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

Disseminated Gonococcal Infection

Stephan Russ, M.D., and Keith Wrenn, M.D. N Engl J Med 2005; 352:e15April 21, 2005

In our morning report discussion today, this image from NEJM was mentioned. The image shows the classic macular (arrows) and pustular lesions (arrowheads)seen in disseminated gonococcal infection.

Seizures in HIV-infected Patients

Today, morning report was a discussion of seizures in patients with HIV. Seizures are common in HIV positive individuals. Always think of HIV-related causes and non-HIV-related causes.

HIV-Related causes of seizure included direct cerebral HIV infection, CNS lymphoma, and opportunistic infections such as CNS Toxoplasmosis (most common), Cryptococcal meningitis, CNS TB (tuberculoma rather than TB meningitis). PML is a possible but uncommon cause of seizures. Some medications (such as Foscarnet used to in treatment of CMV infection) can provoke seizures as well.

Don’t forget the other common causes of seizures in adults such as bacterial meningitis, electrolyte and metabolic disturbances, and drug/EtOH intoxication/withdrawal.

Here is a great review on the topic.
Seizures in HIV-seropositive individuals: NIMHANS experience and review. Satishchandra P, Sinha S. Epilepsia. 2008 Aug;49 Suppl 6:33-41.
http://www.ncbi.nlm.nih.gov/pubmed/18754959

* The image is a CT scan slice showing a ring-enhancing lesion with an eccentric nodule, which also enhances. The corticomedullary location and marked surrounding edema are characteristic of toxoplasmosis.

Aspirin Toxicity

This morning we discussed a case of ASA toxicity. This is a potentially fatal clinical scenario that can occur with acute or chronic ingestion of ASA.

At supertherapeutic doses, ASA absorption is delayed because of pylorspasm and “cement” formation. At high doses, the elimination is via slow renal excretion.

Patients often present with nausea, vomiting, tachypnea, and tinnitus. Altered LOC, ranging from mild to coma, and non-cardiogenic pulmonary edema are severe consequences of ASA toxicity. Investigations often show an anion-gap metabolic acidosis and a respiratory alkolosis (secondary to direct stimulation of the respiratory centre).

Main principles of management are supportive care (A-B-Cs), GI decontamination by activated charcoal, and alkalanization of plasma and urine. Don’t forget to call poison control for any overdose, and check for other co-ingestions.

Give a glucose-containing IVF even in the presence of normal serum glucose as ASA can decrease CNS glucose levels. Call nephrology early as hemodialysis is our ultimate treatment for patients who deteriorate despite supportive care.

Uptodate has a really good review on the topic if you’re interested.

Tumour Lysis Syndrome

This morning we had an engaging discussion about Tumour Lysis Syndrome (TLS). As was also reviewed yesterday at noon rounds, TLS is an oncologic emergency.

It is caused by massive tumor cell lysis with the release of large amounts of potassium, phosphate, and nucleic acids Breakdown of nucleic acids to uric acid leads to hyperuricemia, and the precipitation of uric acid in the renal tubules causes acute renal failure. Calcium phosphate deposition can also contribute to renal failure.

Initiation of cytotoxic therapy in patients with high-grade lymphomas (particularly Burkitts lymphoma) and acute lymphoblastic leukemia is often the trigger to TLS. However, TLS can occur spontaneously.

Management of TLS consists of aggressive intravenous hydration, and the administration of the hypouricemic agents rasburicase (recombinant uric oxidase) or allopurinol.

Here is a recent review on the topic:

The Tumor Lysis Syndrome. Scott C. Howard, M.D., Deborah P. Jones, M.D., and Ching-Hon Pui, M.D.N Engl J Med 2011; 364:1844-1854.
http://www.nejm.org/doi/full/10.1056/NEJMra0904569

Familial Mediterranean Fever

FMF is a rare autosomal recessive disorder characterized by paroxysms of fever and serosal inflammation, seen primarily in several ethnic groups originating in the Mediterranean region. Typical clinical presentations of the disease are recurrent attacks of severe pain (due to serositis at one or more sites) and fever, lasting one to three days, and then resolving spontaneously. In between attacks, patients are entirely well.

