Tuesday, August 4, 2009

Non-Resolving Pneumonia

Factors to Consider in Non-Resolving Pneumonia

(1) Do not confuse "non-resolving pneumonia" with non-resolution of chest x-ray findings. Although radiographic resolution has been used in the past to define this entity, Mittl and colleagues demonstrated that only half of patients with community acquired pneumonia have radiographic resolution at two weeks. Clearance was faster in non-smokers and those treated as outpatients. Having said that, patients with radiographic evidence of pneumonia do require follow-up imaging to ensure resolution and to rule out an underlying mass lesion.

(2) The definition endorsed by the Infectious Disease Society of North America is fairly vague- "a situation in which an inadequate clinical response in present despite antibiotic treatment". As in many things, clinical judgment is paramount - consider ongoing cough with sputum production, fever, performance status, hypoxia and white blood cell count.

(3) The possible etiologies are many and include both infectious and non-infectious causes. Important things to consider are:
  • Time of treatment - Patients treated less than 72 hrs should be considered as inadequate treatment time.
  • Infectious Causes - Consider a pathogen not covered by your treatment (e.g. tuberculosis, non-tuberculous mycobateria, viral or fungal infections) or a resistant organism (e.g. MRSA pneumonia).
  • Non-Infectious Causes - malignancy, interstitial lung disease, heart failure. (The NEJM recently published a report of a patient with assymetric pulmonary edema due to mitral valve dysfunction).
  • Complications of Infection - Empyema or parapneumonic effusion.
(4) Approach to Management
  • Does your patient need ISOLATION? Patients with non-resolving pneumonia should be considered high-risk for tuberculous and influenzae, depending on their epidemiology.
  • Does your patient need urgent antimicrobial treatment? If not, consider stopping all antimicrobials to increase the yield of investigations.

  • Investigations for everyone - blood cultures
  • Investigations to consider - HIV serology, induced sputum, bronchoscopy, CT chest. Very rarely, a patient may need a lung biopsy to make a diagnosis.
  • Patients with a pleural effusion need diagnostic thoracentesis, and chest tube insertion if an empyema is identified.

For the full IDSA guidelines on community acquired pneumonia, including a review of the approach to a non-resolving pneumonia, visit the IDSA website.

Wednesday, July 29, 2009

Salicylate toxicity

Salicylate toxicity is not a common phenomenon in internal medicine, but it is important to recognize it because the management is specific.

A couple of general principles to remember in overdoses and toxidromes:

(1) Assess ABCs early and frequently. Patients can change.
(2) There is no such thing as too much IV access. Patients with toxic ingestions can seize, become hypotensive and do other unpredictable things. You will never be sorry that you asked for two IVs.
(3) Always call POISON CONTROL.
(4) Consider multiple ingestions.
(5) Think about general principles of overdose management, including decontamination.
(6) The patient may need additional monitoring, possibly in the intensive care unit setting. This is particularly true if the level of consciousness if depressed or if there is significant hypotension. Again, remember that patients change and a patient who does not need ICU at one moment may later on.

Salicylate toxicity comes in two forms:
(1) Acute overdoses - often intentional, with self-harm of suicidal intent.
(2) Chronic overdoses - from regular high dose ASA use.

The presentation can be variable and non-specific, although there are some cardinal features.

  • Tachycardia, hyperventilation, fever
  • Altered level of consciousness - related to direct toxicity, hypoglycemia, cerebral edema.
  • Nausea, vomiting
  • Platelet dysfunction
  • Pulmonary edema (especially with chronic toxicity, more common in the elderly)
  • Tinnitus (especially with chronic toxicity)

**The combination of an anion gap metabolic acidosis and a primary respiratory alkalosis (beyond compensation for the metabolic acidosis) should trigger the diagnosis of salicylate toxicity**

Specific Management Guidelines
(1) Alkalanize the urine. This is done by running a sodium bicarbonate infusion, targeting a urine pH of 7.5-8.5. In general, start the infusion at 150-200mL/hr and increase according to your urine pH.
(2) Potassium replacement. For any patient with urine output and a serum potassium <5, consider replacement. Similarly to patients with diabetic ketoacidosis, the total body potassium may be low despite a normal measured serum potassium because of intracellular shift related to acidosis. With alkalanization, you may see a precipitous drop in the serum K.
(3) Nephrology consultation +/- hemodialysis - Consider in patients with severe toxicity, acute renal failure, pulmonary edema. If you are not sure, involve nephrology.
(4) Consider ICU consultation. Consider endotracheal intubation if necessary from the perspective of airway protection. However, mechanical ventilation may not be as effective as the patient's own respiratory drive in correcting their metabolic acidosis.

Monday, July 20, 2009

Bacterial Meningitis

Today we discussed the approach to the diagnosis and management of bacterial meningitis.

For a good general review of bacterial meningitis, read the NEJM review by van de Beek et al. The Infectious Diseases Society of America also provides Clinical Practice Guidelines.

I've focused the discussion here on a few evidence based points that were discussed this morning.

(1) Pre-treatment with antibiotics prior to lumbar puncture may cause the culture to become negative, but should not change the biochemical properties of the CSF. This was shown in a study published by Schaad et al comparing ceftriaxone to cefuroxime where repeat lumbar punctures were done at 24 hours post initiation of antibiotics and were found to be unchanged in terms of WBC count, protein and glucose. Based partly on this data, guidelines recommend that if the patient requires a CT scan prior to LP, antibiotics should be given after blood cultures have been drawn, but prior to CT or lumbar puncture.

