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.

Fever and confusion in a patient with HIV - Wednesday Apr 4, 2012

Thank you Dr. P. Bunce for hosting today’s morning report, and to team 5 for bringing the case.

Today, we discussed a case of a patient with HIV who presented to the Emergency Department with a 1-day history of fever and confusion.

There were 3 learning points that Dr. Bunce made today.

First is the differential diagnosis of confusion (or any altered level of consciousness) can be remembered by the mnemonics DIMS.  It stands for Drugs (prescribed, over the counter, illicit, recreational and intoxication or withdrawal), Infection (can be CNS or systemic), Metabolic (can be organ dysfunction [hepatic encephalopathy, uremic encephalopathy, hypercapnia], electrolytes, endocrine (thyroid, glucose, adrenal), and Structural (which has its own differential such as bleeding, abscess, tumour, stroke, vasculitis, etc…).  Seizure is sometimes on the differential diagnosis depending on the presentation.

The second learning point is that for any patient with HIV presenting to the Emergency Department, it is very important to know these features about their HIV as it changes the differential diagnosis:  what treatment (if any) they are on and their adherence to the medications, HIV related complications (including opportunistic infections, cancers, cardiac, renal dysfunction), most recent CD4 count, the name of their HIV doctor.  It is important to contact that doctor on the next working day.

Third learning point is HIV patients should not be having unprotected sex, and that acquisition of sexual transmitted infection should ring an alarm bell.

During the discussion of the case, we also talked about that pneumococcal pneumonia is still common among HIV patients.  Cryptococcal antigen can be sent in the CSF to rule out cryptococcal meningitis.  Bacterial meningitis should be treated with high dose ceftriaxone, vancomycin, and ampicillin (for listeria) as these drugs have high CNS penetrance.

You can read more about acute bacterial meningitis here.  

Confusion and hyperglycemia - Tuesday April 3, 2012

Thank you Dr. A. Page for hosting morning report and to team 6 for bringing a case.

Today, we discussed the presentation of an elderly person who presented to the Emergency Department with confusion.  This obviously has a broad differential diagnosis and requires a systematic approach.  We discussed one such approach:

- Neurologic (stroke, bleed, tumour, seizure, post-ictal, etc...)

-  Infection (meningitis, abscess, encephalitis, pneumonia, UTI, gastroenteritis, etc ...)

- Drugs, medications, alcohol, substances, intoxication, or withdrawal

- Metabolic/Endocrine (Hypo/hypernatremia, hypercalcemia, hypophosphatemia, thyroid dysfunction, adrenal dysfunction, etc...)

-  Organ dysfunction (usually liver or kidney, and can be respirator [hypercapnia])

As the case progresses, we learned that this patient with a history of type 2 diabetes on metformin had a blood glucose of 83, with serum ketones being positive.  She also had renal injury (presumed acute), and an elevated potassium of 5.4.

We discussed the approach to managing a patient in DKA.  It is important to look for precipitating factors such as infection, ischemia, or medication non-compliance (especially in type 1 diabetics).

In addition to treating the precipitating cause, the management includes fluid resuscitation, correction of anion gap, and proactively ensuring that patients are safe from anticipated electrolytes changes.  It is important to construct a chart to track these changes simultaneously.  FREQUENT monitoring of blood glucose and lab values are important.  This patient’s require an intense level of care and is likely not suitable for a medical ward.

We discussed the use of insulin to correct acidosis (monitored by pH and anion gap).  Initial insulin infusion dose is 0.1unit/kg per hr, but will need to be adjusted based on glucose and anion gap.  The goal of insulin therapy is to correct acidosis and should not be stopped until the goal is achieved.  If blood glucose is dropping quickly, it may be necessary to add glucose containing solution (e.g. D5W or D10W) to prevent hypoglycemia, while maintaining the insulin infusion to correct acidosis.  Once acidosis is corrected, the patient will need to be transitioned to subcutaneous insulin at some point.  This is best done when the patient is eating reliably (less chance of hypoglycemia) and the transition can be done over meal time with appropriate overlap (depending on the type of insulin that is used).

Fluid resuscitation is important (as patient may have had polyuria from hyperglycemia and is often quite volume contracted).  One should monitor electrolytes closely.  With insulin infusion, we expect potassium to be shifted into cells and the patient most likely has total body potassium deficit.  We will likely need to replace this patient’s potassium sooner rather than later.  However, given this patient also had renal injury and is hyperkalemia, it is important to monitor this patient’s electrolytes and urine output closely to ensure she has adequate potassium replacement without the risk of hyperkalemia.  Another electrolyte that we can replace is phosphate.

