Friday, July 10, 2009

Meningitis




Gram positive diplococci in CSF which grew strep. pneumo






Today we discussed meningitis, a serious infection that requires prompt initiation of life or neurological function-saving therapy before confirming the diagnosis. Although the discussant was, well, substandard, some important points still came across

(for those not there, the discussant was me, so no emails necessary)

Some issues that came up:

Common sources of infection in nursing home patients:
1) Urinary tract
2) Pneumonia (would be 'healthcare associated'- different abx coverage)
3) Skin

Reasons for a patient not to improve despite appropriate abx for an infection:
1) Not receiving therapy (non-adherence, vomiting, etc)
2) Resistant organism
3) Wrong diagnosis
4) Source not being penetrated (e.g. underdosed, abscess)
5) Persistent source not dealt with (e.g. osteomyelitis, sacral ulcer)

Common organisms in meningitis:
1) St. pneumo
2) N. meningitidis
3) H. flu
4) Listeria

Order depends on patient; listeria more common in older, immunocompromised. Think of unusual causes in right setting (e.g. cryptococcus, TB). Even though cryptococcal meningitis (which may present subacutely) comes to mind in HIV, invasive st. pneumo infections are far more common in HIV than in the general population.

Important risk factors to ask about:
Travel, contacts, HIV RFs, sinus or ear infections, injection drugs, head trauma.
The lack of all of fever, altered mental status, or neck stiffness virtually rules out meningitis

Some physical exam points:
1) Kernig's and Brudzinski's signs were described a century ago in patients with end-stage TB meningitis. They have low sensitivity, but high specificity.
2) Jolt accentuation (i.e. patient turns own head horizontally at 2-3 /second) is 100% sensitive, but very non-specific. Therefore, lack of it essentially rules out the diagnosis (although the JAMA article excluded immunocompromised patients, so be careful)

Empiric treatment (i.e. before CT scan, before LP. Ideally after blood cultures)
1) ceftriaxone 2g (for NM)
2) vancomycin 1g (for SP- there is pen-resistant SP in the community)
3) ampicillin 2g (if suspect listeria)
4) dexamethasone 10mg (with antibiotics)- see references
5) +/- acyclovir if suspect HSV encephalitis (rash, sz, focal deficits)- need to hydrate aggressively
Tailor Abx once culture result back +/- HSV PCR is back


LP is mandatory! Even though Abx are started, you need a diagnosis.


Causes of very low CSF glucose
1) Bacterial meningitis
2) TB
3) Fungal
4) HSV encephalitis

Some references:








Thursday, July 9, 2009

Vasculitis





p-ANCA immunofluorescence








Today we discussed the diagnosis and management of vasculitis, specifically ANCA-associated vasculitis. These diseases are rare, complex, multisystemic, and present many challenges to everyone involved (including those trying to blog about it). Good thing we had an expert!


When to suspect vasculitis?

1) Multiorgan involvement otherwise unexplained

2) Systemic symptoms (constitutional, etc. ) otherwise unexplained

3) Organ ischemia or infarction (bowel, renal, myocardial, etc)

4) Common condition in uncommon age group (MI, pulmonary edema, etc.)


How to classify vasculitis:

May classify by vessel size, by complement levels, by ANCA associated or not, and other features. Most commonly vessel size (Chapel Hill classification)

Large: Takayasu's, GCA

Medium: Kawasaki's, isolated CNS

Medium +/- small: PAN, Churg-Strauss, Wegener's

Small: HSP, cryoglobulinemia, hypersensitivity, microscopic polyangiitis


Basic features of some vasculitides (not intended to be exhaustive!)

Takayasu's:
pulse deficits, fever, malaise; may cause aortitis or dissection

Giant cell:
>50, sudden onset of pain, stiffness, fever, temporal h/a. Often pulse deficits, aortitis, aortic insufficiency

Kawasaki's
children with acute onset rash, fever, conjunctivitis. Often associated with coronary arteritis

Wegener's
fatigue, malaise, fever, inflammation of sinuses, kidneys, lungs. Also often cutaneous vasculitis. Often cANCA +ve

Microscopic polyangiitis
leukocytoclastic vasculitis, glomerulonephritis, hemoptysis, abdo pain. Often p-ANCA +ve

Churg-Strauss
Asthma, eosinophilia. Renal involvement is rare. p-ANCA often +ve

PAN
Assoc with HBV or HCV antigenemia. Fatigue, HTN, fever, renal failure, rash, mononeuritis multiplex. Marked HTN is classic for acute onset. May present as testicular pain.


Non-vasculitic causes of ANCA positivity

IBD, autoimmune hepatitis, CF, TB, many drugs (esp. PTU, methimazole, hydralazine, minocycline).


Some references for vasculitis diagnosis and management

http://www.bmj.com/cgi/content/full/338/apr22_2/b1461

http://jama.ama-assn.org/cgi/content/full/298/6/655

http://content.nejm.org/cgi/content/short/348/4/333


Wednesday, July 8, 2009

Welcome!

Welcome to Tangents, the Toronto Western Hospital morning report blog.

This was the idea of Isaac Bogoch, one of last year's CMRs, and I'd like to continue his great work this year.

