSTAND
non fluent, no repeat - global aphasia
non fl - can repeat mixed transcortical
fluent - no repeating - wernikes
- can repeat - trans cortical sensory aphasia
UNDERSTAND
non fl--no repeat - brocas
non fl - can repeat - transcortical motor
fl - no repeat - conductive
fl - repeat - no name - nominal
We then entertained the possibility of neurosyphilis or a paraneoplastic syndrome such as paraneoplastic limbic encephalitis.
Neurosyphilis can present with a variable presentation.
"Early" <>
- asymptomatic
- meningitis (with cranial nerve palsies)
- meningovascular -- clinical picture of strokes, recurrent. Part of the differential for stroke in the young.
- otic syphilis -- tinnitus, vertigo, hearing loss
- occular syphilis -- uveitis, retinitis, vitritis
- General paresis (of the insane):
P - personality changes
A - affect changes
R - reflexes (hyper-reflexia)
E - Eye (argyll-robertson pupils)
S - Sensorium - delusions, hallucinations
I - Intellect
S - Speech (abnormal) - Tabes dorsalis: sensory loss (dorsal columns), ataxia, bladder dysfunction, "lightning" pains in legs
CSF should:
- Have a positive VDRL (specific, but not sensitive)
- OR Have a lymphocytic pleocytosis (WBC >20) and/or protein >500mg and positive peripheral serologies
- Be suspected in positive CSF FT-ABs is positive
Thursday, July 31, 2008
Day #31 - Fever of Unknown Origin
Today we discussed a case of true fever of unknown origin.
Epidemiologic Criteria:
Diagnostic tests (beyond initial):
Epidemiologic Criteria:
- Fever x 3 weeks (38.3)
- Failure to find cause despite appropriate initial outpatient/inpatient investigations
- Majority unknown
- Then infection (most commonly TB or occult abscesses), inflammatory, malignancy, other
Diagnostic tests (beyond initial):
- CT abdomen to look for abscess, lymphadenopathy, other pathology. Yield ~20%
- Bone scan (insensitive, but specific with good + LR)
- Liver biopsy -- regardless of hepatomegaly or LFT abnormalities has yield ~15%
- Temporal artery biopsy in the elderly -- yield ~ 15%
- Leg dopplers -- yield 2-6%
- Bone marrow biopsy-- in those with cytopenias or compatable syndromes. Yield ~1%
Friday, July 25, 2008
Thursday, July 24, 2008
Day #24 - Colitis
Today we discussed a gay male with fever, abdominal cramping, tenesmus and bloody diarrhea. The discussant made a very important point -- the clinical context and history are very important in making the diagnosis in acute colitis.
Before making the diagnosis of IBD one should exclude infections by history and special tests. Infections can mimic IBD clinically, radiographically, and endoscopically.
I wanted to talk about the differential diagnosis of bloody diarrhea with fever.
Differential Diagnosis
Infectious
There is also a good case of a patient with fever and diarrhea in the NEJM available here.
Before making the diagnosis of IBD one should exclude infections by history and special tests. Infections can mimic IBD clinically, radiographically, and endoscopically.
I wanted to talk about the differential diagnosis of bloody diarrhea with fever.
Differential Diagnosis
Infectious
- Enteroinvasive infection: Salmonella, Shigella, Campylobacter, E. Coli 0157:H7 (associated with HUS, frequently afebrile), Clostridium difficile, Klebsiella oxytoca
- Associated with receptive anal intercourse: HSV proctitis, gonorrhea, chlamydia (L serovar - AKA LGV/lymphogranuloma venerium), syphilis
- Associated with oral-anal practices or colonic irrigation: intestinal amebiasis
- More chronic, associated with the terminal illeum: intestinal tuberculosis
- Immunosuppressed patients: CMV colitis
- Ulcerative colitis/Crohn's disease
There is also a good case of a patient with fever and diarrhea in the NEJM available here.
Monday, July 21, 2008
TGH "Case of the Week" July 14-18, 2008
30F with known HIV (CD4 unknown, not on treatment) presents with acute onset fever, chills, rigors, and cough with sputum. On exam she is febrile, tachycardic, hypotensive, hypoxemic on room air requiring hi-flow oxygen to maintain saturations >90% and in moderate respiratory distress.
