Happy Holidays

On Monday in dermatology morning report we discussed SJS/TEN.

Here is a great reference that our presenter, Dr. A.D., has recommended.

Happy Holidays everyone and see you in January!

Drug-induced liver injury (DILI)

This morning we discussed drug-induced liver injury (DILI). Many drugs, both prescription and over-the-counter, can cause hepatotoxicity, so a careful medication history should always be obtained when a patient presents with liver enzyme abnormalities.

DILI can range from asymptomatic mild enzyme elevations to fulminate liver failure. Jaundice in addition to elevated enzymes is associated with a worse prognosis than that seen in the setting of isolated ezyme abnormalities (an observation known as "Hy's law").

The most important treatment for DILI is cessation of the offending drug.

Here is a review on DILI.

* H& E stain, liver biopsy, atorvastatin-induced acute hepatitis, Inflammatory cell infilteration of the liver parenchyma consistant with inflammation.

Hypersensitivity Pneumonitis

This morning we talked about hypersensitivity pneumonitis- also referred to as extrinsic allergic alveolitis.

This condition is an immunologic reaction of lung parenchyma to an inhaled agent, particularly an organic antigen. HP has been identified in various groups including farmers, bird handlers, carpenters, and those exposed to various industrial dusts. Mold exposure in poor housing can cause HP.

HP can present acutely with abrupt onset of fever, cough, dyspnea, and diffuse fine crackles. CXR may be normal or show transient patchy opacities. Subacute HP presents with gradual development of productive cough, dyspnea, fatigue, anorexia, and weight loss. Respiratory symptoms are more severe than with acute HP, and radiographic findings more extensive.

Removal from exposure to the inciting antigen leads to improvement in symptoms.

* Many adults and children suffer from chronic cough and respiratory symptoms secondary to mold exposure in poor housing in the Northern Ontario Cree community of Attawapiskat.

Here is the CBC photo gallery of the Attawapiskat Housing Crisit.

"once a chief, always a chief...."

This morning, we reviewed a case of HTLV-1 associated T-Cell lymphoma. The human T-lymphotropic virus (HTLV-I) is a retrovirus.

As we discussed, HTLV-1 is also associated with myelopathy, AKA tropical spastic paraparesis (TSP) which causes progressive weakness and spasticity of one or both legs with hyperreflexia.

HTLV-I is diagnosed by serum serology.

Treatment is not indicated for asymptomatic HTLV-1 infection.

*The title of this post has nothing to do with HTLV-1. I just liked Dr. HPK's quote from this morning!

Alcoholic hepatitis

This morning we reviewed a case of Alcoholic hepatitis at morning report.

Updated Post written by Dr. Wong

Alcoholic hepatitis takes place DURING significant alcohol use. They rarely seek medical attention because the hepatitis is mild and resolves on stopping alcohol for a few days. When they do present to ER, it is usually because symptoms persist despite abstinence. Patients rarely recognize jaundice, but in retrospect will have noticed dark urine.

Alcoholic liver disease can be recognized by the findings of AST > ALT, high GGT and high MCV.

Alcoholic hepatitis presents with AST 80-300 > ALT, low grade fever, a rise in WBC/left shift from baseline (baseline may be low), RUQ tenderness. Mild cases (normal INR) have an excellent survival prognosis. Severe hepatitis (INR > 1.9, Bilirubin > 100 or MELD > 21) has a high mortality risk and steroid therapy should be considered.

Therapy is Prednisone 40 mg OD x 4 weeks, no taper. Therapy is contra-indicated in the setting of infection, GI bleeding or renal failure.

Reassess after 1 week, stop if no improvement in bilirubin.

Nutrition with adequate calories is the other mainstay of therapy.

* Coloured light micrograph of a section through the liver of a patient with alcoholic hepatitis, inflammation of the liver due to heavy alcohol consumption. The normally regular cellular structure of the liver has been disrupted here, and large vacuoles of fat (yellow) are seen. The circular structures at centre are bile ducts.

Hypomagnesemia

This morning we reviewed a case of severe hypomagnesemia .

Patients often present with generalized weakness and non-specific complaints, but VENTRICULAR ARRYTHMIA and neurologic finings such as delirium and coma can also occur.

ETIOLOGY
- GI losses: diarrhea
- Renal losses: renal failure or renal magnesium wasting due to drugs such as diuretics, aminoglycosides, or cisplatin, or rare genetic causes such as Gitleman's disease
- Alcohol: causes renal tubular dysfunction and urinary loss of Mg.
- Decrease PO intake

**Think of Magnesium depletion in refractory hypokalemia or unexplained hypocalcemia.

MANAGEMENT:
Route depends on severity and renal function

If hypomagnesemic-hypokalemic ventricular arrhythmias: give 50 meq of IV magnesium slowly over 8 to 24 hours and repeated as necessary to maintain the plasma magnesium concentration above 0.4 mmol/L or 0.8 meq/L.

Oral replacement is adequate for asymptomatic patient.

Treat the underlying disease.

Hypertensive Emergency

We discuss the approach to and management of hypertensive emergency.

Here is a previous post on that topic.

