Pressure Ulcers - Time to Intervene

We have discussed how difficult it is to assess and manage patients with chronic pressure ulcers.

The highlights of our discussion:

• Many patients develop pressure ulcers for multiple reasons;
• Infection, ischemia, and mechanical factors all need to be considered;
• The patient's total situation needs to be assessed - can they mobilize appropriately?  Is there adequate perception of injury or pressure?  Do they have the resources they need to take care of themselves, and the ulcer, adequately? Are there people looking out for them?

This article is a great review from the BMJ on the entire topic. 

The issue of managing chronic ulcers gets even more complicated when we consider the possibility of underlying osteomyelitis.  The evidence based examination for osteomyelitis is found here.  Another review of osteomyelitis is found here.

The bottom line - managing chronic ulcers takes multiple disciplines, and takes time.  Given the tremendous morbidity they cause, the huge effort it takes to deal with them is a very worthwhile investment in patients' quality of life.

Dizziness, Disease, and Doctors' Dizz-Ease

As clinicians, it is obvious that we don't love dizziness.

Not that we have a problem with the idea of it in general.  It's just that it's so.... common.  Vague.  Banal.  Potentially worrisome.  Hard to understand.  Harder to approach.  Tempting to investigate to the nth degree, with an array of tests that's, well, dizzying, and may well leave you just where you started.  Unsure of what is going on, and your dizzy patient is no better off.


Anybody feeling their head spin yet?

Yet we get referred dizzy patients all the time.  In General Medicine, they usually come with the additional label of "R/O [insert ominous disease here]".  Alarming, except that we know that most dizzy patients have a benign underlying diagnosis - in the sense that their symptoms don't connote a life-shortening underlying disease.  How do we sort this out?

We discussed an approach which tries to maximize the value of information that is already at hand.

First, classify the dizziness into one of 4 basic syndromes:

• Presyncope - the feeling of impending faint.  Look for tunnel vision, "dissociated" hearing, blood pressure changes, orthostatic symptoms, vagal stimuli.
• Vertigo - the illusion, often visual, that the person or the environment is rotating.  Note, patients are aware that this is an illusion!
• Dysequilibrium - patient describes the inability to remain upright, tendency to fall or stumble, feeling as if intoxicated or walking on the deck of a ship at sea.  This is really the subjective feeling of ataxia.
• Ill-defined lightheadedness - a grab bag of other descriptions.  Note, this could include patients who belong in the other 3 categories but you didn't understand their story well!

Next, look for the association:

• Presyncope usually connotes a cardiovascular cause - changes in BP
• Vertigo can be central or peripheral - see below
• Dysequilibrium is often a disorder of cerebellar coordination, dorsal columns or peripheral nerves responsible for proprioception

The following article helps to go over these possibilities:

Differential diagnosis of dizziness (U of T link)

In addition, the more difficult problem of analyzing dizziness in older patients is addressed in this 2 part series:

Dizziness in the older adult, Part 1. Evaluation and general treatment strategies (U of T link)

Dizziness in the older adult, Part 2. Treatments for causes of the four most common symptoms  (U of T link)

When vertigo is the best description of the patient's complaint, the key is to distinguish central from peripheral causes.  Bottom line:

• Peripheral causes of vertigo usually have very well defined presentations, which often match classic descriptions - the prototype for this is BPPV.
• Peripheral causes are very unlikely to be associated with non-horizontal nystagmus.  Note, central causes can be associated with any type of nystagmus.
• Autonomic symptoms are more common with many peripheral causes of vertigo.
• The response to the Dix-Hallpike manoeuvre is usually immediate, dramatic, and fatigues rapidly in peripheral causes of vertigo.

This article takes a statistical approach - what is this likely to be?  Note they focus on what presents in ER, rather than on a general population.

An approach to dizziness and vertigo in the emergency department (U of T link)

And what about central causes?  They are what we really worry about, yet we don't usually have a good approach to them, apart from "get an MRI".  This article goes over these issues.

Central vertigo and dizziness: epidemiology, differential diagnosis, and common causes (U of T link)

Finally, what to do about it?

Here is a very useful article about BPPV .  (U of T Link)  Otherwise, see the link above for treatment of symptoms in dizzy patients in general.

Finally, here is a YouTube animated video of the Dix Hallpike manoeuvre and the associated Epley's manoeuvre which treats BPPV specifically.

Responding to Hyperkalemia

Last week, we discussed the rationale for how we respond to calls about hyperkalemia.  Coincidentally, a new article came out on this topic in the CMAJ.

The essential points in our discussion were:

1.  Make sure it's real - order repeat bloodwork to ensure you don't respond inappropriately to hemolyzed blood samples, mislabelled samples, or problems with blood collection technique that give rise to spuriously high K+ in the tube, but not in the patient.

2.  Assume that it is real until you know otherwise - while waiting on the above, don't hesitate to respond to the K+ value that you do have, especially if it is greater than 6.0, or the clinical setting is likely to promote hyperkalemia (see below).

3.  Assess the consequences of the hyperkalemia.  The most frequently cited thing to do next is to "look for ECG changes".  While this isn't wrong, don't be misled by their absence - a recent review found them to be very infrequent!  The ECG changes are:

• Tall, "tented" or "peaked" T waves
• Loss of P waves
• Shortening of PR interval
• Widening of QRS
• Loss of SA node activity and evolution of a "Sine Wave"
• Asystole

Perhaps more importantly, check for hemodynamic consequences.  Rising K+ levels don't just affect conduction - they also affect contractility, and falling BP may be a result of this.

