Oh the paradox....

Hello Everyone,

Today we discussed a facinating case of stroke in a young patient. Above is a handout looking at the differential and work-up of this type of case.

Click here for a NEJM article looking at paradoxical emboli as a cause of cryptogenic stoke in an older pateint.

http://content.nejm.org/cgi/reprint/357/22/2262.pdf

or an article published in stroke which looks at PFO and stroke in younger patient groups try this reference.

Stroke 1993;24:1865-1873.

For a discussion on whether to close a PFO you could also check out this reference: Circulation 2008; 118: 1989-1998.

Cavitary Lung Lesions....

Today we talked about a person who presented with dyspnea and pleuritic chest pain. The diagnosis was greatly narrowed when he was found to have a cavity lung lesion on chest x-ray. Below is a quick summary of the differential discussed for cavitary lung lesions….

C - Cancer – primary lung cancer (especially squamous cell) and metastatic cancer (colon, renal, breast, melanoma etc)

A – Autoimmune - Wegners, Rheumatoid Nodule (rare), Sarcoid

V – Vascular – Pulmonary Embolism with Infarction

I – Infection
Septic Emboli
TB
MAI
Bacterial – staph aureus, strep, anaerobes, nocardia, actinomyces, klebsiella, pseudomonas
Fungal – Aspergillus, Histoplasmosis, Coccidiomycosis, Blastomycosis, Cryptococcus, PJP
Parasite – Echinococcus

T – Trauma – bullous lung disease

Y – Youth –congenital cystic disease, congenital adenomatoid malformation etc

We ultimately settled on the diagnosis of community acquired MRSA. This form of MRSA tends to be more antibiotic sensitive than the hospital acquired relative. The emerging presence of this organism is not to be ignored – For the Canadian experience with MRSA please see the following CMAJ article http://www.cmaj.ca/cgi/reprint/176/1/54

HSV encephalitis

Today we discussed the case of a young male in his twenties who presented with a prodrome of confusion and lethargy. Based on new onset seizures, fever and a non-purulent LP the demographics and presentation were highly suggestive of HSV encephalitis…

HSV Encephalitis:
· worldwide the most common cause of sporadic fatal encephalitis
· although occurring in all age groups – approx. 1/3 of people are children / adolescents
· almost always HSV-1 (vs HSV-2 which is a more common cause encephalitis in neonates)
· rarely in the context of skin disease / outbreaks

clinical presentation: clinical syndrome is often characterized by rapid onset of fever, headache, seizures, focal neurological signs of <>diagnosis: LP may show nothing or more commonly lymphocytic pleocytosis, increased RBC and protein. uncommon to have a low glucose. LP should be sent for HSV PCR (sensitivity = 98%, specificity = 94-100%). alternatives include brain biopsy of temporal lobe. viral cultures rarely positive.
iamging may show temporal lobe abnormalities (50% sensitivity of CT brain – MRI more sensitive and specific but can be negative). Non-specific EEG findings are noted in 80% of patients.

treatment: early empiric treatment is a priority - iv acyclovir is the treatment of choice

prognosis: if untreated mortality is 70%; even with early treatment up to 2/3 will have residual deficits

differential diagnosis: viral encephalitis (e.g. HIV, west nile), brain tumour, subacute sclerosing panencephalitis, neurosyphillis, post infectious (e.g. Reye’s), acute disseminated encephalomyelitis, other (SLE, subdural, intracerebral bleeding, adrenal leukodystrophy)

Reasons not to climb a ladder....

Today we discussed a case of syncope. Syncope itself has a broad differential but an important differentiation is the divide between cardiac and non-cardiac causes of syncope. We discussed that when a person has a very sudden loss of consciousness (no prodrome) and very rapid recovery we are concerned that the underlying etiology is of the ‘cardiac’ variety. As astute clinician seeing a patient after a syncopal episode will notice injuries such as bruising of the head and face to suggest that someone has fainted suddenly without enough warning to brace their fall.