Neurosyphilis (in non-HIV patient)

This morning we discussed a case of rapidly progressive dementia, likely secondary to neurosyphilis.

Neurosyphilis can occur early or late. It may occur with primary, secondary, or tertiary syphilis. Early neurophysilis can present as stroke, meningitis, meningoencephalitis, cranial nerve deficits, hearing loss (otosyphilis), or visual loss (oculosyphilis). Late neurosyphilis occur decades later and can presents as general paresis, dementia with psychosis (rapidly progressive), or tabes dorsalis (posterior column involvement, bowel, bladder dysfunction).

Syphilis Screen:
CMIA-Chemiluminescent Microparticle Immunoassay (serum)- T.pallidum (IgG/IgM)
VDRL-Venereal Disease Research Laboratory-no longer done at UHN labs.
RPR - Rapid Plasma Reagin Test. Detects total IgG/IgM antibody to syphilis (T. pallidum). Automatically done by lab if CMIA is reactive.

CMIA and PRP are called “syphilis screen” in EPR

Confirmatory Tests:
TP.PA- Treponema pallidum particle agglutination.
FTA.ABS- fluorescent treponemal antibody. Positive confirmatory test(s) are often reactive for life

CSF examination (not done at UHN lab, sent to PHL):
• CSF VDRL is specific but not sensitive
• CSF FTA-ABS is sensitive but not specific

Here is a review of syphilis.

Click here for the Ontario Public Health Lab algorithm for interpreting the MANY permutations and combinations of lab results

* A U.S. Army Educational Commission Poster about Neurosypilis, 1918.

Epidural Abcess

This morning we discussed a case of fever with back pain and our differential included epidural abscess.

If you're thinking about an epidural abscess, you need to image the spine. MRI is the best modality as it is sensitive to pick early signs of inflammation. CT with IV contrast is an acceptable alternative if MRI is not available. Plain X-ray may show changes of advanced osteomyelitis or discitis but is not used to diagnose an epidural abscess.

Here is a previous post and a reference on Epidural Abscesses.

Once in a while my heart flutters really fast...

This morning we discussed a case of CHF decompensation secondary to atrial flutter with rapid ventricular response.

Atrial flutter is an arrhythmia of organized atrial activity that is not a sinus rhythm. It can be seen its own or sometime as a transition arrhythmia between sinus rhythm and atrial fibrillation.

Any disorders predisposing to atrial fibrillation can cause atrial flutter including thyrotoxicosis, obesity, the sick sinus syndrome, pericarditis, pulmonary disease, and pulmonary embolism. Mitral valve prolapse and cardiac surgery are also risk factors for developing atrial flutter.

Atrial flutter is very similar to atrial fibrillation its clinical presentation and should be treated the same in terms of rate control and anticoagulation. Ablations therapy is very successful for atrial flutter, however, so long-term antiarrhythmic medications are infrequently used.

Here is review on managment of Atrial Flutter.

* the hallmark of atrial flutter on ECG is the saw-tooth pattern (also referred as a picket fence pattern).

Light's Criteria for Pleural Effusion

Today at morning report we discussed the Light's Criteria.

Light's criteria for exudative effusion are any of
protein level pleural:serum over 0.5
LDH pleural:serum of over 0.6
pleural LDH over 2/3 upper limit of normal for serum

The combination of the three criteria has a higher sensitivity, but a lower specificity, than each individual criterion. Light's criteria are sensitive for exudate; may have transudates falsely called exudates. If clinical appearance suggests transudate but Light's criteria says exudate, measure albumin in serum vs. pleural fluid. If serum albumin is over 12 greater than pleural fluid almost all have transudative.

Our case had a bloody effusion, which narrows Ddx somewhat to cancer, PE, trauma, infection (inc. pneumonia, TB)

Here is a review of Pleural Effusion by Dr. Light himself!

*A large left sided pleural effusion as seen on an upright chest X-ray.

Ascites

At Gel Rounds we discussed ascites.

Some key points:

Most sensitive findings (i.e. make it unlikely if not present):
1) flank dullness
2) bulging flanks
3) shifting dullness
4) peripheral edema
-history of increased girth, weight gain, ankle swelling

Most specific findings (i.e. make it likely if present)
1) fluid wave
2) shifting dullness

An approach to the examination in liver disease (besides examining the liver itself)

1) Signs of decompensated liver disease
-jaundice, scleral icterus, dark urine (high bilirubin)
-petechiae, ecchymoses (coagulopathy)
-edema (hypoalbuminemia)
-asterixis, level of consciousness (encephalopathy)

2) Signs of portal hypertension
-ascites
-splenomegaly
-dilated abdominal veins (extreme of this is caput medusae)
-hemorrhoids

Reference:

Click here for JAMA rational clinical exam on ascites.

* using the ultrasound, we looked at the Pouch of Morrison, which is a potential space between the liver and the right kidney. This is the first spot to check if you suspect a small amount of ascites. The picture shows Morison's pouch with fluid present (red arrows).

Pericarditis

At physical exam rounds today, we reviewed Pericarditis.

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, and 3. ventricular diastole.

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

Treatment: In most cases of idiopathic pericarditis, high dose NSAIDS are effective. Steroids and colchicine also may have a role.


Here is a review article on the topic.