The chest x-ray is taken and appears below:
Questions:
1) What is the most likely microbiological diagnosis?
2) What is the differential diagnosis?
3) What tests would you order to make your diagnosis?
4) What empiric treatment would you initiate in the ED?
BONUS: What "management strategy" would you employ in the ED and what journal was the study published in?
Thank you to the people who submitted answers. The "contest" is closed for this week. The winner will be notified in person.
"Answers"
1) The most likely etiologic agent to cause a lobar pneumonia in a patient with HIV is still streptococcus pneumoniae. In fact, patients with HIV are at an increased risk of getting pneumococcal infections and should all be vaccinated with the polysaccharide vaccine.
2) The differential diagnosis includes lobar pneumonia with the other organisms of community acquired pneumonia including haemophilus influenzae, moraxella cattharalis, and Staphylococcus aureus. Of particular concern in a patient who is rapidly deteriorating is community acquired MRSA necrotizing pneumonia.
Other causes would include Legionella pneumophillia and if risk factors such as underlying structural lung disease enteric gram negative organisms.
Upper lobe pneumonia should prompt concern for tuberculosis, although in this case the acquity and sepsis-syndrome argue more strongly in favor of bacterial pneumonia.
PCP tends not to be lobar and consolidative and the classic x-ray appearance looks more like bilateral peri-hilar interstitial infiltrates.
Fungal pneumonias like cryptococcal pneumonia, blastomycosis, invasive aspergillosis are unlikely and would not generally have this radiographic appearance and acute presentation.
3) Blood cultures should be sent ASAP (ideally before antibiotics) as they may be positive in up to 25% of cases of pneumococcal pneumonia. Sputum cultures should also be sent for conventional culture, legionella culture and TB culture. I would not recommend sputum for PCP in this case.
Urinary antigen detection for pneumococcal antigen is used in some centres (not here). Urinary antigen testing for legionella can help make this diagnosis.
CD4 testing in acute illness may not be helpful as the acute illness could cause a decrease in the counts; however, it would not be unreasonable as if the CD4 count was >200 rare causes are much more unlikely.
4) In a septic patient with community acquired pneumonia you need to cover broadly for the most likely pathogens. There are many ways to do this and in some cases what you choose will depend on recent antibiotic exposure.
In this case a combination of VANCOMYCIN 1gIV q12h and LEVOFLOXACIN 750mg IV/PO q24h would be appropriate. This would cover MRSA and quinolone resistant pneumococcus, the usual pathogens including the majority of pneumococcus, unusual pathogens like legionella, and many enteric gram negatives.
BONUS: The management strategy to be employed is "Early Goal Directed Therapy in Sepsis"
The chest x-ray is taken and appears below:
Questions:
1) What is the most likely microbiological diagnosis?
2) What is the differential diagnosis?
3) What tests would you order to make your diagnosis?
4) What empiric treatment would you initiate in the ED?
BONUS: What "management strategy" would you employ in the ED and what journal was the study published in?
Thank you to the people who submitted answers. The "contest" is closed for this week. The winner will be notified in person.
"Answers"
1) The most likely etiologic agent to cause a lobar pneumonia in a patient with HIV is still streptococcus pneumoniae. In fact, patients with HIV are at an increased risk of getting pneumococcal infections and should all be vaccinated with the polysaccharide vaccine.
2) The differential diagnosis includes lobar pneumonia with the other organisms of community acquired pneumonia including haemophilus influenzae, moraxella cattharalis, and Staphylococcus aureus. Of particular concern in a patient who is rapidly deteriorating is community acquired MRSA necrotizing pneumonia.
Other causes would include Legionella pneumophillia and if risk factors such as underlying structural lung disease enteric gram negative organisms.
Upper lobe pneumonia should prompt concern for tuberculosis, although in this case the acquity and sepsis-syndrome argue more strongly in favor of bacterial pneumonia.
PCP tends not to be lobar and consolidative and the classic x-ray appearance looks more like bilateral peri-hilar interstitial infiltrates.
Fungal pneumonias like cryptococcal pneumonia, blastomycosis, invasive aspergillosis are unlikely and would not generally have this radiographic appearance and acute presentation.