(2) Concurrent administration of dexamethasone with or prior to the first dose of antibiotics reduces mortality. This difference was shown in a 2002 study published in the NEJM. In this study of a combined group of patients with both streptococcus pneumoniae and with neisseria meningitidis, although the difference was largely evident in the s. pneumoniae group. The dose of dexamethasone used was 10 mg Q6H and this is the current standard of care.

(3) As shown in this brief report, re-insertion of the stylet post lumbar puncture decreases the risk of post-LP headache.

(4) Which patients need a CT brain prior to lumbar puncture? Although the vast majority of CTs done in these patients are normal, the IDSA guidelines recommend CT for anyone with an altered LOC, focal neurologic deficits, papilledema, an immunocompromised state, history of CNS disease or new onset seizure. I've linked the NEJM article supporting these guidelines here.

Saturday, July 18, 2009

Physical Exam - Aortic Stenosis

To determine if a systolic murmur is related to aortic stenosis, consider the following predictive factors:

The following factors are SENSITIVE (help to rule OUT aortic stenosis)
No systolic murmur
No radiation of murmur to right clavicle

The following are SPECIFIC (help to rule IN aortic stenosis)
Pulsus parvus
Plusus tardus
Decreased S2
Brachioradial delay
Apical carotid delay
Mid-late peaking murmur

Two very good evidence based evaluations supporting this are the JAMA Rational Clinical Exam Series paper on systolic murmurs and the JGIM paper on aortic stenosis. Both come from Toronto clinicians, and are linked here and here.

Monday, July 13, 2009


Today we discussed the evaluation of a new pleural effusion in the context of a history of smoking and possible occupational asbestos exposure. The approach to pleural effusions is reviewed here.

One interesting disease that was brought up today was malignant mesothelioma. Although most commonly found as a pleural based malignancy, mesothelioma is probably best described as a cancer of serosal surfaces and can rarely present as peritoneal disease with ascites or pericardial disease.

The incidence of malignant mesothelioma is expected to rise until at least 2020, an epidemiologic phenomenon that lags behind known exposure to asbestos. In fact, in parts of the developing world, asbestos is an ongoing exposure, and therefore mesothelioma may be an ongoing problem for many years.

The diagnosis of mesothelioma can be difficult, and the sensitivity of cytology of pleural or ascitic fluid is quite variable, ranging from 33-84%, often necessitating needle or thorascopic biopsy. The disease usually presents at an advanced stage when large effusions have reached the point of symptoms, and median survival is less than one year from the time of diagnosis. Management is typically palliative, and may include local management such as pleurodesis or chronic drainage, or systemic therapy. Occasionally surgery is required to manage complications of locally advanced disease.

A good NEJM review is available.

Tuesday, July 7, 2009

Welcome to "The Pulse", a blog of educational activities at TGH. This blog was started by Isaac Bogoch last year and will be continued onwards this year. All errors, omissions and mis-representations are his.

Today at morning report, we discussed the approach to a patient with an altered level of consciousness. The facilitator provided a framework for the differential diagnosis:

1. Neurologic causes - including stroke, CNS infections, dementing illnesses such as Lewy Body dementia, normal pressure hydrocephalus and others.

2. Metabolic causes - including electrolyte abnormalities (think sodium and calcium!), endocrinopathies (e.g. thyroid disease).

3. Medications - overdose, intoxication, withdrawal. Also consider over-the-counter and alternative therapies.

4. Major medical illness. Both liver and kidney dysfunction can present with altered level of consciousness.

5. Psychiatric illness. Depression can present in atypical ways, particularly in the elderly.

We also talked about the basics of the workup and management of stroke. A good general review article on stroke can be found in the New England Journal of Medicine 2007, Vol 357 (6), pp 572-579. A link to the abstract is found here

I would encourage you to consult the Canadian Stroke Network best practice guidelines on stroke management, linked here. Although practice guidelines often represent a combination of evidence and expert opinion, they can be helpful resources and can direct you to the peer-reviewed literature.

Hope you are all enjoying the first week. Let me know how I can help make this a great experience for you!


Wednesday, June 24, 2009


This will be the last Morning Report Blog update of the academic year. I hope this was a valuable learning experience for you. It's been a good time.

Your CMR, 2008/2009



First, think about the underlying etiology:

1. Trauma: this can be overt, like a crush injury or a bit more subtle, like immobilization in an elderly person who falls and is unable to get up for some time. Also think about immobilization in patients with a decreased level of consciousness or during prolonged operation.

2. Physical activity: rhabdo may occur in those who either perform excessive physical activity (eg. marathons), in those who are doing significantly more physical activity than they are used to (eg. couch potato who goes on run for 1st time in 10 years), or in situations where hyperthermia may occur (eg. jogging in the Sahara). Also, don't forget seizures as a common etiology.

3. Drugs/Toxins: as always, we should consider prescribed drugs (eg statins, colchicine), and non-prescribed drugs (eg. alcohol, cocaine, ecstasy). There are always a few cases per year of rhabdomyolysis from wild mushroom poisoning.

4. Infections: many viruses (eg. cytomegalovirus, Coxsackievirus, Epstein-Barr, Influenza, adenovirus, HIV), bacteria (eg. pyomyositis), sepsis, and parasitic (Falciparum malaria).