Rhabdomolysis

This morning we discussed a case of rhabdomyolysis.

Here is a previous blog post on the topic.

*myoglobinuria

Miller Fisher Syndrome

Guillain-Barré syndrome (GBS) is an immune-mediated polyneuropathy characterized classically by ascending weakness and absent reflexes. GBS is a heterogeneous disease with several variants. Miller Fisher Syndrome (MFS) is a variant that presents with opthalmoplegia, ataxia and areflexia.

In patients with GBS, CSF has elevated protein and normal WBC. In about 85% of patients with MFS antibodies against GQ1b (a ganglioside component of nerve) is positive, though this testing is not routinely performed.

Here is review of Guillain-Barre Syndrome.

* Dr. C. Miller Fisher, Canadian neurologist who first described the MFS variant of GBS in 1956. He was a stroke neurologist who contributed greatly to our understanding of lacunar stroke, and strokes related to atrial fibrillation.

SSRI and SIADH

This morning we talked about the association between SSRIs and SIADH.

The article we talked about was a review, by Dr. Liu, of case reports involving various SSRIs and hyponatremia. This study found that the majority (83%) of patients with this complication were over the age of 65. The average time to onset of hyponatremia was 13 days (range 3 to 120 days). This finding has since been confirmed through a prospective study.

Take home message is that elderly patients are at increased risk of hyponatremia associated with SSRIs.

Here is the abstract for the above article.

Here is a great review article about SAIDH.

Mitral Regurgitation

In physical exam rounds yesterday, we examined a patient with mitral regurgitations.
Here is a previous post on Mitral Regurgitation.

*Doppler ultrasound of the heart showing mitral regurgitation: there is abnormal leakage of blood backward (blue is flow away from the probe) through the mitral valve during systole.

Antimitochondrial antibody

Antimitochondrial antibody is present in 95% patients with Primary Billiary Cirrhosis. The antibody assay is 95% sensitive and 98% specific for PBC (except if it's done by indirect immunoflorescence).

There has been suggestion that the presence of antimitochondrial antibodies may predict the eventual development of PBC in asymptomatic people based on a small study. About 13% of first-degree relatives of patients with PBC have circulating antimitochondrial antibodies, suggesting they may be susceptible to developing PBC. The clinical significance of this finding remains to be determined.

Here is a great review on Primary Billiary Cirrhosis.

*Immunofluorescent stain shows antimitochondrial antibodies on a liver biopsy specimen.

Endocarditis

This morning we discussed a case of subacute bacterial endocarditis secondary to Strep viridans.

Here is a previous post on endocarditis with some great review referrences.

* Viridans Streptococcus is a term for a large group of commensal streptococcal bacteria that are either α-hemolytic, producing a green coloration on blood agar plates (hence the name "viridans", from Latin "vĭrĭdis", green), or nonhemolytic.

Hypertension

This morning we discussed a case of Hypertensive Emergency.

Here is a previous post on this topic.

* William Harvey (1578–1657)the first physician who described the systemic circulation of blood being pumped around the body by the heart in his book "De motu cordis" which became the basis for our current understanding of hypertension.

Hypophosphatemia

Hypophosphatemia is secondary to decreased intestinal absorption (such as in Vit D deficiency), increased urinary excretion (such as in hyperparathyroidism), or shift into the cells (such as in refeeding syndrome).

Symptomatic hypophosphatemia occur when serum phosphate concentration reaches 0.64 mmol/L. Worrisome symptoms of hypophosphatemia are related to ATP depletion, causing metabolic encephalopathy, impaired myocardial contractility, respiratory failure due to weakness of the diaphragm, a proximal myopathy, Rhabdomyolysis, dysphagia, ileus, and hematologic abnormalities.

Hypophosphatemia should be replaced aggressively even if the patient is not overtly symptomatic, since develop myopathy and weakness.

IV phosphate is potentially dangerous, since it can precipitate with calcium causing hypocalcemia, renal failure due to calcium phosphate precipitation in the kidneys, and possibly fatal arrhythmias. So, if IV therapy is necessary in the patient with severe symptomatic hypophosphatemia, it should be given by slow infusions (over a long period of 4-12hrs).

Paraneoplastic Erythrocytosis

There are 5 types of tumor commonly associated with the overproduction Epo:

1. Hepatocellular carcinoma: Epo elevation doesn’t always cause erythropoiesis because of RBC production inhibition by malignancy.

2. Renal cell carcinoma: In about 1-5% of patients.

3. Hemangioblastoma

4. Pheochromocytoma

5. Uterine myomata: clue will be absence of anemia in patients with menorrhagia. RBC overproduction is reversed following myomectomy.

*Contrast-enhanced MRI image of a patient with Hb=194, showing renal cell carcinoma(arrow).

HIV and Pneumococcal Disease

Although we automatically think about opportunistic and atypical infections in immunocompromised patients, it is important to note that , similar to non-HIV infected patients, Streptococcus pneumoniae, is the most common bacterial pathogens of CAP in patients with HIV.

As was discussed this morning, HIV infection substantially increases the risk of invasive pneumococcal infection, particularly among those patients with a low CD4 count <200, and those not on therapy. This increased risk may be partially explained by the observation that HIV infected individuals have a predisposition for pneumococcal nasopharyngeal colonization.