Common manifestation are peritonitis, pleuritis, synovitis and an erysipelas-like skin lesion. Other less common findings are pericarditis, orchitis and recurrent aseptic meningitis also can occur. As was mentioned this morning, an increased incidence of some vasculitides, such as polyarteritis nodosa and Henoch-Schönlein purpura, has been described. Kidney involvement with these processes may be particularly common.

As discussed this morning, the most important long term complication of FMF is secondary (AA) amyloidosis which occurs insidiously and progressively. Amyloid A deposition occurs in the kidney, spleen, liver, and gut. Renal involvement is the dominant feature of FMF-related amyloidosis.

Colchicine is the mainstay of treatment of FMF, both to prevent attacks as well as prevent the development and progression of amyloidosis. Research is underway evaluating the role of anti-TNF-alpha therapy and IL-1 receptor blockade in severe FMF.

Here two good articles are treatment and clinical manifestations of FMF if you're interested.
http://www.ncbi.nlm.nih.gov.myaccess.library.utoronto.ca/pubmed/19530512
Familial Mediterranean fever. Ben-Chetrit E, Levy M. Lancet. 1998;351(9103):659.

Hepatocellular Carcinoma Risk Factors

A number of important risk factors for the development of hepatocellular carcinoma (HCC) have been identified, including the following:

- Hepatitis B carrier status
- Chronic hepatitis C infection
- Cirrhosis of almost any cause
- Hereditary hemochromatosis
- Environmental toxins (alfatoxin that commonly contaminates corn, soybeans and peanuts; contaminated drinking water; betel nut chewing)
- Tobacco and alcohol abuse
- Non-alcoholic fatty liver disease and diabetes mellitus
- Alpha-1 antitrypsin deficiency
- Epidermal growth factor polymorphisms

Also, it should be noted that HCC has been known to occur in patients without any identifiable risk factor.

For the coffee-lovers among us: several observational studies have implicated coffee consumption as a protective factor for liver cancer, including HCC. A meta-analysis estimated that consumption of two or more cups per day was associated with a 43% reduction of liver cancer. The benefit was observed in individuals with and without liver disease. The presumed mechanism surrounds the fact that coffee contains large amounts of antioxidants suggesting biological plausibility for the protective effect. The authors also noted that coffee and caffeine have been linked to lower liver enzyme levels and a reduced risk of cirrhosis, potentially further contributing to biological plausibility (Larsson SC, Wolk A. Coffee consumption and risk of liver cancer: a meta-analysis. Gastroenterology. 2007;132(5):1740)

Diarrhea in HIV-infected patients

Diarrhea can cause significant morbidity in HIV-infected patients, and can be due to a myriad of causes from infectious pathogens, malignancy and even medications. Before the use of HAART, chronic diarrhea was a large cause of AIDS-defining conditions. However, in the current era the infectious causes of diarrhea in HIV-infected individuals in declining. Key to the evaluation of diarrhea in HIV-infected individuals is a thorough history that includes duration of symptoms, frequency and characteristics of stool, amount of weight loss, and the presence of other abdominal symptoms and constitutional symptoms. Additionally, all medications should be reviewed. A careful physical examination is key to help determine the degree of wasting or to identify any particular findings that may point to specific diseases. For example, fever and wasting may suggest an underlying opportunistic infection. Initial investigations should include stool examination and cultures, and blood cultures. Abdominal CT imaging and endoscopy may be considered if the initial non-invasive work-up is non-diagnostic.

Below is a list of several key causes of diarrhea in HIV-infected individuals:

Bacterial: salmonella, campylobacter, MAC, TB, C. difficile, shigella
Viral: CMV, herpes simplex, adenovirus, norwalk
Protozoal: microsporidium, cryptosporidium
Fungal: histoplasmosis, coccidiomycosis
Gut neoplasms: lymphoma, Kaposi’s sarcoma
Pancreatic insufficiency
Infectious pancreatitis: CMV, MAC
Drug-induced pancreatitis: didanosine, pentamidine
Tumor invasion: lymphoma, Kaposi’s sarcoma
Idiopathic: “AIDS enteropathy”

Is my patient delirious?

