...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.