For this reason, the Centers for Disease Control and Prevention (CDC) recommends that all HIV–infected patients be vaccinated (preferably early in the disease while they still have the ability to mount an effective antibody response).

Here is a review on the topic.

Invasive pneumococcal disease in patients infected with HIV: still a threat in the era of highly active antiretroviral therapy. Jordano et al. Clin Infect Dis.38(11):1623.

* Chest radiograph of an HIV positive individual with a CD4 cell count above 200 cells/mm3, revealing right upper lobe consolidation. Sputum and blood cultures were positive for Streptococcus pneumoniae.

Hypercalcemia associated with Malignancy

We discussed a case of hypercalcemia this morning and reviewed the mechanisms by which malignancy can cause hypercalcemia.

1. Direct metastases to bone: These mets trigger the production of inflammatory cytokines and stimulate ostoclasts. Sometimes osteoclasts are directly stimulated by tumor cells via Osteoclast Activating Factors (eg IL6) in multiple myeloma or lymphoma.

2. PTH related peptide: this is the most common cause of hypercalcemia from non-metastatic solid tumors. Classically in squamous cell lung Ca

3. PTH: this is rare! only a few case reports of PTH being released from tumors

4. Calcitriol: a very common mechanism for hypercalcemia in the lymphomas.

Here is a great review article.
*CT scan of a patient presenting with Ca=3.1, who subsequently was found to hav have small cell lung cancer.

This morning we talked about a variety of different cases. One of them, involved a patient with a presentation of swollen warm painful knee. Here is a previous morning repot blog post on approach to monoarthritis.

*The Gout by James Gillray. Published May 14th 1799.

Hormone Replacement Therapy

This morning we briefly talked about the Women’s Health Initiative (WHI)and hormone replacement therapy. WHI was a set clinical trials including two hormone trials in healthy postmenopausal woman 50-70. The hormone trials were stopped early due to increased risk of cardiac events, VTE, stroke and breast cancer. The study did show benefits in reducing fracture and colorectal cancer risk.

Subsequent analysis of the WHI noted that the increased risk of CHD tended to depend on the timing of exposure, with no excess risk observed in younger menopausal women.

Current recommendations are as follows:

Moderate to severe menopausal symptoms can be treated with short term HRT in peri- or postmenopausal women (and no contraindications to estrogen). HRT should be stopped before five years. HRT should not be used as primary or secondary prevention of CAD.


Here is Endocrine Society’s statement on HRT.

Lets SIGN OUT? at TWH!

Handing over. We do it often. And the information we transfer is critical to patient safety. This morning we talked about SIGN OUT? as a template for our signovers.

S: Is the patient sick? Code status!!!
I: Identifying data
G: General hospital course
N: New events
O: Overall health status right now
U: Upcoming possibilities (if and then statements)
T: Tasks to complete overnight
?: Questions

Every team will function differenly, but sticking to consisten hand over template an style keeps communication flowing, and patients safe.

* it's 5pm...have you Singed Out yet?!

VTE and Malignancy

The questions of screening for an occult malignancy comes up often when a patient presents with unprovoked VTE. There are multiple observational studies that have confirmed the increased incidence of malignancy among those with VTE, however, none has shown improved survival with aggressive diagnostic testing. None of these studies are prospective.

As a result, the current recommendations is that all patients with idiopathic DVT should be evaluated with careful history. A past history of cancer should be a red flag. Other symptoms such as loss of appetite, weight loss, fatigue, pain, hematochezia, hemoptysis, and hematuria should also raise suspicion about cancer.

A complete physical examination (including digital rectal examination and testing for fecal occult blood, pelvic examination in women), and routine laboratory testing (complete blood count, chemistry panel including electrolytes, calcium, creatinine, and liver function tests), urinalysis and CXR should also be performed. Furthermore, age-appropriate cancer screening (PSA, FOB and C-scope, mammogram) should be offered.

Any abnormality observed on initial testing should then be investigated aggressively.

HCV-associated Cryoglobulinemia

Cryoglobulins are immunoglobulins that precipitate in cold and dissolve with warming.

HCV infections is associated with Type II or essential mixed cryoglobulinemia (polyclonal IgG and a monoclonal IgM rheumatoid factor directed against the IgG) and Type III or mixed cryoglobulin (polyclonal IgG and rheumatoid factor IgM).

Deposition of antigen-antibody complexes in small and medium-sized arteries leads to the clinical findings of cyroglobulinemia. It is unclear, however, why cryoglobulins are produced and which antigen triggers this process. HCV RNA itself may serve as the inciting agent.

Clinical features include palpable purpura, nonspecific systemic symptoms, arthralgias, lymphadenopathy, hepatosplenomegaly, peripheral neuropathy, and hypocomplementemia (low C4).

Here is a review on the topic.

*image is papable purpura (non-blanching erythematosus papules) found in a patient with chronic HCV infection with mixed cryoglobulinemia.

"Did the green onion make me yellow"?

Hep A is an RNA virus that spreads by the fecal-oral route. HAV is more prevalent in low socioeconomic areas with lack of adequate sanitation and poor hygienic practices. International travel is the most common risk factor in USA (and Canada).