Delirium is a very common medical problem in elderly patients admitted to hospital. The 4 key features that characterize delirium include: (1) disturbance of consciousness with reduced ability to focus, sustain, or shift attention; (2) a change in cognition or the development of a perceptual disturbance that is not better accounted for by a pre-existing, established, or evolving dementia; (3) the disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day; and (4) there is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by a medical condition, substance intoxication, or medication side effect.

The Confusion Assessment Method (CAM) is a simple tool that can be used by clinicians to integrate their observations and identify when delirium is the most probable diagnosis. In medical and surgical settings, the CAM has a sensitivity of 94-100% and a specificity of 90-95%.

Confusion assessment method (CAM) for the diagnosis of delirium

1. Acute onset and fluctuating course
- Usually obtained from a family member or nurse and shown by positive responses to the following questions: "Is there evidence of an acute change in mental status from the patient's baseline?"; "Did the abnormal behaviour fluctuate during the day, that is, tend to come and go, or increase and decrease in severity?"

2. Inattention
- Shown by a positive response to the following: "Did the patient have difficulty focusing attention, for example, being easily distractible or having difficulty keeping track of what was being said?"

3. Disorganized thinking
- Shown by a positive response to the following: "Was the patient's thinking disorganized or incoherent, such as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject?"

4. Altered level of consciousness
- Shown by any answer other than "alert" to the following: "Overall, how would you rate this patient's level of consciousness?"
Normal = alert
Hyperalert = vigilant
Drowsy, easily aroused = lethargic
Difficult to arouse = stupor
Unarousable = coma

The diagnosis of delirium requires the presence of features 1 AND 2 plus either 3 OR 4.

Does my patient have COPD?

We are often faced with many patients who are given a label of obstructive airway disease based on a history of smoking and wheezing. But in many instances patients with these features do not have obstructive airway disease. Dr. Straus and colleagues identified 4 elements on history and physical examination that were significantly associated with a diagnosis of obstructive airway disease:

1. Smoking at least 40 pack-years (LR + 8.3)

2. Self-reported history of chronic obstructive airway disease (LR + 7.3)

3. Maximum larygeal height less than 4cm (LR + 2.8)

4. Age at least 45 yrs (LR + 1.3)

The presence of all 4 of these elements has a LR + 220, rulling in a diagnosis of obstructive airway disease.

Click on the following link to see the abstract: http://http//jama.ama-assn.org/content/283/14/1853.abstract

Adrenal Insufficiency

The clinical presentation of adrenal insufficiency is variable and depends on whether the onset is acute (leading to adrenal crisis) or chornic, with symptoms that are often vague and insidious. The key to making the diagnosis of adrenal insufficiency is a high level of clinical suspicion. The signs and symptoms of adrenal insufficiency depend upon the rate and extent of loss of adrenal function, whether mineralocorticoid production is preserved, and the degree of stress. The following is a list of key clinical features of primary adrenal insufficiency:

• weakness


• fatigue


• anorexia


• orthostatic hypotension


• nausea


• vomiting

The following is a list of key laboratory abnormalities of primary adrenal insufficiency:

• hyponatremia


• hyperkalemia


• hypoglycemia


• lymphocytosis


• eosinophilia


• hypercalcemia (rarely)