5. Electrolyte: primarily hypokalemia and hypophosphatemia from any cause.

6. Endocrinopathy: mostly in hypothyroidism, but may also be seen in DKA/HONK - probably from hypophosphatemia.

7. Those who are more prone: people who have myopathies may be more prone to developing rhabomyolysis. Think about those with poly/dermatomyositis, malignant hyperthermia, or rare congenital myopathies.

Other: paraneoplastic syndromes

What should I watch out for?

  1. Hyperkalemia: lots of potassium can be released from muscle cells. Monitor this and the ECGs closely.
  2. Renal failure: watch out. Myoglobin is toxic to the renal tubules and can cause acute tubular necrosis.
  3. Other electrolytes: hyperphosphatemia (released from muscle cells), hypocalcemia.


This primarily revolves around finding and reversing precipitants, and aggressive fluid administration to prevent myoglobin-induced ATN. There is debate whether the best fluids are saline or if sodium bicarbonate added to D5W works best. Also, keep a close eye on the potassium.

A good link:

A strange case of rhabdomyolysis from CMAJ.

Tuesday, June 23, 2009


Evaluation for Malnutrition:
  • General Inspection: look for grooming, BMI <19, cachexia
  • Vital signs: increased HR if intravascularly volume depleted
  • Head & Neck: alopecia and brittle hair, glossitis (Iron, B12), bleeding gums (Vit C), angular cheilitis (Iron)
  • Abdominal Exam: look for ascites, hepatomegaly, splenomegaly
  • MSK: Muscle wasting. Pay particular attention to temporal muscle wasting, deltoids - note a 'boxing off' appearance, triceps, and quadriceps muscles. Also assess if ribs can be visualized through pectoral muscles. Note subcutaneous fat loss in these areas as well.
  • Neuro: look for loss of deep tendon reflexes, peripheral neuropathy, optic atrophy, and evidence of subacute combined degeneration of the cord (B12).

A Rational Clinical Exam article from
JAMA was published by local talent explains how to determine if your patient is malnourished via the Subjective Global Assessment. See below

Thursday, June 18, 2009

"Elite" or "Advanced" Morning Report

Today we had a Morning Report session with our friends from Mt. Sinai and Toronto Western Hospitals. We discussed a very interesting case of a person with shortness of breath in the context of rheumatoid arthritis.

  • Please see the Mt. Sinai Blog for details here.
  • More on interstitial lung disease can be found here.

Friday, June 5, 2009

A total overreaction

(the syndrome of Reactive arthritis pictured left)

Reactive Arthritis
- (formerly known as Reiter's Syndrome)

What is it? A post infectious immunologic phenomenon resulting in arthritis.

How long after an infection does it develop? a few days to a few weeks. This lag-time may make it difficult to know what the offending pathogen was.

Which pathogens are associated? Think about two big systems....GI and GU
  • GI: Yersinia, Salmonella, Shigella, Campylobacter
  • GU: Chlamydia, and possibly Gonorrhea

What does the syndrome look like?
The arthritis is usually an asymmetric oligoarthritis,. Enthesitis is common and may affect the achilles tendon or plantar fascia on the calcaneus. Conjunctivitis or uveitis is seen, as is balanitis - Hence the adage "Can't pee, can't see, can't climb a tree". A classic dematologic manifestation of reactive arthritis is keratoderma blennorrhagica - scaly lesions on the palms and soles. See picture below.

Is there any genetic predisposition to developing Reactive Arthritis? Yes.

What is it? HLA-B27 is present in just under 50%.

How do we treat it? NSAIDs work well, like indomethacin or naproxen. In severe cases, DMARDs like sulfasalazine may be used.

Why is it called Reactive Arthritis now instead of Reiter's Syndrome? an interesting paper can be found here.

(keratoderma blennorrhagica pictured left)

Wednesday, June 3, 2009



No, this is not just an infection of children anymore - we are seeing measles more frequently in adults. This is usually in those with no history of primary vaccination.

Classic Measles: there is about a 14 day incubation period where the virus replicates and spreads via lymphatics and hematogenously. Initial symptoms include fever, coryza, conjunctivitis, cough, and general malaise. Koplik's spots may be seen as well - these are small, raised lesions in the buccal mucosa that are whitish or blue in colour (see photo below). These are pathognomonic for measles and can be visualized roughly 2 days prior to the classic rash.

The exanthem of measles typically starts on the face and moves to the trunk and extremities, sparing the hands. It is a blanchable maculopapular rash (see photo above). Patients may start to feel better a couple of days after the rash appears, and the rash typically will start to fade after 4ish days.

Diagnosis: can be confirmed with serology. Send off measles IgM - this should be positive a few days after the exanthem appears. Measles IgG will be detectable two weeks after the exanthem.

What to do? this is a very contagious virus, so patients with suspected measles should be in respiratory isolation and the Infection Control service should be contacted. Treatment revolves mostly around supportive care - fluids, antipyretics, and monitoring for/treating bacterial suprainfections like pneumonia or otitis media. Vitamin A is given to children with measles in countries where vitamin A deficiency is prevalent.

  • A neat case and image of Koplik's spots can be found here.
  • Check out the epidemiology of measles in North America here.

(Koplik's Spots in the buccal mucosa)

Tuesday, June 2, 2009


Today we discussed prognostic tools for pneumonia - the PORT and CURB65 scores. You can read more about these here.

