Sick after Travelling - Monday April 16, 2012

Thank you to Dr. D. Frost for hosting morning report and for team 6 for brining the case.

We discussed a case of a previously healthy person returning from travels to the Caribbean who presented with fever at home, abdominal pain, nausea/vomiting, headache, pleuritic chest pain, and general unwell.  She also had an elevated WBC of 25.  She had recent antibiotics exposure (amoxicillin) prior to her travel for a URTI that resolved.

We discussed that it is important to consider both travel-related and un-related causes of fever.  For travel-unrelated causes, the differential diagnosis includes infectious (UTI, pyelonephritis [our patient had R CVA tenderness], gastroenteritis, C. diff [our patient had recent antibiotics exposure], pneumonia, meningitis, etc…], inflammatory, malignancy (primary hematologic or non-hematologic), drugs.

For travel-related causes, it is important to think of infection, but also thromboembolic disease.  We discussed the important points on history that should be asked.  This starts from pre-travel advice and immunization, to prophylaxis taken and patient adherence to them during (and after) the trip.  A detailed itinerary of travel including dates and location, as well as activities under taken.  Ask especially about insect bites, sexual encounters, exposure to animals, and exposure to food and water.  It is also important to know the health of the patient and treatment taken while away.  It is important to clarify the date of return and onset of symptoms as incubation periods sometimes give a clue to the diagnosis.

It is extremely important to consider malaria as a possible diagnosis, and appropriate tests need to be undertaken to rule out this possibility.  Some (among many other) possibilities include dengue fever, typhoid fever, and viral illnesses (HIV, hepatitis, HTLV [given region of travel]).  In our patient, we suspect she may have had leptospirosis.

We have discussed a number of resources.  The CDC Travel website has a list of destination-based synopsis as well as the “Yellow Book”.  You can also find disease specific information on this website.  The site can be accessed here.  The GIDEON (Global Infectious Diseases and Epidemiology Network) web site can be accessed here.  The GeoSentinel Surveillance Network also published in 2007 a review of etiologies of febrile illness broken down by region of travel.  The article can be accessed here.

Nephrotic syndrome - Friday April 13, 2012

Thank you to Dr. E. Cole for hosting a special nephrology morning report and to team 6 for bringing the case.

We discussed a patient with known nephrotic syndrome (heavy proteinuria) and presented with renal vein thrombosis.  We discussed that other than the usual signs and symptoms of nephrotic syndrome, two complications are frequent infections and thrombosis.  We also discussed the differential diagnosis of edema from a pathophysiologic point of view.  The 3 mechanisms or increased hydrostatic pressure, decreased oncotic pressure, and increased capillary vessel permeability.  Some disease processes that increase hydrostatic pressure include heart failure, volume overload secondary to renal failure, DVT, obstructed lymphatics, or portal hypertension from liver disease.  Some disease processes that decrease oncotic pressure include decreased albumin synthesis from liver disease, nephrotic syndrome (losing protein), or protein-losing enteropathy.  Capillary vessel permeability is sometimes secondary to trauma or inflammation.

For Amuse Bouche, we posed of question of calculating the post-test probability given the likelihood ratio and pre-test probability.  The pre-test probability given was 20%, and the positive likelihood ratio was 16.  To do this, we:

1.  Convert the pre-test probability to pre-test odd.

2.  Multipley the pre-test odd with the likelihood ratio to obtain the post-test odd.

3.  Covert the post-test odd to post-test probability.

In our case:

1.  Pre-test odd = pre-test probability / (1 – pre-test probability).  In our case, this is 0.2/0.8 = 0.25.

2.  Then we get post-test odd = pre-test odd X LR = 0.25 x 16 = 4.

3.  Then we get post-test probability from post-test odds by this formula:  probability = odds / (1 + odds).  In this case, post-test probability = 4/(1+4) = 0.8.

Therefore, the post-test probability is 80%.

Fall and Cavitating Lung Lesion - Thursday April 12, 2012

Thank you to Dr. A. Detsky for hosting today’s morning report and to team 8 for bringing the case.