HAV infection usually results in an acute, self-limited illness and only rarely leads to fulminant hepatic failure in those with underlying liver disease, especially chronic hepatits C infection.

The manifestations also vary with age: HAV is usually silent or subclinical in children. In contrast, infection in adults can vary in severity from a mild flu-like illness to fulminant hepatitis. The incubation period averages 30 days (range 15 to 49 days). Symptoms include fatigue, malaise, nausea, vomiting, anorexia, fever, and right upper quadrant pain followed by dark urine, light stools, jaundice, and pruritus. Lab investigations show marked elevations of serum aminotransferases (usually >1000 IU/dL), bilirubin, and alkaline phosphatase.

Acute HAV infection is diagnosed by the detection IgM anti-HAV in serum.

The treatment is supportive care.

* image: the most widespread hepatitis A outbreak in USA affected 640 people (killing 4) ,in late 2003, was blamed on tainted green onions at a restaurant.

Statin-induced muscle injury

Muscle injury with statin therapy can range from myalgias to myositis to rhabdomyolysis. Muscle symptoms usually begin within weeks to months after starting statins and usually return to normal over days to weeks after drug discontinuation.

You should warn your patients about new onset muscle pain and weakness when you start a statin. A CK level should be obtained at baseline, but routine monitoring of serum CK levels is not recommended.

Patients with acute or chronic renal failure, liver disease, and hypothyroidism are at higher risk of developing muscle injury. Clinical symptoms or a CK level >10X the upper limit of normal should prompt a drug discontinuation.

Pravastatin and fluvastatin appear to have much less intrinsic muscle toxicity than other statins. After the CK has returned to baseline, patients may be tried on a statin less likely to cause muscle toxicity with careful monitoring.

Here is review on the topic.

An assessment of statin safety by muscle experts. Thompson PD, Clarkson PM, Rosenson RS, National Lipid Association Statin Safety Task Force Muscle Safety Expert Panel. Am J Cardiol. 2006;97(8A):69C.

Antibiotics in COPD exacerbation

The use of antibiotics in exacerbations of COPD is based on small placebo-controlled trials and large retrospective population studies. They found that antibiotics improve clinical outcomes in severe COPD exacerbations. There is little evident for the use of antibiotics in mild exacerbation.

A recent cochrane review on the topic concluded that "in COPD exacerbations with increased cough and sputum purulence antibiotics, regardless of choice, reduce the risk of short-term mortality by 77%, decrease the risk of treatment failure by 53% and the risk of sputum purulence by 44%; with a small increase in the risk of diarrhoea These results should be interpreted with caution due to the differences in patient selection, antibiotic choice, small number of included trials and lack of control for interventions that influence outcome, such as use of systemic corticosteroids and ventilatory support. Nevertheless, this review supports antibiotics for patients with COPD exacerbations with increased cough and sputum purulence who are moderately or severely ill".


Choice of antibiotics is an area where not a great deal of evidence exists. Most initial trials were with Amoxicillin, Doxycyclin and Septra. However, these antibiotics are no longer considered first-line for treatment of pathogens such as H.Flu and M. catarrhalis that maybe responsible for COPD exacerbations. When deciding on the antibiotic choice, risk factors such as older age (>65 years), comorbid conditions (especially cardiac disease), severe underlying COPD (defined as FEV1 <50 percent), frequent exacerbations (three or more per year), and antimicrobial therapy within the past three months should be taken into account.

The GOLD guidelines recommend antibiotic therapy for patients with:

1) Severe exacerbation requiring mechanical ventilation
2) With three cardinal symptoms of increased sputum purulence plus either increased dyspnea or increased sputum volume
(thought they don’t provide any guidance regarding the choice of antibiotics)

WITHDRAWN: Antibiotics for exacerbations of chronic obstructive pulmonary disease.
Ram FS, Rodriguez-Roisin R, Granados-Navarrete A, Garcia-Aymerich J, Barnes NC. Cochrane Database Syst Rev. 2011 Jan 19;(1):CD004403.

4 for 2, 2 for 4

This morning we reviewed the drugs involved in treatment of active tuberculosis.

The initial phase of treatment usually consists of two months of therapy with four drugs--typically isoniazid, rifampin, pyrazinamide, and ethambutol. The continuation phase in most cases consists of isoniazid and rifampin for four months (remember “4 for 2, 2 for 4”).

Treatment requires careful monitoring for drug toxicity. Baseline transaminases, bilirubin and ALP, CBD, creatinine, and uric acid should be obtained. When starting ethambutol, patients should be referred to ophthalmology for visual acuity and red-green color discrimination testing. Patients should be monitored closely for signs of hepatic toxicity.

Here is a recent update on TB management.
Current concepts in the management of tuberculosis. Sia IG, Wieland ML. Mayo Clin Proc. 2011 Apr;86(4):348-61

* Ghon's complex, seen in left middle field in the above image, is a lung lesion caused by tuberculosis that consists of a calcified focus of infection and an associated lymph node.