As part of our differential diagnosis of Chest Pain, the topic of pericarditis came up.

Clinical presentation: usually a sudden onset of retrosternal chest pain with a pleuritic component to it, often relieved by sitting up. You may hear a pericardial rub - this is classically described as a triphasic, high-pitched sound. The 'tri' refers to:
  1. atrial systole
  2. ventricular systole
  3. ventricular diastole

It may be a transient phenomenon so listen again if you don't hear it. Classic situation...you hear the pericardial rub, admit and treat the patient. When your attending reviews the case the next morning they can't hear it - even though you swear on your life that you heard one. Solution: when you hear a pericardial rub, get your friend to have a listen as well, so in the morning both of you can say you heard it.

ECG: may show diffuse, concave ST elevations that do not fit any particular vascular territory. PR depression is also seen. Check out the ECG above.

Treatment: In most cases of idiopathic pericarditis, high dose NSAIDS are effective. Steroids and colchicine also may have a role. Interestingly, newer evidence suggests that colchicine may be a good first line agent. Here is a link to the article published in Circulation. Have a look and decide for yourself.

Other Links

Monday, June 1, 2009

Addressing DRESS

DRESS syndrome - Drug Reaction with Eosinophilia and Systemic Symptoms, also known as drug hypersensitivity reactions.

These commonly present 2 weeks after initiating a new medication with:
  • Fever
  • Rash: papular, macular, bullous
  • Lymphadenopathy
  • Arthralgias
  • Hepatitis
  • Eosinophilia

Medications which are commonly associated with DRESS syndrome include "aromatic" anticonvulsants (phenytoin, carbamazepine, and phenobarbitol) - but can occur with other anticonvulsants as well. Other classic DRESS syndromes occur with NSAIDs, abacavir, and allopurinol. Treatment revolves around discontinuing the culprit agent, supportive care, and perhaps steroid therapy.

In the case of abacavir, hypersensitivity reactions are known to occur more frequently in those who are HLA B5701-positive, and screening programs are now widely used to prevent this adverse reaction.

Friday, May 29, 2009

Community-Acquired Pneumonia

(the Stanly Cup, pictured left)

Community-acquired pneumonia is extremely common. When patients present with this condition, we are often faced with a situation in the ER where we either admit pateints to hospital, or decide to treat in an out-patient setting. How do we decide? There are two major ways to do this.....
  • "Gestalt": take a careful history and physical exam, look at the bloodwork and chest x-ray, think about the patients' social situation and the time of day (or night), and put all the information into context and make a decision.
  • Clinical Prediction Rules: There are a few of these, however the Pneumonia Severity Index (derived from PORT score) and CURB65 score are most widely used.

Pneumonia Severity Index: Here is a link to the original article from NEJM. Points are given for various clinical/historical feaures and patients are categorized into one of 5 classes. Class I, II, have very low all-cause mortality rates at 30 days and can usually be treated as outpatients. Class IV, and V have higher rates of morbidity and 30-day all cause mortality - these patients should be admitted to hospital.

: This is a much simpler scale requiring only 5 pieces of information. Here is a link to the original article in Thorax. Each feature is worth 1 point...then just add them up.
  • C: confusion- disorientation to person, place, time
  • U: urea >7 mmol/L
  • R: respiration rate >30 breaths per minute
  • B: Blood pressure- systolic <90 or diastolic <60 mmHg
  • 65: age >65 years
30-day mortality rates are 0.6% with a score of 0, and 1.7% with a score of 1. Scores of 4 have roughly 15% 30-day mortality rates - oy vey (come find me if you don't know what that means). Patients with scores of 0 or 1 can most likely be treated as outpatients. 3 points or more should be brought into hospital, and 4 or more points should likely be evaluated by the ICU.

Remember, these scales are helpful tools meant to assist you - they are not substitutions for good clinical judgment.

Thursday, May 28, 2009

Gonococcal Infection: a few syndromes

Pictured: Image from NEJM, a case of disseminated GC infection. Click here for the link. Note the tenosynovitis and 'countable' pustules.

Gonococcal Infection - syndromes:
  • Localised inflammation of involved mucous membrane: urethritis, vaginitis, pharyngitis, etc.
  • Pelvic inflammatory disease
  • Fitz-Hugh and Curtis syndrome: inflammation of the liver capsule, from direct extension of the organism in a patient with pelvic inflammatory disease.
  • Arthritis dermatitis syndrome: migratory arthralgia, tenosynovitis (Achilles, wrist,etc.), pustular lesions - usually not very many...they are "countable". Fever is common here.
  • Septic arthritis
  • Other very rare: meningitis, endocarditis

Link: updated treatment guidelines can be found here

Wednesday, May 27, 2009

Arthridites Associated with Inflammatory Bowel Disease

(above: monoarthritis in a patient with IBD)

Spondylitis and Sacroiliitis

  • HLA B27 in 50-75% with axial arthritis
  • Prolonged morning stiffness which improves with exercise
  • Unrelated to GI disease...'disease discordant'
  • Sacroiliitis may be asymptomatic
  • Treatment: Back exercises, NSAIDs, maybe methotrexate

Peripheral arthritis

  • Type 1
  • Acute and pauciarticular peripheral arthritis
  • Associated with flares of bowel disease....'disease concordant'
  • Self limited with no joint deformity
  • Knee most common site affected

  • Type 2
  • Polyarticular damage especially at MCPs
  • Migratory
  • Persist for months
  • Can have exacerbations and remissions
  • Treatment: NSAID/COX-2, sulfasalazine, methotrexate

Monday, May 25, 2009

HIV+ with Shortness of Breath

(a complex parapneumonic effusion pictured left)

Today we discussed the diagnosis and management of Parapneumonic Effusions. Check out some details here.