Differential Diagnosis of Syncope:

Neurally medicated: constitutes approximately 20-25% of cases. This category includes vasovagal attacks, situational syncope and carotid sinus syncope. Of this group, vasovagal syncope is by far the most common. Consider vasovagal syncope in people when the event is preceded by pain, fear, extreme emotional stress, micturition or when someone has been standing for long periods of time.

Cardiac disease (up to 20%): includes abnormality any part of the heart i.e. pericardium, myocardium and valves. In addition to organic heart disease consider also arrhythmias. Finally a rare cause that was discussed today - the atrial myxoma – could be considered in particular in those people who have positional syncope such us when bending down.

Orthostatic hypotension: Should be identified on physical exam by postural vitals. This category included volume depletion, medication medicated orthostasis, autonomic dysfunction etc.

Neurologic Disorders: vertebrobasilar ischemia

Unknown: up to 1/3 of syncope used to be considered to have no obvious etiology however with improved diagnostics e.g. tilt table testing for neurally mediated mechanisms this number is likely lower now.

Unifying Diagnosis

A few days ago we talked about a fascinating case involving a person presenting with chest pain and found to have both pericarditis and a lobar pneumonia. To unify the diagnosis we looked at the differential for pericarditis that includes but is not limited to:
· Infectious Causes: viral (coxsakie virus A, B, echovirus…); bacterial (s. pneumonia, s. aureua…); TB; fungal (histoplasmosis, blastomycosis..)
· MI associated: acute vs Dressler’s syndrome
· Metabolic: uremia, hypothyroidism
· Neoplasm: lymphoma, breast, lung, RCC, melanoma
· CVD: SLE, RA, scleroderma, polyarteritis
· Vascular: aneurysm, trauma, cardiac surgery
· Other: drugs (hydralazine), radiation, sarcoid

We also had the chance to look at an ECG which showed some (but not all) of the changes we associate with pericarditis including diffuse ST elevation, PR segment depression (elevation in aVR), concave morphology to ST segment elevation.

For more information on pericarditis look at this NEJM review:

http://content.nejm.org/cgi/reprint/351/21/2195.pdf

Finally, the team discussed some clinical trial evidence for the treatment of pericarditis. The colchicine in addition to conventional therapy for acute pericarditis (COPE TRIAL) can be found at the link below!

http://www.circ.ahajournals.org/cgi/content/full/112/13/2012

Just add water....

JUST ADD WATER.......

Today we talked about a classic internal medicine case: hypernatremia. We divided our approach by etiology into “low total body sodium”, “water losses” and “sodium addition”.

Low Total Body Sodium:
These patients may be divided into renal or extra renal losses. The renal losses include osmotic diuresis (mannitol, glucose, urea). Extra renal losses tend to be sweating and diarrhea. Urine sodium helps to differentiae these two in that urine sodium will be >20mEq/L in an osmotic diuresis while it would be expected to be <10mEq/L with diarrhea and excessive sweating. The recommended treatment approach would be hypotonic saline.

Water Loss (Normal total body sodium):
Again the approach to these patients can be divided into renal and extarenal causes. Renal causes include both nephrogenic and central diabetes insipidus. Extra renal water loss tends to be insensible losses from respiratory tract or skin. Urine sodium is less helpful to differentiate this group as in both cases it will be variable. The treatment of choice is replacement of the water.

Increase total body sodium:
There are a number of causes of increase body sodium including endocrinopathies and exogenous administration (chloride, bicarb, saline admin). Endocrine causes include primary hyperaldosteronism and less commonly Cushings. Urine sodium will tend to be >20 mEg/L in these patients. Treatment is again replacement of the water deficit.

For more information / a slightly different appraoch you can review the NEJM review article: http://content.nejm.org/cgi/reprint/342/20/1493.pdf

More Morning Report Updates

Hello,

FYI....not only can you continue following Morning Report updates from the Toronto Western Hospital at this site, you can also follow Morning Report from the Toronto General Hospital here: 

www.morningreporttgh.blogspot.com.

Enjoy,

Your CMRs