Dysphagia

Today's highlighted some of the areas of medicine less commonly featured in morning report.

The case involved a 38-year-old woman with a history of GERD and a motor vehicle collision several years prior to her admission. She presented with a 5-month history of progressive dysphagia, first to solids then to liquids with globus sensation.  She had lost a significant amount of weight.  There were no systemic features to suggest a connective tissue disorder such as systemic sclerosis.  There were also no bulbar or cranial nerve features to suggest a central nervous system cause.  Finally, she had no fatigability suggestive of a myasthenic cause.  As the case progressed, an extensive number of ‘outside’ investigations was revealed including an esophagogastroduodenoscopy, motility study, and barium swallow which effectively ruled out an intraluminal cause of dysphagia.  It was then revealed that there were substantial psychosocial stressors and, when the psychiatry consult-liason team was involved, her presentation was consistent with a somatoform disorder.

Important learning points from today:

-Dysphagia is a common symptom with a wide differential diagnosis

-It is helpful to divide dysphagia into obstructive (extrinsic/intrinsic mass, peptic strictures) and propulsive (achalasia, neuromuscular disorders, central nervous system/coordination) causes

-We discussed salient historic features that can help differentiate them – these include a progressive dysphagia from solids to liquids (more consistent with an obstructive cause) compared to dysphagia which begins with solids and liquids (consistent with a neuromuscular cause)

-We briefly discussed the infections in an immunocompromised host that would lead to esophageal dysphagia including opportunistic infections with Herpes group viruses, or esophageal candidiasis

-We discussed features of brainstem and bulbar disease and the importance about acquiring those symptoms when taking a dysphagia history (dysphonia, dysarthria, nasal vocal changes, hoarseness, etc.)

-Importantly, we discussed the concept of psychiatric or somatoform disease as a diagnosis of exclusion and that it can be challenging to deem someone having been ‘investigated enough’ for ‘organic’ causes of symptoms

Further Reading:

Mathog, R. H., & Fleming, S. M. (1992). A clinical approach to dysphagia. American journal of otolaryngology, 13(3), 133-138.

Melanoma and Hypercalcemia

Oncology Morning Report

Today's case involved a 43-year-old man with metastatic melanoma who presented with generalized weakness and hip pain.  He was admitted with a mild hypercalcemia of 2.8mmol/L.  He was hydrated overnight, and his bone pain will be investigated with imaging studies today.

There were several valuable learning points, as this patient represents a very common scenario encountered at this hospital:

-Hypercalcemia of malignancy can occur for a variety of reasons.  A review from the NEJM is attached with a clinical scenario

-Treatment relies on intravenous fluids to help correct the metabolic abnormalities associated with hypercalcemia (diuresis, acute kidney injury) and can also include bisphosphonate therapy (pamidronate 90mg IV, or zoledonate 4mg IV)

-Cancer patients also have a higher incidence of primary hyperparathyroidism, so checking an intact PTH level is important

-We discussed opioids and the management of cancer-associated pain, and cancer-associated nausea

-We discussed malignant melanoma and particularly the lack of efficacy of traditional therapies (alkylating agents and anti-metabolites) with some new effective therapies on the horizon (BRAF inhibitors, Tyrosine Kinase inhibitors, immunotherapy)

-We discussed choosing wisely in terms of the appropriateness of brain imaging in patients with newly-diagnosed cancer; to review, the only indications are 1) symptoms suggestive of CNS disease warranting investigation, 2) melanoma and 3) lung cancer of any type

Further Reading:

Johnson, D. B., & Sosman, J. A. Therapeutic Advances and Treatment Options in Metastatic Melanoma. JAMA Oncology.

Stewart, A. F. (2005). Hypercalcemia associated with cancer. New England Journal of Medicine, 352(4), 373-379.

Marcocci, C., & Cetani, F. (2011). Primary hyperparathyroidism. New England Journal of Medicine, 365(25), 2389-2397.