We also discussed an approach to patients with HIV who present with shortness of breath.

A few things to consider...
  • Is this an HIV or non-HIV related condition?
  • What is this patient's immune status (last CD4+ count and Viral Load)
  • Is this patient on Antiretroviral therapy?
  • Is this patient taking the appropriate prophylactic therapy (eg. Septra for PJP)
  • Are there other Tuberculosis risk factors?
  • Can the past medical history help me here?
HIV-related causes of shortness of breath:

1. Infectious
  • Community acquired pneumonia: >10x more likely in HIV + patients with CD4+ counts less than 200. Watch out for parapneumonic effusions and empyema. S. pneumoniae is common.
  • Pneumocystis Carinii Pneumonia or Pneumocystis Jirovecii Pneumonia or PCP or PJP... whatever you want to call it, this is still the most common AIDS-defining opportunistic infection. You can read more on this here.
  • Viral: Influenza, CMV
  • Tuberculosis must be considered, but also think about non-tuberculous mycobacteria as well, like MAC (usually disseminated rather than pulmonary)
  • Fungal: Cryptococcus, Histoplasma, Coccidioides. Also think about Aspergillus - though more common in neutropenia.
2. Malignant:
  • Lymphoma: non-Hodgkins > Hodgkins
  • Kaposi's sarcoma and associated Castleman's Disease
  • Metastatic disease
3. Other:
  • Cardiovascular: think about cardiomyopathy or other cardiac risk factors associated with HIV as a cause for shortness of breath
  • Pulmonary Hypertension
  • Drug toxicity
  • Inflammatory conditions
A Good Link:

Thursday, May 21, 2009

Lemierre's Syndrome

(pictured left: image from NEJM...arrow pointing to a thrombosed jugular vein)

Lemierre's Syndrome

What is it?
a septic thrombus of the jugular vein.

Which bacteria are implicated? usually oral flora, and typically Fusobacterium species.

How does one get it? typically after acute pharyngitis, there may be a small abscess or erosion of the mucosa. Bacteria can then invade the peri-pharyngeal space which houses the carotid sheath (encasing the jugular vein), and neck musculature.

How do patients present? more common in younger patients with a prodrome of a sore throat. They commonly have a fever, and possibly tenderness over the thrombosed vein. Septic emboli frequently spread to the lungs so an element of respiratory distress may be seen.

Treatment? use a beta-lactamase resistant beta-lactam. Surgical exploration may be required. The role of anticoagulation is controversial.

A great reference: check out this case

Tuesday, May 19, 2009

The Solitary Pulmonary Nodule

An Approach to the solitary pulmonary nodule.....

Differential Diagnosis:

  • Malignant: can be primary (adenoCa, squamous, large cell, or small cell), or metastatic
  • Infectious: Granuloma from TB or fungal infection (eg. histoplasmosis, coccidiomycosis), abscess, aspergilloma
  • Vascular: arteriovenous malformation, infarction
  • Inflammatory: Wegener's granulomatosis, rheumatoid nodule
  • Benign neoplasm: hamartoma, lipoma
Risk Factors for Malignancy:
  • Size greater than 3 centimeters
  • spiculated border
  • "eccentric" calcification pattern (see above image; calcium deposition is off-centre)
  • doubling time of the nodule is between 20 and 400 days
  • Clinical clues: constitutional symptoms, smoking history
As always:
  • Take a good history and physical exam
  • Get an old Chest X-ray
  • If you susptect malignancy: Get a tissue sample with Bronchoscopy vs Video-Assisted Thorascopic Surgery vs Open Thorascopy
A good link:

Friday, May 15, 2009


We have previously discussed our physical exam and diagnostic approach to Ascites here.

The mainstays of treating pancreatitis includes identifying an underlying cause and correcting it (eg. gallstone, hypertriglyceridemia, hypercalcemia, etc.), pain control and fluid resuscitation. Other issues that should be considered are feeding status and preventing infection.

1. Infection: patients are prone to infection by translocation of gut organisms if pancreatic necrosis is present. There is debate in the literature whether prophylactic antibiotics are indicated, and this uncertainty is reflected in guidelines from gastroenterology societies - one recommends it, one does not. Take a look at this Cochrane review and decide for yourself: http://www.cochrane.org/reviews/en/ab002941.html

2. Feeding: The classic teaching was that we do not feed our patients with acute pancreatitis. Newer evidence suggests that early oral feeding is alright if the patient can tolerate it. Here is a good meta analysis from the BMJ.