We did also have a side discussion (with images) about the topic of mucormycosis (a fungal infection seen sometimes in the immunocompromised or diabetes).

To learn more about diabetic ketoacidosis, I point you to a local resources developed here at the UHN:  http://www.udiabetes.ca/dka.html.

AML in the Emergency Room - April 2, 2012

Thank you to Dr. Raymond Jang for hosting, and to team 8 for brining the case.

Briefly, a young man with previous AML (treated with allogenic stem cell transplant 5 years ago) presented with fever, chills, and tachycardia.  He also has graft vs. host disease and previous line infections (pseudomonas and CNST), and still has indwelling lines.

We talked about the key considerations when a patient presents to the Emergency Department with a cancer related issue.  It is important to know:

- Is the patient sick or not sick?

- What cancer treatments had been received so far and their responses?

-  Is treatment curative or palliative?

- What is the prognosis?

- Is there anything reversible?

- What are the complications of cancer itself or its treatments?

For AML, there are 5 complications that we focused on today:

-  Fever/infection:  This is what our patient presented with.  We talked about the importance of looking for a source and controlling the source, appropriate antibiotics (this patient had previous pseudomonas infection, and CNST), and fluid resuscitation.

-  Tumour lysis syndrome (TLS).  We unfortunately did not have enough time to talk about this.  You can read more here.

-  Disseminated intravascular coagulation (DIC).  Diagnosed with blood film, INR, PTT, and fibrinogen.  Support with blood products (including fresh frozen plasma and cryoprecipitate as appropriate).

-  Leukostasis.  We talked about the main organs at risk are brain, heart, and lungs.  We talked briefly about the agent hydroxyurea.

-  Cytopenias.  This is managed supportively with blood products.

You can read more about AML here and Graft vs. Host disease here.

Welcome to TGH Team Medicine - April 2012

See everyone at 8 am sharp on Monday April 2, 2012 on the 13th floor of Toronto General Hospital.

Terence

Decompensated cirrhosis

Today in morning report was a case of decompensated liver failure. For more on this topic, see a prior post here.


We also discussed about the management of spontaneous bacterial peritonitis. See a nice review of cirrhosis and ascites in NEJM here.

Hemolytic anemia

Today's morning report was an interesting case of hemolytic anemia: check out a prior post on the topic here, with a few links at the bottom to review articles.

Non-resolving pneumonia

Today in morning report was a great case of non-resolving pneumonia. For more, see a prior post here.

See the IDSA guidelines here, and skip to recommendation #38 to read about the work-up of a pneumonia that fails to respond to therapy.

Levamisole toxicity

Today's amuse-bouche was a case of a levamisole-related cutaneous vasculitis syndrome. A few quick points: 

• Recent trend in cocaine being adulterated by levamisole, 
• An anti-helminth agent in the 1960s first identified as a cocaine adulterant in the USA in 2003 
•  Now found in majority of cocaine seized at US borders, common in Canada also
• Proposed that levamisole potentiates the psychotropic effects of cocaine, and that producers intentionally add it during the cocaine manufacturing process 
• Associated with a cutaneous vasculitic syndrome 
• Purpuric lesions and/or cutaneous necrosis 
• Involves the ears in ~50% of reported cases 
• Lab associations: neutropenia + pANCA and + cANCA

More in a case-series review here.

Hyponatremia

Today in MR we had a case of hyponatremia. See a prior post here with links to a few good review papers.

Neurologic presentations of HIV infection

Last week in morning report was an excellent case of ptosis and diplopia in a patient with HIV infection. This is a big topic, but a few points about neurologic involvement in HIV:


1) Acute seroconversion reactions: 


-Although rare, acute neurologic presentations at the time of HIV infection do occur, including aseptic meningitis, Bell's palsy, and inflammatory neuropathies. CSF testing for HIV may be positive in these patients.


2) Opportunistic infections: A variety of OI can manifest with neurologic presentations:


- Progressive Multifocal Leukoencephalopathy (PML): a demylenating CNS disease caused by JC virus, mostly in patients with CD4 counts less than 100. Usual presentation is a subacute deterioration in mental status with possible focal neurologic signs/symptoms, with fever and headache not usually present.


- Cytomegalovirus (CMV): although 60% of the population have evidence of exposure to CMV, patients with HIV and CD4 counts less than 50 and other immunocompromised states are at risk of clinical disease from reactivation. CMV can infect and reactivate throughout almost the entire spectrum of the CNS and PNS- from the brain to peripheral nerves. For this reason, the neurologic presentation can be any combination of encephalitis, ventriculitis, myelitis, gangionitis and peripheral polyneuropathy. 