The goal is to briefly summarize the topics discussed and give you links to some more detailed resources if you're interested.

Please feel free to give me any feedback on how to make it more useful to you.

David



UGIB

On Tuesday, we discussed issues related to upper GI bleeds.


Gastric ulcer with ASA tab in it!

Issues that came up:

DDx
-Ulcer (NSAIDS, H pylori) DU in 2nd/3rd part of duodenum suggests Zollinger-Ellison. Gastric ulcer: think of gastric cancer
-Varices (EtOH, hepatitis). High pressure venous system = big bleed
-Mallory-Weiss tears: vomiting hx. This is partial, vs. Boerhaave: rupture
-Esophagitis/gastritis (reflux, NSAID)
-Portal HTN gastropathy (like varices in stomach)
-Others: Dieulafoy's lesion, epistaxis, many others.

Checklist approach to acute UGIB management
1) Large bore IV access- at least 2
2) Group and screen, be ready to transfuse
3) Reverse any coagulopathy
4) PPI- IV or PO
5) Octreotide if known varices or high probability of variceal etiology
6) GI consult, possible urgent endoscopy

H. Pylori:
Acquisition: usually from childhood due to contaminated drinking water. Spread can occur person to person, especially within households.
Diagnostic tests:
Serology: Sensitive, but does not differentiate active vs. past infection
Urea breath test: Differentiates active vs. previous infection
Biopsy: Gold standard

Ferritin in Fe deficiency:
From Guyatt et al:
Likelihood ratios of Fe def (compared to gold standard of bone marrow bx):
Ferritin: LR
>100: 0.13
45-100: 0.46
18-45: 3.12
<18: 41.47
Cutoff of 41 is 98% Sn and 98% Sp

Some useful references- may need U of T computer to access full text.

Friday, June 19, 2009

Dont decompensate......


Decompensated Cirrhosis / encephalopathy consider:


  • SBP and other infection
  • portal vein thrombosis
  • variceal haemorrhage / upper GI bleed
  • constipation
  • narcotics / medications
  • dehydration
  • hypokalemia
  • hepatocellular carcinoma

Here is a link for a recent article on cirrhosis management : Lancet. 2008 Mar 8;371(9615):838-51.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1B-4S0JSP4-15&_user=1166899&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000051839&_version=1&_urlVersion=0&_userid=1166899&md5=5581813824abf0c779fe91e89e3be860

Thursday, June 18, 2009

Isnt it ELITE!!


Here is a link to the ELITE morning report ..... ILD






Friday, June 12, 2009

Pneumocystis jirovecii pneumonia


PJP is the most common AIDS deifining opportunistic infection in HIV-infected individuals. The presentation in most people (>85%) includes fever, progressive cough and dyspnea. It is generally subacute developing over days to weeks. Other constitutional symptoms are common.
Radiology:
A large percent of initial CXR imaging is normal in people with PJP. As the disease progresses diffuse bilateral interstitial or alveolar infiltrates develop. Discrete infiltrates, cysts, nodules and pleural effusions have been described. If a patient suddenly deteriorates dont forget to think about the pnumothorax which is not an uncommon complication of this disease (see above). a HRCT maybe very helpful in times when the CXR is normal.
Diagnosis:
The diagnosis is confirmed based on demonstration of PJP in sputum (sens 50-90%) or BAL (sens >95%). Laboratory data is not particularly helpful for diagnosis but the 2 most common abnormalities are an elevated LDH and low CD4.
Treatment:
Anti-PCP treatment....first line is TMP-SMX - other considerations include tolerance, iv vs oral therapy. Duration 21 days.
Steroids: As people typically worsen 3-5 days into treatment with an inflammatory response, steroids become the standard of treatment in severe infection. This is defined as a PaO2 <70>35 on ABG. The original studies in this area came out of Toronto so check out this link.....
" The possible role of corticosteroid therapy for pneumocyctis pneumonia in the acquired immune deficiency syndrome" J Acquir Immune Defic Syndr. 1988;1(4):354-60

Friday, June 5, 2009

Milk 'does the body good'



Today we reviewed how to interpret a blood gas. There are many ways to do this but the approach generally follows a few simply steps....here is an example:


6 simple steps…

1. What is the pH?
2. Is the primary disturbance respiratory or metabolic?
3. Is there appropriate compensation?
4. If this is a metabolic acidosis is there an anion gap?

  • what is the delta – delta?
  • is there an osmolar gap?

5. what is the A-a gradient?

We also had a brief discussion of 'milk alkali syndrome' which is a syndrome characterized by the triad of hypercalcemia, alkalosis and renal insufficiency. This syndrome is most often precipitated by excessive ingestion of calcium carbonate preparations in predisposed individuals. In the acute presentation of this syndrome the patient develops symptoms within a week of the treatment. They have symptoms of hypercalcemia, including nausea, vomiting, weakness, and mental changes with psychosis or depressed sensorium. The also have severe metabolic alkalosis, a normal to elevated plasma phosphate concentration, and acute renal insufficiency. Withdrawal of milk and alkali leads to rapid relief of symptoms and the return of normal renal function.