This is a good review article from NEJM touching on most of these topics

Wednesday, May 13, 2009

Physical Exam for Pulmonary Hypertension

Physical Exam for Pulmonary Hypertension:
  • JVP: may be elevated with prominent A waves (from right ventricular hypertrophy). CV waves are seen in tricuspid regurgitation. A positive Kussmaul's sign and Abdominal Jugular Reflux will be seen if there is right ventricular failure.
  • Inspection of the precordium: look for an apical beat. This may be displaced when left ventricular failure is the cause of pulmonary hypertension. Also look for right ventricular heaves.
  • Palpation: palpate for a right ventricular heave and sub-xyphoid impulsations (from RV hypertrophy). You may also find a palpable P2. There may be a pulsatile liver edge from tricuspid regurgitation.
  • Auscultation: listen for a normal S1 and loud S2. There may also be a split S2. You may hear a right sided S3 in right ventricular failure, or a right sided S4 in right ventricular hypertrophy. Finally, listen for the murmur of tricuspid regurgitation - a systolic murmur best heard at the left lower sternal border that classically gets louder with inspiration (Carvallo's sign).
  • Other: patients may have peripheral edema, and rarely ascites.

Links: here is a good review article on the causes of pulmonary hypertension.

Tuesday, May 12, 2009

Thyroid Cancers

(psammomma body in Papillary thyroid cancer)

There are many types of thyroid malignancies

  • Papillary carcinoma: Very common, spreads via lymphatics, more common in woman (3:1) aged 30-50, very high cure rate. Psammomma bodies are seen on histology.
  • Follicular carcinoma: The second most common thyroid cancer behind Papillary. This spreads hematogenously, so distant metastases are more common. It typically presents in the 40-60 year old age group with a cold thyroid nodule. It is difficult to distinguish between a follicular adenoma and carcinoma on cytology - so often a partial thyroidectomy is preferred over a fine needle aspiration for diagnosis.
  • Medullary carcinoma: This originates from C-cells (involved in calictonin production). This commonly affects families and is associated with the Multiple Endocrine Neoplasia syndromes. We discussed these here.
  • Anaplastic carcinoma: These are very undifferentiated tumors. Fortunately they are uncommon as the cure rate is low and life span is usually measured in months
A few other thyroid cancers to remember:
  • Lymphoma
  • Metastatic disease
Here is a good approach to the Thyroid Nodule.

Monday, May 11, 2009

Less is More...

The Syndrome of "Leser and Trelat" came up today in our discussion. It is certainly not that common, but one we should know about. This is a rapid eruption of seborrheic keratoses which can be pruritic and have an inflammatory base. It is a paraneoplastic condition commonly associated with intraabdominal malignancies - particularly gastrointestinal adenocarcinoma.

Here is a case from NEJM.

Monday, April 27, 2009

my mumps,......my mumps my mumps my mumps...check it out.

Please pardon the horrible Black Eyed Peas reference.

A great "Advanced Morning Report" today. We discussed a case that was likely Mumps.

More details can be found here.

Friday, April 24, 2009


(hyperthermia can cause rhabdomyolysis)

1. "....What are you lying on? This is a giant question...a maximus question....are you crushed by this?"..... this was in the context of patients found either unconscious or unable to get up for prolonged periods of time. He is referring to rhabdomyolysis. The 'maximus' comment must refer to the gluteus maximus, and the 'are you crushed?'....for sure that is for crush injuries. We discussed rhabdomyolysis here.

2. "...Let's think about cardiac causes of syncope...hey....Adam is here today...". Yep, this is a Stokes-Adams Attack, named after William Stokes and Robert Adams - two Irish physicians.

3. "...Sometimes you have overt alcoholics, then there are social drinkers...I'm thinking of the smallest room in the house..." So what's the smallest room in the house? The closet. He was referring to "closet alcoholics". We discussed alcohol related issues here, seizure disorders here, and toxic alcohol ingestions here.

4. "....Think about Captain Morgan!...". This was said in the context of him shaking his arms and head - convulsing. "Yes...this is a 'Rum Fit'". Also known as an alcohol withdrawal seizure. Remember your CAGE questionnaire to screen for alcohol-related problems:
  • do you feel the need to Cut back your drinking?
  • do you ever feel Annoyed at people critiquing your drinking?
  • do you ever feel Guilty about your alcohol consumption?
  • do you ever have an Eye opener? (Alcohol first thing in the morning)

  • 1 point is given every time your patient answers "yes" to a question. ....then you just add up the points.
  • Most patients with alcohol dependence will have a score of 2 or greater. About 80% of patients without alcoholism will score 0 points.
Here is a paper from JAMA written by local talent on the utility of alcohol screening tools.

Wednesday, April 22, 2009

There is the artist formerly known as Prince...

....and the pneumonia formerly known as Pneumocystis Carinii Pneumonia. Many people still refer to it as PCP , but you will also hear it called Pneumocystis Jirovecii Pneumonia (PJP). Either is fine. It is a common respiratory opportunistic infection in HIV+ individuals. Those with a CD4 count less than 200 are at the greatest risk. It is a protozoa, and is found ubiquitously in soil - we are all exposed, but this organism poses few problems to healthy immune systems.

The classic clinical presentation is dyspnea with subacute onset, and a dry cough. Patients may have a low-grade fever, tachycardia, and tachypnea. The chest exam is variable - you may hear crackles...you may have a normal exam (in up to 50% of cases). The Chest X-ray often reveals bilateral interstitial infiltrates, but virtually any abnormality may be seen.

Remember, we can make the diagnosis roughly 90% of the time with history and physical exam alone. Still, it is nice to confirm your diagnosis by isolating an organism. Methenamine silver or Immunofluorescent stains on induced sputum (or bronchoalveolar lavage) has a high sensitivity and specificity.

Treatment: TMP-SMX in high doses. This has some interesting complications associated with it (see below). If patients are allergic to sulfa drugs or have complications, other agents can be used, such as TMP-Dapsone, or Atovaquone.