We discussed a man who presented with fall and found to have a cavitating lung lesion on the right side.  We discussed the approach to a patient with fall.  As with most medical problems, we begin by ensuring the stability of the patient.  In a patient with fall, patient may become unstable if he/she had a intracranial bleeding.  We also discussed that epidural bleeding can have “lucid” period.  The second question is whether the problem is new or old, and if old, what were the previous diagnoses and treatment.  Thirdly, is there one problem or multiple problems.

Specifically with fall, we want to assess any complications of fall (intracranial bleed, fractures, lacerations, etc…).  Then, we want to identify the etiology of fall.  Broadly speaking, it can be classified into multifactorial (sarcopenia, deconditioning, mechanical), syncope (cardiac, neurologic), and others.

We then focused on discussion on a very short differential diagnosis of a cavitating lung lesion:  TB, fungal infection (especially aspergilloma), pneumonia (especially anaerobic), and cancer.  The patient will require sampling of the lesion either via bronchoscopy or interventional radiology.

In the medical setting, our main focus on preventing falls is on treatment of osteoporosis which was based on bone mineral density, but has since been broadened to assessment of fracture risk.  Dr. A. Detsky and Dr. A. Cheung wrote a commentary in JAMA urging us all to look at the many other factors that contribute to fall (including sarcopenia, and the role of muscle strength, balance, etc…).  You can see a copy of the article here (full text via U of T Library here).

Heart failure - Wednesday April 11, 2012

Thank you Dr. H. Rakowski for hosting a special cardiology morning report, and to team 5 for bringing the case.

Today, we discussed a man who had a history of hypertension, atrial fibrillation, and heart failure, who presented with a 1-week history of increasing shortness of breath on exertion (NYHA 3, worsened to 4), increased abdominal girth, and bilateral leg edema.

We discussed an approach to the chronic etiology of heart failure, as well as acute triggers for decompensation.  Common etiologies of heart failure include hypertension, diabetes, and coronary artery disease.  However, each part of the heart can give rise to heart failure.  These include cardiomyopathy, pericardial disease (constriction or effusion), ischemia, arrhythmia, and valvular lesions.  Also, the most common cause of right heart failure is left heart failure.  However, lung pathology (e.g. COPD, obstructive sleep apnea, pulmonary hypertension, PE) can also give rise to right heart failure.  The JVP is sometimes helpful in distinguishing right heart failure from cirrhosis.  Common acute triggers for decompensation include salt and fluid indiscretion, medication non-adherence, infection, and ischemia.

We discussed the basic investigations in someone presenting with apparent heart failure symptoms, including ECG and CXR.  We also looked at echo images for our patient.  Visiting the cardiologist reporting echocardiogram on the third floor can be very helpful.  Our patient had a large right pleural effusion that is not adequately explained by the lack of LV dysfunction shown in the echocardiogram.  A leg Doppler, CT chest and/or thoracentesis is likely the next step given his previous history of colon cancer.

Although we did not focus on management of heart failure in today’s morning report, you can find an article in Lancet about medical therapy of heart failure here, and the Canadian Cardiovascular Society heart failure guidelines can be found here.

Sepsis - Tuesday April 10, 2012

Thank you to Dr. A. Page for hosting morning report and to team 7 for bringing the case.

We discussed a patient referred to internal medicine for sepsis.  She had a history of cholangiocarcinoma (with biliary stenting) and recently had chemotherapy (about 14 days ago).  She presented with chills at home, temperature 37.4 in hospital, tachypnea, tachycardia, some diarrhea, nausea/vomiting.  She did have an indwelling line, bilateral decreased breath sounds at bases, and tender/enlarged liver.  She also had anemia, neutropenia, thrombocytopenia, acute kidney injury (Cr 600), and a low bicarb.

We discussed the definition of sepsis (systemic inflammatory response syndrome caused by infection [or suspected to be caused by infection]).  SIRS requires meeting >= 2 of the following 4 criteria:  fever or hypothermia, HR > 90, RR > 20 or PaCO2 < 32, WBC > 12 or < 4 or > 10% bands.  Our patient met the criteria for SIRS.  The team appropriately looked for/monitor for infection by sending off appropriate cultures (urine, NP swab, blood cultures, hepatitis serologies, stool for C+S, C. diff), CXR, and ordering abdominal imaging (pending).