The Right dose at the Right time

This morning we discussed a case of fever and headache. We reviewd the approach to diagnosis and treatment of bacterial meningitis. Two key points from our discussion were:

1. Antibiotic therapy should not be delayed for any reason and should be given immediately after blood cultures are obtained. Dexamethasone should be given shortly before or at the same time as the first dose of antibiotics, when S. pneumoniae is suspected.

2. The "meningitis doses" of the empiric antibiotics in patients with normal renal function is: Vancomycin 1.5-2g IV q12, Ceftriaxone 2 g IV every 12 hours, and if Listeria suspected Ampicillin 2gr IV q4hr.


Here is a previous post on Meningitis.

*Steptococcus Pneumoniae, a gram postive cocci in chains, is the most common cause of community acquired bacterial meningitis in adults.

A case of bloody diarrhea

Today we discussed a case of bloody diarrhea caused by Enterohemorrhagic E. coli (EHEC), strain O157: H7.

Patients with this infection generally present with bloody diarrhea, mild leukocytosis, abdominal pain, but no fever. This bacteria produces a toxin called the Shiga toxin which can result in the dreaded Hemolytic-uremic syndrome (HUS)- the major systemic complication of EHEC infection. HUS is characterized by the triad of acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia

The treatment of EHEC infection consists of supportive care and monitoring for the development of microangiopathic complications. Administering antibiotic therapy to patients with EHEC is not recommended (Grade 1B- though the evidence is only in children <10).

Here is a review article on the topic.

Escherichia coli O157:H7 and the hemolytic-uremic syndrome.Boyce TG, Swerdlow DL, Griffin PM. N Engl J Med. 1995;333(6):364.

* Romanian greenhouse employees destroy tons of cucumbers for fear of E. coli. In May 2011, a new Shiga toxin-producing EHEC strain, O104:H4, was identified as the cause of an outbreak in Germany and other countries in Europe.

"a case of abnormal bone softening"

We talked about a case of newly diagnosed Multiple Myeloma. Here is a previous blog post on the topic.

*Sarah Newbury, the first reported patient with multiple myeloma. (A) Bone destruction in the sternum. (B) The patient with fractured femurs and right humerus. (C) Bone destruction involving the femur. Reported by Solly 1844.

Combined ASA and Plavix in setting of Acute Stroke

This morning we talked about the evidence behind dual therapy with ASA and plavix in the setting of acute stroke.

A large study called the MATCH trial, with over 7500 patients, did not find any benefic with the combined use of aspirin and clopidogrel but found significant increase in the risk of bleeding complications.


The FASTER trial, a much smaller study with 392 patients with TIA or mild stroke, compared either aspirin plus clopidogrel (300 mg loading dose, then 75 mg daily) or aspirin alone. The trial ended prematurely due to slow recruitment. At 90 days, there was no statistically significant difference between the groups but a trend toward decreased primary outcome measure of combined ischemic and hemorrhagic stroke (7.1 versus 10.8 percent).

Silk Road Disease

This morning we discussed a case of oral ulcers and our differential diagnosis included Behcet’s disease.

This disorder is a systemic vasculitis that can effect veins of variable sizes. The disease is characterized by relapsing episodes of oral and genital ulcers, skin lesions, and ocular lesions, and can affect other systems including vascular, gastrointestinal, and neurological systems.

It occurs most frequently in an area that coincides with the Old Silk Route, so the disease is sometimes referred to as the Silk Road Disease.

Mainstay of treatment is immunosuppression with corticosteroids, azathioprine, cychlophosphamide, cyclosporine A, and more recently biologics including interferon-alpha, anti-tumour necrosis factor alpha agents.


Here is a recent feview article on the topic.

Behçet's disease--a contemporary review. Mendes D, Correia M, Barbedo M, Vaio T, Mota M, Gonçalves O, Valente J. J Autoimmun. 2009 May-Jun;32(3-4):178-88. Epub 2009 Mar 26.


* The image is a picture of Hulusi Behçet, a Turkish dermatologist and scientist who first described the illness in 1936.

Tachycardia-induced Cardiomyopathy

We discussed a case of tachycardia-induced cardiomyopathy this morning. This condition results from prolonged periods of rapid ventricular heart rates, and often improves with heart rate control with a good prognosis in most patients.

Patients may present with palpitations, fatigue, decreased exercise tolerance, or symptomatic congestive heart failure.

Treatment of tachycardia-mediated heart failure is the same as any other heart failure (eg, ACE or ARB inhibitors, beta blockers, diuretics), with aggressive control of heart rate.

Here is a recent review article on the topic

Tachycardia-induced cardiomyopathy: evaluation and therapeutic options. Lishmanov A, Chockalingam P, Senthilkumar A, Chockalingam A. Congest Heart Fail. 2010 May;16(3):122-6.


* Chest x ray showing cardiomegaly (panel A) in a patient with tachycardia (panel B). Panel C shows improved cardiomegaly after 3 months of aggressive heart-rate control (panel D). Images in Cardiology. Heart 2001;86:642.

Diabetic Autonomic Neuropathy

This morning our we talked about diabetic autonomic neuropathy (DAN) in long-standing diabetes.