4.  Assess the setting for possible causes.  This isn't just a follow-up step - start thinking of this RIGHT AWAY.  Your immediate management may be guided by this.  The approach to diagnosing the cause looks for each of:

• high intake (almost always in combination with reduced clearance, and almost always involving a physician administering potassium somehow);
• reduced clearance - renal compromise (lowered GFR) is by far and away the most common association with hyperK.  Look out for meds that also affect renal K handling, eg. spironolactone.
• shift -  the big player here is acidosis, which you need to identify early in order to help the K.

Special mention:  ALWAYS ascertain whether the patient is on Digoxin.  Hyperkalemia related to digoxin toxicity requires specific management! (Get the full article from U of T here.)

5.  Start Managing the K+!

• Get help.  Trying to manage patients on your own, especially when they have potassium levels >6.5, can set them up for disaster if things get out of control quickly. Get the crash cart if there are ECG changes or the patient is symptomatic, or if the K level is >7.0.  At a minimum have a nurse nearby to handle all the IV access issues and assist monitoring the patient.
• Protect the heart.  Give Calcium salts (CaCl2 or Ca gluconate), usually as a rapid infusion over 2-10 minutes.  In pre-arrest situations, you may need to give by direct injection over about 30 sec.  (Always have ECG monitoring in place for this.)  NB.  This does nothing for the K level.  It only buys you time.  However, it can have some dramatic clinical effects - I have personally raised someone's BP from 60 to 90 systolic with Ca gluconate alone.
• This is one of the differences with digoxin toxicity - DON'T give Ca salts to these patients!
• Start shifting the potassium.  You can give nebulized ventolin as a start.  10 units of REGULAR insulin followed by 50 mL of 50% dextrose will also bring the K+ down somewhat. 
• If the patient is extremely acidotic, and not volume overloaded, you should consider infusing sodium bicarbonate to assist in shifting the potassium back into cells.  This is NOT part of the routine management of this problem - only done in specific situations!
• Start eliminating the potassium.  All the shifting in the world won't solve the problem, unless the total body K+ has been brought down to normal.  
• If the patient makes any urine at all, it's worth trying to assist K excretion via the kidneys, using loop diuretics.  This can be the most efficient route of K excretion.
• Otherwise go for the GI route to excrete K.  Use K-binding resins (prefer calcium resonium for volume overloaded patients, rather than sodium polystyrene, because it avoids loading them with sodium).  Remember that resins without sorbitol cause a lot of abdominal pain, and not much K excretion - give them plenty of sorbitol to help things move along osmotically.

6.  All of this may not be enough.  Patients with very little renal function may only get their potassium down reliably with dialysis.  If you are seeing a patient with newly diagnosed renal failure, treat as above, and get help from a nephrologist to assess whether dialysis should be instituted on an emergency basis.

Low Platelets and a 'rash'

A 60 year old man was referred to the ED by his primary care physician because of a platelet count of 6.

He had been generally well and had a past history of appendectomy (age 30), hypertension, and diet controlled type 2 diabetes. He had gone to his PCP 2 days ago because of a 'rash' on his legs, and bloodwork done at that time showed a hemoglobin of 136, WBC 6.2, and plts 6. The PCP called him this morning and told him to go to ED. He has not developed any new symptoms.

You are the internist consulted. What is your approach?

Strep viridans bacteremia

It happens, from time to time, that a patient who is febrile, hypotensive, confused, or otherwise acutely ill has blood cultures drawn and is found to have Strep species in them.  A short time after that, the lab may call the ward and give further identification - the Strep belong to the viridans group.

The reflex reaction to this may be - does this patient have endocarditis??  It's an important question to answer.  Traditional teaching about Strep viridans is that it is the primary causative organism of what we used to call "subacute" bacterial endocarditis.  While we don't look at endocarditis quite the same way any more, it is still true that viridans bacteremia is a major diagnostic criterion under the Duke system of estimating the likelihood of infective endocarditis.

However, that's not the end of the story with Strep viridans.  It has important other sources, primarily in the gut and oral cavity.  When it arises de novo, one should ask the following questions:

1.  Could this patient have infective endocarditis?  (note - IE hasn't given up first place!)
2.  Is there a possibility of an underlying cancer involving the mouth or GI tract?
3.  Is this a patient with impaired immunity?  (these bacteremias may occur more easily, for example, in patients with hematologic malignancies, with or without chemotherapy)
4.  Does the patient have an indwelling vascular access device?
5.  Irrespective of 2 through 4, could this patient have infective endocarditis?

A recent paper (from Slovakia)  [Mrazova, et al. "Prospective national survey of viridans streptococcal bacteraemia risk factors, antibacterial susceptibility and outcome of 120 episodes" Scandinavian journal of infectious diseases (2005)] shows a current snapshot of the associations of different diseases with Strep viridans bacteremia.

The rule of thumb regarding treatment of Strep viridans bacteremia should be followed here:  When in doubt, and when there is no compelling contraindication, treat this as infective endocarditis, according to current guidelines.