For her pan-cytopenia, we discussed the need to look for bleeding (given anemia and low platelet count).  Supportive therapy includes transfusion of RBC (threshold of 70).  For platelet of < 10, platelet transfusion to prevent spontaneous intracranial hemorrhage.  Whether to support WBC with GCSF is controversial.  The evidence is that it decreases duration of neutropenia by a small amount.  Some people will give it.  Dr. Page also pointed out that prophylaxis against infection has the unfortunate effect of patients being infected with infections that are not prophylaxed against, or drug resistant organisms.  Given this presentation, it is also important to look at her blood film over night to rule out fragments (TTP, DIC).  Fibrinogen should also be measured.

The patient did grow gram-negative organisms in the blood.  She was on Piptazo and Vancomycin (for the line).  We are reminded that Piptazo has a broad coverage, but does not cover ESBL organisms or atypical organisms (if we think she has community acquired pneumonia).  We also discussed the hypothetical situation of someone with known gram-negative bacteremia (sensitivity unknown yet) who is already on broad-spectrum coverage (Piptazo or meropenem), but continues to deteriorate.  In this situation, it is important to ensure source control (e.g. rule out abdominal abscesses), and that antibiotics coverage may be broadened by adding aminoglycoside (if renal function allows).

As a side note, we also discussed re-activation of hepatitis B when someone is being immunosuppressed (from chemotherapy, organ transplant, etc…).  Lamivudine is usually indicated in these situations.  We discussed that this risk is highest with Hep B S Ag positivity, but is possible with Hep B S Ab positivity as well if someone is immunosuppressed enough.

Although we did not focus on this aspect of management, you can find the Surviving Sepsis Campaign here.  Also, today’s Amuse Bouche was based on a new Rational Clinical Exam Series:  “Does this patient with liver disease have cirrhosis?”  You can find the article here.

Thrombocytopenia - Apr 9, 2012

Thank you to Dr. Alan Detsky for doing morning report on Thursday April 5.  Unfortunately, I was post-call and did not blog.

Today, we thank Dr. David Frost for hosting morning report and thank you to team 5 for bringing the case.

We discussed a case of a 75 year-old woman who presented with bleeding for 2 days after a dental procedure and found to have severe thrombocytopenia (platelet count of 1, Hb 91, MCV 75, WBC 4.4), with normal INR and PPT.  We discussed the approach to the bleeding patients include thrombocytopenia/platelet dysfunction or coagulopathy.  In our case, it is thrombocytopenia that is the major issue.  We discussed the major life threatening diagnoses that must be ruled out overnight:  ITP, TTP/HUS, DIC, HIT, drugs.  Other causes may be related to drugs, malignancy (especially lymphoma), infections (e.g. HIV, Hep C), and autoimmune disorders (e.g. SLE).

One of the most important investigations (other than CBC and coagulation parameters) is the blood film.  The diagnosis and management of the patient will be very different if schistocytes (or fragments) are present.  In the absence of fragments on blood film, normal coagulation studies, no signs of hemolysis (LDH, bilirubin, haptoglobin), no heparin or other drug exposure, the initial diagnosis overnight was ITP.

The management focuses on stopping the bleeding, and therapy for ITP.  Whereas it is controversial in patients with ITP who are not actively bleeding, patients who are actively bleeding may benefit from platelet transfusion.  Acutely, therapy for ITP includes steroids (prednisone or dexamethasone), and/or IVIG (IVIG in combination with steroids will raise platelet count quicker).  Other options sometimes used with the help of a hematologist include other agents (e.g. rituximab, vincristine, etc…), and splenectomy.  Newer agents in the future may include thrombopoietin receptor agonists that stimulate platelet production.

In the patient discussed, it is important to exclude secondary causes given her age and anemia.  Secondary causes include infection (e.g. HIV, HCV), malignancy (e.g. lymphoproliferative disorder), drugs, and autoimmune diseases (SLE, APLA, Evans syndrome, etc…).  Appropriate investigations (serologies, bone marrow) are required.

You can read the 2011 American Society of Hematology evidence-based practice guideline for ITP here.