DAN is a common and distressing complication that can affect any or all parts of the autonomic nervous system (ANS). Many organs are innervated dually by the parasympathetic and sympathetic fiber. DAN can cause hypo- or hyperactivity of each or all parts of the ANS.

Clinical manifestations can include the cardiovascular system (tachycardia, exercise intolerance, cardiac denervation leading to silent ischemia, orthostatic hypotension), GI system (esophageal dysfunction, gastroparesis, diarrhea or constipation, fecal incontinence), GU system (erectile dysfunction, neurogenic bladder), skin (impaired sweating), and metabolic dysfunction(hypoglycaemia unawareness).

Here a review article on the topic.
Diabetic autonomic neuropathy. Vinik AI, Freeman R, Erbas T. Semin Neurol.(4):365-7.

* A plain abdominal radiograph showing a very dilated stomach (arrows) secondary to diabetic autonomic neuropathy (Images in Clinical Medicine NEJM)

Water Intoxication

This morning, we discussed a case of hyponatremia.

Remember that disorders of sodium are really problems with water balance, so it is helpful to think of hyponatremia as excess free water. Prior to being able to test for serum sodium concentrations, the clinical syndrome that is now known as hyponatremia, characterized by confusion, muscle cramps, fatigue, delirium, seizures, and death, was called “water intoxication” syndrome.

Here are two previous post on hyponatremia.
Hyponatremia
Hyponatremia - no it's Hyperhydroemia


* MRI scan of person with central pontine myelinolysis (Saggital view, the dark area inside the circle is the region of damage). CPM is a devastating consequence of rapid fluctuations in sodium status.

Equilibrium

Today in morning report a few of the presented cases had disorders of equilibrium with the two cardinal symptoms of either vertigo – an illusion of bodily or environment spinning- or ataxia- incoordination of limbs or gait.

Disorders of disequilibrium can be produced by conditions that affect the vestibular pathways, the cerebellum, or sensory pathways in the spinal cord or peripheral nerves.

We considered the diagnosis of stroke in all of the above cases. A recent article in CMAJ called "Does my dizzy patient have a stroke" addresses that same question. Here is the article.

*Jean Louis Forain's 19th Century Tightrope Walker. How many organ systems is the performer using to maintaining her balance in the dark?

Is This Patient Malnourished?

In our physical exam rounds today, we examined a patient for signs of malnutrition, and reviewed the JAMA RCE article on the topic.

The gist of the articles is to know the “Subjective Global Assessment” which includes the following:
•History (Weight change,Dietary intake change,GI symptoms,Functional capacity)
•Physical exam (Loss of subcutaneous fat, Muscle wasting, Edema)

Based the above, you can categorize patients into “well-nourished”, “moderately malnourished”, or “severely malnourished”. These categories then correlate with patient likelihood of being admitted, and post-operative complications.

Here is the article.
http://www.ncbi.nlm.nih.gov.myaccess.library.utoronto.ca/pubmed?term=is%20this%20patient%20malnourished%20detsky%20JAMA

* Given our topic of conversation, I like to remind everyone of the famine in East Africa. A devastating drought and crumbling infrastructure have created one of the worst hunger emergencies in our generation. If you would like to make a donation, the Government of Canada has created the East Africa Drought Relief Fund, and will match your donations.

An aspirin a day? ASA in secondary prevention of CVD.

This morning we briefly mentioned the Antithrombotic Trialists' Collaboration overview article. This group reviewed the results of 195 randomized trials of aspirin, among more than 135,000 high-risk patients with prior history of cardiovascular or cerebrovascular events. The following are the major conclusions:

• Aspirin, significantly reduced the relative risk of subsequent vascular events (nonfatal MI, nonfatal stroke, and vascular death) by approximately 22 percent.
• There was no difference in efficacy between doses of 75 to 150 mg/day (called low-dose aspirin) and 160 to 325 mg/day (called medium-dose aspirin).

Here is the link to the paper if you like.
Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. Antithrombotic Trialists' Collaboration. BMJ. 2002;324(7329):71.

http://www.ncbi.nlm.nih.gov.myaccess.library.utoronto.ca/pubmed?term=BMJ.%202002%3B324(7329)%3A71.

* A French advertisement for aspirin from 1923. Aspirin (name originally coined by they Bayer company in 1897) lost its status as a registered trademark became a generic name in many countries. Today, Aspirin, with a capital "A", remains a registered trademark of Bayer Canada.

...and the QT was 580!!

Amuse-Bouche at today’s morning report was prolonged QT interval on the ECG. This conditions is associated with an increased risk of torsades de pointes, which is a life threatening polymorphic ventricular tachycardia.

Long QT can be genetic or acquired. Drugs are a common cause of prolonged QT. Among them are:
• Antiarrhythmic drugs such as sotolol, amiodarone, quinidine, procainamide
• Macrolide and floquinolone antibiotics
• Certain psychotropic medications like TCAs, haloperidol, methadone

Drug-induced prolonged QT is an idiosyncratic event, but there are some identified risk factors.
• Rapid IV infusion of the drug
• Electrolyte abnormalities (hypokalemia, hypocalcemia or hypomagnesemia)
• Use of other drugs known to prolong the QT interval
• Congenital long QT syndrome
• Underlying cardiac abnormalities
• Hypothyroidism
• Females
• Patients with stroke

Here is a review article on the topic.
Long QT syndrome: diagnosis and management. Khan IA. Am Heart J. 2002 Jan;143(1):7-14
http://www.ncbi.nlm.nih.gov/pubmed/11773906

* The term “torsade de pointes” means “twisting around the points in ballet where the dancer rotates around an imaginary axis. On the ECG, the QRS complex appears to twist around the electrical baseline with a continuously changing point of origin, reminiscent of the ballet movement.