3) Blood cultures should be sent ASAP (ideally before antibiotics) as they may be positive in up to 25% of cases of pneumococcal pneumonia. Sputum cultures should also be sent for conventional culture, legionella culture and TB culture. I would not recommend sputum for PCP in this case.
Urinary antigen detection for pneumococcal antigen is used in some centres (not here). Urinary antigen testing for legionella can help make this diagnosis.
CD4 testing in acute illness may not be helpful as the acute illness could cause a decrease in the counts; however, it would not be unreasonable as if the CD4 count was >200 rare causes are much more unlikely.
4) In a septic patient with community acquired pneumonia you need to cover broadly for the most likely pathogens. There are many ways to do this and in some cases what you choose will depend on recent antibiotic exposure.
In this case a combination of VANCOMYCIN 1gIV q12h and LEVOFLOXACIN 750mg IV/PO q24h would be appropriate. This would cover MRSA and quinolone resistant pneumococcus, the usual pathogens including the majority of pneumococcus, unusual pathogens like legionella, and many enteric gram negatives.
BONUS: The management strategy to be employed is "Early Goal Directed Therapy in Sepsis"
Friday, July 18, 2008
Day #18 - Cirrhosis
Today's case was of a 52 year-old man who presented with new diagnoses of cirrhosis with ascites, portal hypertension and probable variceal bleed who also had a new diagnosis of diabetes mellitus. The discussant showed us, although in his own uniquely tangential way, the type of clinical reasoning that great physicians use in arriving at a diagnosis.
There are a number of valuable teaching points today:
1) Ascites:
Etiology
History
The team today also mentioned that they had performed a paracentesis in order to evaluate the ascites. This is important as paracentesis can:
The Serum Albumin-Ascites Gradient (SAAG) is a valuable tool in deciding if the ascites is due to portal hypertension. SAAG = Serum albumin - Ascites Albumin. If <11 style="font-style: italic;">It should also be prevented in cirrhotic patients post GI bleed using TMP/SMX 1DS PO BID x 7d or CIPROFLOXACIN 500mg PO BID x 7d
The diagnosis can be made on the paracentesis:
Initial treatment is with CEFTRIAXONE 2g IV q24h with coverage narrowed to the culture data. You need only treat for 5 days.
Patients should get 1.5g/kg of 25% albumin within 6h then 1g/kg on day 3.
NB: Think of missed perforation if multiple organisms grow in the culture or if the WBC count in the fluid is much greater than 1000.
There are a number of valuable teaching points today:
1) Ascites:
Etiology
- Elevated Hydrostatic Pressure --> CHF, constrictive pericarditis, Budd-Chiari, cirrhosis, IVC occlusion
- Decreased oncotic pressure --> malnutrition, nephrotic syndrome, protein losing enteropathy, cirrhosis/liver failure
- Increased fluid production in peritoneum --> infection (TB), neoplasm
History
- Increased abdominal girth and ankle swelling are the most sensitive (greater than 85%)
- Past history of hepatitis or cancer are the most specific (greater than 85%)
- Not likely if no bulging flanks, no flank dullness and no shifting dullness
- Likely if fluid wave, shifting dullness, and peripheral edema (LR+3.8/-0.2)
The team today also mentioned that they had performed a paracentesis in order to evaluate the ascites. This is important as paracentesis can:
The Serum Albumin-Ascites Gradient (SAAG) is a valuable tool in deciding if the ascites is due to portal hypertension. SAAG = Serum albumin - Ascites Albumin. If <11 style="font-style: italic;">It should also be prevented in cirrhotic patients post GI bleed using TMP/SMX 1DS PO BID x 7d or CIPROFLOXACIN 500mg PO BID x 7d
The diagnosis can be made on the paracentesis:
- PMN >250 (LR + 6 LR - 0.2)
- WBC >1000 (LR + 9)
- Inoculation of blood culture bottles (fill them with required volume) can improve yield of the C/S
Initial treatment is with CEFTRIAXONE 2g IV q24h with coverage narrowed to the culture data. You need only treat for 5 days.
Patients should get 1.5g/kg of 25% albumin within 6h then 1g/kg on day 3.
NB: Think of missed perforation if multiple organisms grow in the culture or if the WBC count in the fluid is much greater than 1000.