Gout and Shoulder Pain

Today's case involved a 33-year-old man with end-stage renal disease on hemodialysis due apparently to hypertensive nephrosclerosis.  The man had had left shoulder pain for around one year, and was given a presumptive diagnosis of pseudogout and treated as such without resolution.  On admission his physical examination did not strongly suggest an articular or periarticular process.  X-ray and CT imaging showed a large lytic lesion in the humerus, which is being further characterized by MRI with a view toward biopsy. The current diagnosis remains unclear, but we look forward to hearing more about this in the future!

We discussed multiple medical expert and non-medical expert topics, learning points include:

-We discussed that the differential diagnosis for shoulder pain includes articular processes (gout, pseudogout, hemarthrosis, septic arthritis, etc.) as well as non-articular processes (referred pain from MI or diaphragmatic irritation, a bony lesion, a muscular problem, venous thrombosis, etc.)

-A first diagnosis of gout/pseudogout should probably involve a diagnostic arthrocentesis of the affected joint when the diagnosis is not clear.

- We discussed gout, and the approach to treatment which includes NSAIDS (when there isn’t a contraindication, typically naproxen 250-500mg BID with some gastroprotection) followed by colchicine therapy for 6 weeks.  Do not start allopurinol or other urate-lowering agents during an acute flare of gout.

Further Reading:

• 
  
• New perspectives on the management of gout, a common primary care disorder. [Postgrad Med. 2012]
• Gout. [N Engl J Med. 2011]

Nuki, G. (2006). Treatment of crystal arthropathy—history and advances. Rheumatic Disease Clinics of North America, 32(2), 333-357.

Aseptic Meningitis

Today's case involved a 52-year-old man with a past medical history of type 1 diabetes mellitus on insulin pump and dyslipidemia who presented to hospital with a 10-day history of hemicranial headache.  He also had some mild alterations in mental status, diplopia, blurred vision, and nausea.  His initial physical examination was normal, but evolved to feature a possible abducens palsy as well as some ptosis.  His neuroimaging (MRI) was normal.  He went on to have a lumbar puncture which showed a normal opening pressure and a pleiocytosis (88 WBC, all lymphocytes) as well as elevated protein.  Viral and infectious tests are pending at this point.  It was further revealed that he may have had some mosquito exposures as well as having spent some time in Vermont and Vancouver.

Learning points:

-We discussed the differential diagnosis of headache which I like to break down into “Red Flag” features or the absence of red flag features.  These are things like focal neurologic deficits, thunderclap headache (maximal intensity reached within one minute), signs of raised intracranial pressure, visual deficits, altered mentation, fever, age, or worsening frequency/intensity with other medical conditions.

-Further than that, headaches can be broken down into primary headache disorders (migraine, tension, cluster) and headaches secondary to other problems (infections, vascular phenomena, raised intracranial pressure, and mass effects).

-We discussed the differential diagnosis to a unilateral ptosis which includes problems with the sympathetic chain (Horner’s syndrome), problems with the third cranial nerve (pupil-sparing lesions such as ischemic injuries and non-pupil-sparing such as compressive lesions), neuromuscular problems, and central nervous system/nucleus problems

-We discussed Lyme disease and its propensity to cause an aseptic meningitis picture, along with other infections such as West Nile Virus (which can produce a host of neurologic syndromes), and HIV acute seroconversion illness

-We discussed some of the infections that diabetic patients get that we do not typically see in non-diabetic patients including malignant otitis externa, emphysematous pyelonephritis and emphysematous cholecystitis

Further Reading:

Lee, B. E., & Davies, H. D. (2007). Aseptic meningitis. Current opinion in infectious diseases, 20(3), 272-277.