Patients with Headache

Headaches are a very common medical complaint. In assessing patients with headaches, we must determine who has a serious cause of a headache and who requires neuroimaging. A Rational Clinical Exam article from JAMA entitled "Does this patient with headache have a migraine or need neuroimaging?" helps to outline an approach to headache. After a systemic review of the literature, the best predictors of a migraine were summarized by the mnemonic POUNDing: Pulsation, duration of 4-72 hOurs, Unilateral, Nausea, Disabling). If a patient meets 4 out of the 5 criteria, the likelihood ratio (LR) for definite or possible migraines is 24. For neuroimaging, several clinical features were found on pooled analysis to predict the presence of a serious intracranial abnormality: cluster-type headache (LR 10.7), abnormal findings on neurological examination (LR 5.3), undefined headache (LR 3.8), headache with aura (LR 3.2), headache aggrevated by exertion or valsalva (LR 2.3), and headache with vomiting (LR 1.*). It should be noted that no clinical features were useful in ruling out significant pathologic conditions. To see the full Rational Clinical Exam article click here http://jama.ama-assn.org/content/296/10/1274.full.pdf+html?sid=80cae855-c34e-401a-a365-34f964dfe247

Dabigatran for anticoagulation in Afib

Dabigatran is an oral, direct thrombin inhibitor. Its efficacy and safety relative to warfarin was evaluated in the RE-LY trial, at 2 doses. It was the first randomized trial to demonstrate that an alternative oral anticoagulant is superior to adjusted-dose warfarin. Over 18,000 patients with non-valvular atrial fibrillation and at least 1 stroke risk factor were were randomly assigned to receive oral dabigatran at one of two doses (110 or 150 mg) twice daily, or adjusted dose warfarin (INR 2-3). The primary study outcome was stroke or systemic embolism. After a median follow-up 2 years, rates of the primary outcome were 1.69%/yr in the warfarin group, compared with 1.53%/yr in the group that received 110 mg of dabigatran (P<0.001), and 1.11%/yr in the group that received 150 mg of dabigatran (P<0.001). The rate of major bleeding was higher in the warfarin group, compared to the lower dose dabigatran group. This study concluded that in patients with atrial fibrillation, dabigatran given at a dose of 110 mg was associated with rates of stroke and systemic embolism that were similar to those associated with warfarin, as well as lower rates of major hemorrhage. To see the full article click here http://www.nejm.org/doi/full/10.1056/NEJMoa0905561#t=article

Clubbing

Today in morning report we discussed a patient, who among other problems, was clubbed.

Clubbing is the enlargement of the terminal segments of the fingers and/or toes that results from the proliferation of the connective tissue between the nail matrix and the distal phalanx. It develops in the context of a number of neoplastic, infectious, inflammatory and vascular conditions.

Features on physical exam that make clubbing more likely include changes in nail-fold angles, as well as changes in the shape, depth, and width of the terminal phalanges.

1) Phalangeal Depth - This ratio compares the depth of the distal phalanges to the inerphalangeal areas. Normally, this is less than 1. Once this ratio exceeds 1, clubbing is more likely.

2) Nail Fold angles - Two angles are commonly discussed: the profile angle and hyponychial angle.

a) The profile angle can be estimated by the angle the nail projects from the nail fold. normally this is about 160 degrees but exceeds 180 degrees when the finger is clubbed.

b)The hyponychial angle compares two lines, (1), from the DIP joint to the nail fold and (2), from the nail fold to the point where the nail meets the finger tips. This angle is should not exceed 190 degrees normally and if it does, clubbing is likely present.

3) Nail bed squishiness - Palpation of the nail bed in clubbed fingers tends to be spongier than a normal nail with the sensation that the nail is floating.

Check out the JAMA rational clinical exam series here for an evidence based review.

Grade 4 Left Ventricles

Today in morning report, we discussed a patient presenting with complications related to their grade-4 left ventricle. Much of our discussion focused on the management of these patients. Specifically, what about device therapy? Here is a summary:



Device Therapy
This really came to the forefront with the MADIT-2 trial where patients with a history of MI and severe LV dysfunction (grade 3 or worse) after optimal medical therapy had prophylactic ICDs placed. This showed improved survival. The SCD-HeFT trial looked at amiodarone vs. ICDs and again, device therapy appeared superior. Cost effective analysis has been favourable, but controversial. Check out this editorial for another look.