Steroids? Yep. If the PaO2 is less than 70, this is very helpful. Of note, this was a major breakthrough in medicine and was discovered by local talent here in Toronto.

What else? Watch these patients closely. There is often a profound inflammatory reaction to the dying organisms, and patients often get worse on day 2-ish of treatment. That is why the steroids are added in severe disease.

  • Treatment guidelines for HIV can be found here.
  • Treatment guidelines for Opportunistic infections are here.
  • A great review of PCP from NEJM here.
  • Local talent publishing on an interesting complication from high dose trimethoprim-sulfamethoxazole.

Below: Methenamine silver (top) and Immunofluorescent (bottom) stains on induced sputum showing PCP.

Tuesday, April 21, 2009

Would you like fries with that?

Today we discussed Non-Alcoholic Fatty Liver Disease.

We have previously discussed the etiology of liver diseases here, and some complications of liver disease like ascites here, and spontaneous bacterial peritonitis here.

I don't know about you, but I'm dying for a burger right now.

Check out this review from CMAJ on Non-Alcoholic Fatty Liver Disease.

Monday, April 20, 2009

No Country for Old ________........

(Does this man have acromegaly?)

Multiple Endocrine Neoplasia
(MEN) syndromes can often be a bit confusing. It should be considered in those with....uhhhh....endocrine neoplasia - at multiple sites.

MEN 1: An autosomal dominant disease with mutations in the MENIN gene.
Remember "the 3 P's":
  • Pituitary tumors: particularly the anterior pituitary.
  • Pancreas: islet cell tumors like Insulinomas, Glucagonomas, and VIPomas.
  • Parathyroid hyperplasia, usually in all glands.

MEN 2: Also an autosomal dominant disease. The mutation is in the RET proto-onco gene.

  • MEN 2A: aka Sipple Syndrome
  • Medullary thyroid cancer; typically bilateral. In non-MEN disease this is mostly unilateral.
  • Pheochromocytoma in about 50%. Also can be bilateral.
  • Parathyroid hyperplasia
  • Men 2B
  • Medullary thyroid cancer: as above.
  • Parathyroid hyperplasia: as above.
  • Marfanoid habitus: high arched palate, pectus excivatum.

Friday, April 17, 2009


(Modigliani's Paul Guillaume Novo Pillota. In Paris' Musee d'Orangerie)

1. "....if you are anemic with your chronic renal failure, are you drinking the Tour de France drink?..." Okay...this one isn't too tough. He is referring to erythropoietin, a glycoprotein hormone produced by interstitial fibroblasts in the renal cortex, responsible for stimulating red blood cell production. Patients with chronic renal failure commonly have anemia secondary to low levels of this hormone. It is also a common performance enhancing drug which some famous athletes on the Tour de France were caught with recently.

2. "....is is hard to diagnose rheumatoid arthritis? No, they are usually deviant...". I liked this one. He is referring to ulnar deviation of the metacarpal bones in RA. Other common findings in the rheumatoid hand include swelling of the small joints - namely the MCPs and the PIPs, swan neck and boutonniere deformities in the fingers, median nerve entrapment, and trigger fingers (from nodules forming on tendon sheaths).

3. "...do you do math? Adding and subtracting? C'mon...this is a crisis!..." This was mentioned in the context of an elderly person on longstanding prednisone for a hemolytic anemia. "Adding"? "Crisis"? In a person on steroids? Yes, this is an Addisonian Crisis (adrenal crisis). Patients may present with clinical evidence of volume depletion, nausea, vomiting, shock, abdominal pain, and hyperkalemia with or without hyponatremia and hypoglycemia.

4. "...is it dangerous to take antibiotics? Is this a difficult hospital...?" Hmmm...'antibiotics'? 'Difficult'? Yep, this has got to be Clostridium difficile infection. A good review by local talent can be found here.

5. "...you look unflappable....is it frosty in here?...." I really liked this one. We were discussing a case of an elderly gentleman who presented with 1 week of malaise. He is referring to some signs of renal failure, including asterixis (unflappable - may also be seen in hepatic encephalopathy or hypercarbia), and the uremic frost. We don't really see uremic frost all that much - it's from severe uremia such that there are nitrogenous deposits on the skin Here's a case from NEJM with picture below.

Thursday, April 16, 2009

Oh Schist!(....ocyte)

Microangiopathic Hemolytic Anemia (MAHA):

It is important to rule out the microangiopathic hemolytic anemia's when you see a CBC with anemia and thrombocytopenia. After a very detailed history and physical exam, a few additional tests must be done to clinch the diagnosis:
  • Hemolyitic work up: LDH, unconjugated bilirubin, haptoglobin
  • Coomb's test: to assess for autoimmune hemolytic anemia
  • Blood film: looking for schistocytes
If there your patient has biochemical evidence of hemolysis and schistocytes on the blood film then this is likely MAHA. Note that a positive Coomb's test in autoimmune hemolysis will typically be associated with spherocytes on the blood film - this is not MAHA

What are some of the more important causes of MAHA?
  1. Thrombotic Thrombocytopenia Purpura: presents with a classic pentad of fever, neurologic changes, renal failure, hemolytic anemia, and thrombocytopenia....although most patients have only 2-3 of these features. A great case-based approach to TTP can be found here.
  2. Hemolytic Uremic Syndrome: on the same spectrum as TTP, more common in children, and as the name implies it has a renal failure phenotype. Here is a cool paper from JAMA looking at the risk of developing HUS after treating E. coli 0157:H7 strains.
  3. Disseminated Intravascular Coagulation: check for coagulopathy with an INR, PTT, fibrinogen, and fibrin degradation products.
  4. HELLP Syndrome: a variant of pre-eclampsia with hemolysis, elevated liver enzymes, and low platelets. Read more about this here.
  5. Malignant Hypertension. More on this here.