Ascites

We talked about examination manoeuvres for clinically diagnosing ascites today in our physical exam rounds. Here is a good review of the topic in a previous post.

http://morningreporttwh.blogspot.com/2009/07/ascites.html

* The image is a painting of Bacchus, the Greek god of wine by Henri Millot,1730. How many stigmata of alcoholic cirrhosis can you identify in him?

Is it hot enough yet?

Given the recent heat wave in Toronto, morning report was aptly about a case of heat stroke today. As we discussed today, the most important causes of severe hyperthermia (greater than 40ºC) are heat stroke, neuroleptic malignant syndrome, thyroid strom, and malignant hyperthermia.

Heat stroke is diagnosed based on history, physical examination and the context in which symptoms developed (eg, high temperature and no air conditioner). Diagnostic studies are nonspecific. Heat stroke can cause cardiovascular, renal, or hepatic dysfunction or coagulopathy.

The management of heat stroke consists of ABC, rapid cooling, and treatment of complications.

Here is a recent review of the topic.

Heat-related illness. Becker JA, Stewart LK. Am Fam Physician. 83(11):1325-30
http://www.ncbi.nlm.nih.gov.myaccess.library.utoronto.ca/pubmed/21661715

Toxic Epidermal Necrolysis

This morning we discussed an unsolved mystery that involved a skin biopsy showing TEN. Toxic Epidermal Necrolysis (TEN) a severe type of hypsersensitivity reaction, affecting the skin and mucus membranes, that occurs in response to medications and some infections.

Treatment includes stopping the offending agent and supportive care including treating the complications such as superimposed skin infections.

Here is a recent review on the topic if you like to read more!
Toxic epidermal necrolysis and Stevens-Johnson syndrome: a review.
Gerull R, Nelle M, Schaible T. Crit Care Med. 2011 Jun;39(6):1521-32.

*The above picture is Mycoplasma pneumoniae, which is rarely associated with TEN

Systemic Lupus Erythematosis

This morning, we discussed a case of first presentation of lupus. Here is post from last year on the topic
http://morningreporttwh.blogspot.com/2010/07/systemic-lupus-erythematosus.html

* Contrary to popular belief, British singer Seal wasn't bitten by a seal and didn't wrestle a wild boar. His facial scars are manifestations of discoid rash of lupus.<

Neurologic Manifestations of Vitamin B12 Deficiency

In our discussion this morning about the causes of “fall and dementia” we briefly touched on Vitamin B12 deficiently. Vitamin B12 is a water soluble present in animal products (meat and dairy). B12 is involved in myelin synthesis, and hence, it’s deficiency has neurologic consequences.

Neurologic manifestations of B12 deficiency is the classic subacute combined degeneration of the dorsal (posterior) and lateral spinal columns. SCD manifests as symmetrical primarily lower limb neuropathy with loss of vibration and position sense, which can result in ataxia.

Other neurologic findings in B12 deficiency include axonal degeneration of peripheral nerves and central nervous system symptoms including memory loss, irritability, and dementia.

Interestingly, not all patients with neurologic abnormalities secondary to Vit B12 deficiency have hematologic manifestations.

Here is good review of B12 deficiency.
Current concepts in the diagnosis of cobalamin deficiency. Green R, Kinsella LJ. Neurology. 1995;45(8):1435.

*the picture is an axial image of the spinal cord of a patient with B12 Deficiency. Blue is where myeline is stained and you can see the loss of myeline latterally and posteriorly.

Cutaneous Manifestations of Sarcoid

Sarcoidosis is a multisystem disease characterized by the presence of noncaseating granulomas in tissues such as the skin, lung, lymph nodes, eyes, joints, brain, kidneys, and heart. Cutaneous lesions may present with a variety of morphologies, including papules, nodules, plaques, and infiltrated scars.

One-third of patients with sarcoidosis have skin lesions. These lesions can be the presenting finding of the disease. Some of these lesions are nonspecific, but others are highly suggestive of sarcoidosis. There are many different types of lesions.

Here are a few common skin findings in Sarcoidosis:
Lupus pernio (first picture) : Lupus pernio is a violaceous or erythematous indurated papules, plaques, or nodules that are primarily distributed on the central face (though can also happen in the extremities and buttocks)
Erythema nodosum (second picture): raised tender inflammatory nodules over lower legs. Common and non-specific.

If you’re interested in reading more on sarcoidosis, here is a great review article.

Sarcoidosis. Michael C. Iannuzzi, M.D., Benjamin A. Rybicki, Ph.D., and Alvin S. Teirstein, M.D.N Engl J Med 2007; 357:2153-2165.
http://www.nejm.org/doi/full/10.1056/NEJMra071714