The MADIT-CRT trial looked at relatively asymptomatic patients (NYHA class 1 and 2) with depressed LV function (less than 30%) and prolonged QRS durations and found that CRT decreased rates of CHF exacerbations.

Recently, results of the RAFT trial were presented in NEJM and found that "among patients with NYHA class II or III heart failure, a wide QRS complex, and left ventricular systolic dysfunction, the addition of CRT to an ICD reduced rates of death and hospitalization for heart failure." More adverse events were noted, however.

All in all, this is a rapidly progressing area in medicine and it may not be too long until we find ourselves here!

Toxic Epidermal Necrolysis

Today in Morning Report, we discussed the case of toxic epidermal necrolysis likely secondary to allopurinol use.

Allopurinol and its metabolite, oxipurinol (alloxanthine), decrease the production of uric acid by inhibiting the action of xanthine oxidase, the enzyme that converts hypoxanthine to xanthine and xanthine to uric acid. Indications are most commonly for disorders of hyperuricemia (urate nephropathy, tumor lysis sydrome prophylaxis, and gout). When used for gout, most would agree that >3 flares/year (or tophaceous deposition) would merit its use. Incidentally discovered hyperuricemia is not an on-label indication.

With regards to the side-effect profile, the biggest concern, as seen in our patient, is toxic epidermal necrolysis. This is a very rare, but acute and potentially fatal skin reaction in which there is sheet-like skin and mucosal loss. It exists in a spectrum with Stevens-Johnson Sydrome and is mainly differentiated by the degree of epidermal involvement.

Treatment is mostly supportive but begins with the discontinuation of the offending drug. Wound care is very important to prevent excess fluid loss and secondary infections. In severe cases, consultation with a burn unit may be appropriate. Adjunct treatment with corticosteroids, cyclosporin, cyclophosphamide and IVIg have been trialed with variable success.

TEN is reviewed nicely at this link, check it out for a summary on the diagnosis and treatment.

Hyperkalemia

Last week, a patient with hyperkalemia was discussed in morning report.

Causes of hyperkalemia always come down to renal handling of potassium. Dietary (or iatrogenic!) intake of potassium may play a role, but most clinical scenarios revolve around limitations in excretion.

Management options include:
1) Stop the exogenous potassium - this seems simple but is embarassing when missed.

2) Stop offending drugs - this is not the right time for any potassium sparing diuretics or ACE inhibitors

3) Shift the Potassium - This does not equal excretion and is only a temporary fix. Classically, a high glucose load (1 amp of D50W) with an intravenous insulin chaser (1o units iv) is the mainstay cocktail. Other options include intravenous sodium bicarbonate and inhaled beta agonists (8 puffs with aerochamber). Interestingly, beta agonists may be more efficacious than previously believed (see the article below).

4) Dump the Potassium - at the end of the day, you need to rid the body of the excess. A number of options exist. High dose furosemide (assuming this is not oliguric renal failure) is an effective way to mobilize potassium. Potassium binders are often used (kayexalate) but are slow and have other side effects (colonic necrosis!). Finally, hyperkalemia refractory to medical management is an indication for hemodialysis.

Check out CMAJ for a very recent review.

Aches and Pains

Today we discussed an interesting case of a man with fevers and progressive muscle pain and weakness. Among the many things on the differential diagnosis was Giant Cell Arteritis.

GCA (formerly known as temporal arteritis) should be considered in patients with new headaches, abrupt onset of visual disturbances, symptoms of polymyalgia rheumatica, jaw claudication, unexplained fever or anemia, high erythrocyte sedimentation rate and/or high serum C-reactive protein.

A temporal artery biopsy is part of the workup but can be negative in some patients who have the disease (7-13% will have a negative unilateral biopsy but a postive bilateral biopsy).

The treatment for GCA are glucocorticoids. Prednisone at 1mg/kg is the commonest initial therapy with tapering initiated after 4 weeks (providing a normalized ESR).

Here is a link to a NEJM review on the topic and here is a look at the topic in the JAMA rationale clinical exam.