Tuesday, July 8, 2008
Day #8 - The Bacteremia that Won't Go Away
Today the discussant described evaluating for exit site and tunnel infections and differentiated these from catheter tip infections with bacteremia. We then talked about diagnosis and management of line-related infections focussing of a few specific pathogens. Here are a few take-away points:
One should obtain paired, labeled blood cultures from the periphery and line in question. The differential time to positivity can help determine whether the line is the source of the infection as follows
We also talked about two interesting pathogens involved in this case:
One should obtain paired, labeled blood cultures from the periphery and line in question. The differential time to positivity can help determine whether the line is the source of the infection as follows
- Line and blood simultaneously positive suggests that the line is not the focus
- Line positive 2 hours before periphery suggests that the line is the focus
- Line positive and blood negative may suggest colonization only
- Failure to remove the focus/line can be associated with adverse outcomes including metastatic infection and death.
- Changing over a wire or reinsertion at the same side is not ideal but sometimes the only solution.
- If the line is not medically necessary and is easy to remove without complication it should probably be removed in most line related infections.
- One should be vigilant for evidence of metastatic infection or complications.
- Recurrent bacteremias with the same organism are highly suggestive of an occult/endovascular focus.
We also talked about two interesting pathogens involved in this case:
- Staphylococcus lugdunensis which is a coagulase-negative staphylococci which has virulence similar to Staphyloccocus aureus and is a cause of endovascular infections such as native-valve infective endocarditis
- Achromobacter xylosoxidans ss xylosoxidans which is a rare gram negative rod which has been known to cause infections such as bacteremia and more rarely pneumonia, abscesses and meningitis. Patients with malignancies seem to be particularly at risk.
Monday, July 7, 2008
Decision making in Community Acquired Pneumonia
Read a great article published in CID on Aug 1, 2008. SMART-COP predicts people with CAP who will require admission to intensive care requiring ventillatory or vasopressor support. It does so better than the PORT score or CURB-65 which really only predict death.
Friday, July 4, 2008
Day #4 - Acute Monoarthritis
Today the discussant spoke about the approach to acute monoarthritis. It was a very articulate presentation and your participation was excellent.
To clarify the point on treatment:
VIDEO: How to do an arthrocentesis of the knee
Highlights include:
Risk Factors: Age, DM, rheumatoid arthritis, joint surgery, hip/knee prosthesis, HIV infection, skin infection, (unprotected sexual intercourse for GC)
History: Pain and swelling are present >80% of the time; fever is present only 60% rigors and chills less than that.
Synovial Fluid Exam (LR less than 0.1 rules out; LR >10 rules it in)
To clarify the point on treatment:
- CEFTRIAXONE 2g IV q24h will cover most organisms including GC, most streptococci, Staph. aureus and many gram negatives. It is not the ideal agent for Staph. aureus, so if it turns out to be methicillin *sensitive* staph. aureus you should change to ANCEF (1g IV q8) or CLOXAILLIN (2g IV q6)
- Is MRSA a possibility or is this a prosthetic joint? --> ADD VANCOMYCIN (renal dose)
- Is there reason to worry about pseudomonas? --> I would suggest VANCO+CEFTAZADIME and ID consult.
- Prosthetic Joint = Call ortho. Probably should not be admitted to medicine if septic prosthetic joint is the main reason they are in hospital -- they need to go to the OR for wash-out and, in my experience, this is much less likely if they are admitted to GIM instead of orthopedics. Should get ID consult as well.
VIDEO: How to do an arthrocentesis of the knee
Highlights include:
Risk Factors: Age, DM, rheumatoid arthritis, joint surgery, hip/knee prosthesis, HIV infection, skin infection, (unprotected sexual intercourse for GC)
History: Pain and swelling are present >80% of the time; fever is present only 60% rigors and chills less than that.
Synovial Fluid Exam (LR less than 0.1 rules out; LR >10 rules it in)
- WBC <=25,000 unlikely septic arthritis (LR 0.32) unless immunosuppressed
- WBC >=25,000 LR 2.9
- WBC >=50,000 LR 7.7
- WBC >100,000 LR 28
- PMNs <90%>
- PMNs >90% LR 3.4
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