- Cryptococcus neoformans: an encapsulated yeast found throughout the world. It usually is cleared by the immune system, but in immunocompromised patients, including HIV patients with CD4 counts less than 100, it can remain in a latent state that can disseminate to organs, with the CNS being particularly common. The usual presentation is that of a subacute menigoencephalitis, with fever, headache and malaise. It can also present with complications of increased ICP, including seizure.


- Toxoplasma gondii: intracellular protazoan with high seroprevalence in the population, with most primary infections being asymptomatic or flu-like. Reactivation can occur in immuno compromised hosts, usually in patients with HIV and CD4 counts less than 200. Usually casues an encephalitis and presents with fever, headache, and focal neurologic signs or seizures. 


3) Neoplasms: primary CNS lymphoma is usually a high grade B-cell lymphoma and almost always related to Epsetin -Barr Virus (EBV). It usually presents in HIV patients with CD4 counts less than 100 with headache, changed mental status, focal neurologic signs or seizures. 


4) Immune reconstitution inflammatory syndromes (IRIS): a group of syndromes casued by the inflammation generated by a reconstituted immune system in the first 4-8 weeks after starting on combined antiretroviral therapy. Usually seen in HIV patients with CD4 counts less than 50 being started on therapy for the first time in the setting of an opportunistic infection. Typically presents as a paradoxical worsening of course in patients with HIV encephalitis, cryptococcal meningitis  toxoplamsamosis encephalitis and PML.


5) HIV associated peripheral neuropathies: many peripheral neuropathic syndromes have been reported in the context of HIV infection, with the most common being a distal peripheral sensory neuropathy. Modifiable risk factors include use of neurotoxic medications, diabetes and alcohol abuse.


6) HIV-associated vacuolar myelopathy: an entity of unclear pathophysiology affecting the spinal cord neurons, more often the dorsal column. It presents with often initial errectile dysfunction and hyper-refexia, but progresses to asymmetric spastic leg weakness, dorsal column vibration/position sensory loss, and ataxic gait.


7) HIV Associated neurocognitive disorders (HAND): this is a group of neurocognitive changes thought to be a spectrum of a subcortical process that primarily affects attention/concentration, psychomotor speed, memory/learning, information processing, and executive function, while language and visuospatial abilities are often relatively unaffected.


More on diagnosis of these conditions from a review article here.

Elevated liver enzymes

Today in MR was a case of elevated liver enzymes. See here for a previous post on the topic.

Weekly Amuse-Bouche Links

For more on this week's amuse-bouche topics see the following links:


- Pendred's syndrome here
- Dermatologic findings in dermatomyositis here
- Familial Adenomatous Polyposis here
- Limb lead reversal here

Hyperkalemia and Renal Tubular Acidosis

We had a great case of hyperkalemia in MR, likely due to an underlying type IV renal tubular acidosis in the setting of diabetes.

A prior post on hyperkalemia here, with a link at the bottom to a recent CMAJ article on management.

A prior post on renal tubular acidosis here, with a good review from the Archives here.

Hypercalcemia

Morning report today was a case of hypercalcemia. More from a prior post here.

Medullary Thyroid Cancer

Yesterday in morning report we had a really interesting case of medullary thyroid cancer presenting with chronic diarrhea and complicated by heart failure, likely secondary to amyloidosis.

A little more about medullary thyroid cancer (MTC):

- MTC can be either sporadic or inherited. Inherited forms involve mutations to the RET proto-oncogene and can be either be alone or as part of one of the Multiple Endocrine Neoplasia syndromes- MEN 2A or MEN 2B.

- MEN 2A is characterized by MTC with hyperparathyroidism and/or pheochromocytoma

- MEN 2B is characterized by MTC with typical phenotyic features such as marfanoid body habitus or mucosal neuromas with or without pheochromocytoma.

- Most patients present with a thyroid mass, but some present with symptoms of local spread such as dysphagia, dyspnea, or hoarseness. Roughly 10% will present with systemic symptoms related to the production of neuroendocrine mediators such as calcitonin, resulting in bone pain, flushing, and/or diarrhea.

- Those that present with systemic symptoms usually have metastatic disease.

- More in a review from Cancer here

We also found out through our group searching excercise that MTC is associated with secondary amyloidosis casued by calcitonin.

-A good related article sent out by Dr. Abrams here.

- More on amyloidosis from a prior post here.