Decompensated Heart Failure and Alternative Medicine

Today's case involved a 77-year-old man referred to medicine for progressive dyspnea of around one year’s duration.  He experienced orthopnea and increased leg swelling. He is also known for aortic stenosis, a history of congestive heart failure, and hypertension as well as a JAK-2 positive myeloproliferative disorder.  His physical examination was consistent with decompensated heart failure.  Further history was obtained which included some naturopathic remedies consisting of unknown infusions and blood ozonation by some sort of German machine.

Learning points:

-Dyspnea is a common presenting complaint to an emergency department; it is essential to remain open to diagnostic possibilities regarding its etiology – common players include decompensated heart failure, exacerbations of chronic pulmonary diseases, and venous thromboembolic disease.

-Historical points that help you rule in a diagnosis of heart failure are: previous admissions for heart failure, orthopnea, paroxysmal nocturnal dysnpea, leg swelling, dysnpea on exertion, needing several pillows for sleep and/or sleeping in a seated position

-On physical examination, inspiratory crackles, peripheral edema, a positive abdominojugular reflex, an elevated JVP, and an S3 can be helpful findings

-Dealing with people seeking ‘alternative’ medical advice in conjunction with allopathic (our) medicine can be challenging for several reasons:  We are not taught what many of these therapies are.  Our previous mantra that they are unlikely to help but are probably not harmful is likely untrue – many of these therapies present harms and risks to patients.  We sometimes see providers of alternative therapies as taking advantage of desperate people from a financial and hope perspective.  Finally, it seems as though we, as a hospital, are expected to ‘pick up the pieces’ when these therapies fail or cause harm to patients

-Maintaining a degree of composure and openness regarding alternative medicine while providing advice to people is essential to our therapeutic relationships

-Many people are on proton pump inhibitors and other chronic medicatons which do have harms and are rarely ‘debrided’ from their medication list by their usual practitioners

Further Reading:

Srivastava, R. (2012). What's the alternative? The worldwide web of integrative medicine. N Engl J Med, 366(9), 783-785.

Wang, C. S., FitzGerald, J. M., Schulzer, M., Mak, E., & Ayas, N. T. (2005). Does this dyspneic patient in the emergency department have congestive heart failure?. Jama, 294(15), 1944-1956.

Sometimes Heart Failure is just Heart Failure

Respirology Morning Report

The case featured a 77-year-old man with a history of rheumatic heart disease comprised of AS/MS, ‘heart failure,’ atrial fibrillation, and a possible diagnosis of interstitial lung disease worked up at another hospital.  He presented with dyspnea of around one month’s duration and had signs and symptoms consistent with right-sided heart failure (predominantly).  He was diuresed to ‘euvolemia’ and continued to have some breathlessness.  His CT imaging was inconsistent with idiopathic pulmonary fibrosis, and more consistent with pulmonary edema due to decompensated left-sided heart failure.  He has since responded to diuresis.

The imaging below is classical imaging of idiopathic pulmonary fibrosis featuring basilar and subpleural disease in contrast to our patient.

There were multiple valuable learning points from today’s morning report:

-The epidemiology of interstitial lung disease in people at the higher extremes of age is such that idiopathic pulmonary fibrosis is the usual culprit.

-We talked about an approach to suspected IPF.  This involves taking a history predominantly to rule out non-idiopathic contributors to interstitial lung disease such as: drugs, autoimmune conditions, exposures/pneumoconiosis/hypersensitivity pneumonitis among others.  Once ILD is suspected imaging is typically an important diagnostic step.  CT imaging patterns consistent with IPF include a subpleural/lower lobe-predominant pattern, reticular pattern, honeycombing, and sometimes ground glass appearances.

-It is challenging to diagnose an interstitial lung disease on physical examination.  Helpful findings include clubbing, findings associated with secondary causes (skin discoloration, hand findings in RA, etc), and characteristic “Velcro” sounding crackles in late inspiration suggestive of fibrotic lung.  These can be contrasted with the fine, early inspiratory crackles caused by alveoli full of fluid in pulmonary edema, and coarse, non-specific crackles caused by airway secretions.  Most of the time, a high-resolution CT of the chest is helpful as well as pulmonary function tests.  Plain X-rays are more helpful to rule out another process such as a pneumothorax or very obvious congestive heart failure findings.