Wednesday, April 15, 2009

Mitral Regurgitation

Mitral regurgitation is common. When you hear this murmur and are trying to determine the underlying cause, think about the individual components of the mitral valve, and particular disease states which may affect them. Let's start at the annulus, and work our way down:

  1. Annulus: This may be dilated from cardiomyopathies, or calcified in diseases like rheumatic fever or chronic renal failure.
  2. Leaflets: The mitral leaflets can fail in a number of disease states, including infectious endocarditis (acute or chronic), rheumatic fever, autoimmune conditions (SLE, scleroderma), myxomatous degeneration (MVP), connective tissue diseases (eg. Marfans), and congenital malformations.
  3. Chordae: These can be damaged or rupture under ischemic, infected, or traumatic conditions and in rheumatic heart disease.
  4. Papillary Muscle: These muscles can rupture after trauma or infarct. They become 'dysfunctional' under ischemic conditions, or when the LV becomes dilated (myopathy or aneurysm). Papillary muscle can also become infected, and rarely can have infiltration with amyloid deposits or granuloma (eg. sarcoid).
Here is a good review on the evaluation and management of mitral regurgitation from NEJM.

Tuesday, April 14, 2009

"Shot through the heart, and you're to blame.....You give love a bad name "......Bon Jovi, circa 1986

Pericarditis: an approach....
  1. Idiopathic: many patients do not have an underlying etiology established. We assume that many of these patients have a 'viral' pericarditis.
  2. Infectious:
    • Viral: classically Coxsackie, Echovirus, and Adenovirus, but certainly others.
    • Bacterial: think about Staph and Strep species, and never forget TB (mycobacterial)
    • Fungal: Histoplasmosis, Aspergillosis, Blastomycosis
    • Parasitic: Toxoplasomosis, Echinococcus
  3. Malignant: usually metastatic disease like lung or breast cancers, or lymphoma.
  4. Autoimmune: Think about lupus, rheumatoid arthritis, and mixed connective tissue diseases.
  5. Metabolic: Uremic pericarditis is common, and hypothyroidism can cause a pericardial effusion.
  6. Cardiac: a pericarditis can be seen early after an infarction, or sometimes within 3-4 weeks afterwards....the so called Dressler's Syndrome.
  7. Drugs: can cause a drug-induced lupus. Common culprits include procainamide, INH, and hydralazine.
  8. Other things: Radiation, Trauma.

Monday, April 13, 2009


Some principles in the management of acute COPD exacerbations:

1. Stability: patients should be in a setting where their vital signs can be monitered closely.

2. Oxygen: can be delivered with increasing capacity. Note that if you are requiring more intense oxygenation, consider other etiologies of hypoxia such as pulmonary embolism. Oxygen can be delivered by....
  • nasal prongs
  • venturi masks (delivered in increasing FiO2's)
  • non-rebreathing masks
  • non-invasive positive pressure ventilation
  • intubation
3. Anticholinergic Agents: short acting ones like Ipratropium Bromide, in frequent and large doses.

4. Beta Agonists: also short acting ones like Salbutamol, also in frequent and large doses.

5. Steroids:
administered PO for most, or IV if your patient is very ill and/or will not tolerate PO meds. Commonly used doses include Prednisone 40-60 mg PO daily, or Methylprednisolone 125 mg IV given 2 times per day. Treatment usually lasts from 5-10 days.

6. Antibiotics:
Indicated in moderate to severe exacerbations. This includes patients who have 2/3 of:
  • increased dyspnea
  • increased sputum purulence
  • increased sputum production
or those requiring invasive ventilation.

7. When the dust settles: After the acute event it is important to counsel patients on smoking cessation, ensure they have their proper vaccines, re-evaluate their medications and ensure they are taking them properly, and possibly arrange for pulmonary rehabilitation.

A good paper on infections in COPD from NEJM.
A review on the management of COPD exacerbations in a case-based approach.

Thursday, April 9, 2009

Serum-Ascites Albumin Gradient

Calculate your Serum-Ascites Albumin Gradient:

If greater that 11 g/L: This is considered a transudate and is likely related to portal hypertension. Think about cirrhosis, CHF (right sided), constrictive pericarditis, or Budd-Chiari syndrome.

If less than 11 g/L: This is considered an exudate and is not related to portal hypertension. Think about pancreatitis, peritoneal carcinomatosis, peritoneal TB, serositis, or low albumin states like nephrotic syndrome.

(Physical exam manoeuvres for ascites, from the JAMA rational clinical exam. Link provided below).

  1. JAMA's, Does This Patient Have Ascites?
  2. Here is a great article on managing cirrhosis and ascites from NEJM.

Wednesday, April 8, 2009

Follow the arrows...it's that easy

An interesting Morning Report today on DKA - first presentation.

Here is a good approach to the confused patient.

You can read about precipitants to DKA here.

Check out the management of DKA/HONK here.

(the great Shane McConkey, pictured below)