Further Reading:

Sahni, P., & Shapera, S. Idiopathic Pulmonary Fibrosis: an update.

Nephrotic Syndrome

Nephrology Morning Report

The case involved a woman admitted with back pain who had a medical history of Sjogren’s disease and rheumatoid arthritis.  She was noted to have peripheral edema and periorbital edema, heavy proteinuria, a normal serum creatinine, and hypoalbuminemia of 18g/L.  She went on to receive a kidney biopsy which demonstrated immune complex deposition and some features consistent with cryoglobulinemia.  Her serum cryocrit was 1% (which is abnormal).  There is no final diagnosis as of yet, but her nephrotic syndrome is thought to be related to one of her existing autoimmune diagnoses.

There were multiple learning points discussed:

-There are different ways of quantifying proteinuria.  Firstly, a dipstick only measures albumin and is a point of care test.  A 24-hour urine collection for protein will give you an exact amount of all types of protein in the urine as well as an amount of creatinine (in mmol).  The normal excretion of creatinine in a 24-hour period is 5-15mmol.  A spot protein/creatinine ratio will quantify all types of protein against the number of mmol of creatinine, so it acts as a surrogate for a 24-hour collection when you estimate the amount of creatinine a person would excrete.

-The differential diagnosis of edema (whether dependent or independent of gravity) can relate to the Starling forces: cardiac pump failure (or any venous problem such as thrombosis) can increase venous pressure allowing filtration of fluid from the vascular to extravascular compartment.  Low oncotic pressure from hypoalbuminemia impairs the blood’s ability to retain fluid/sodium in the intravascular compartment and allows it to be filtered out.  Impaired lymphatic drainage can lead to edema.  Impairment in vascular tone caused by medications such as amlodipine can also lead to edema.  Finally, impaired filtration of salt/water as a result of renal insufficiency can also be a cause.

-We discussed nephrotic syndrome: it was broken down into primary renal lesions (which are typically at the glomerular level and include minimal change disease, focal segmental glomerulosclerosis, and membranous disease) and secondary causes (SLE, viruses such as the hepatitides, other autoimmune diseases, drugs such as penicillamine/gold/NSAIDs, malignancies such as lymphomas, amyloidosis).

-The hallmark features of nephrotic syndrome include proteinuria, lipiduria, coagulopathies as a result of loss of anticoagulant factors in the urine, hypoalbuminemia, and a preserved GFR.

-There are a number of ways that multiple myeloma (a clonal plasma cell dyscrasia in which B-cells secrete a monoclonal immunoglobulin) leads to renal disease.  Cast nephropathy (“myeloma kidney”) occurs as a result of filtered immunoglobulin light chains depositing in the tubules and impairing their function.  Monoclonal IgG deposition disease (MIDD or sometimes light chain deposition disease) occurs as a result of deposits of immunoglobulin in the basement membranes of renal tissue.  To distinguish from AL amyloidosis, MIDD deposits do not stain positively for typical amyloid stains (Congo Red).  AL amyloidosis involves deposition of amyloid plaques in renal basement membranes.  Other frequent causes in multiple myeloma include hypercalcemia and volume depletion.

-We did not discuss the hyponatremia, but patients with nephrotic syndrome can classically have one of the “hypervolemic” hyponatremia syndromes.

-Sjogren’s disease can lead to a tubulointerstitial problem, and both it and rheumatoid arthritis are associated with distal renal tubular acidosis.  These would typically be non-anion gap metabolic acidoses.

Further Reading:

Hebert, L. A., Parikh, S., Prosek, J., Nadasdy, T., & Rovin, B. H. (2013). Differential diagnosis of glomerular disease: a systematic and inclusive approach. American journal of nephrology, 38(3), 253-266.