Necrotizing Fasciitis

During this ambulatory internal medicine selective, I have had the opportunity to assess several patients referred to our clinic for possible cellulitis.Skin and soft tissue infections are common but recognizing the dangerous ones that need prompt admission and treatment from those that can be treated with oral antibiotics as an outpatient is crucial. One of the most notorious soft tissue infections is necrotizing fasciitis, an infection that spreads quickly along fascial layers and can lead to the development of toxic shock syndrome resulting in organ failure and death. There are two clinical types of necrotizing fasciitis, Type I which is a polymicrobial infection with anaerobes (bacteroides, peptostreptococcus) and a facultative anaerobe (enterobacterales or non group A streptococcus) and Type II which is a monomicrobial infection with streptococcus pyogenes (group A strep). 

 

Signs & Symptoms: Signs and symptoms of necrotizing fasciitis typically develop acutely (over the course of hours).

 

Early signs and symptoms:

• Red, warm, swollen area of skin, not well demarcated that spread quickly (mark the area of erythema)
• Severe pain or edema beyond the area of redness
• Fever

Late symptoms:

• Ulcers, blisters, black areas or skin colour changes
• Crepitus of the skin
• Oozing/pus
• Dizziness
• Fatigue
• Nausea
• Diarrhea
• Tachycardia, tachypnea, hypotension

Common Findings on Bloodwork/Imaging:

• WBC: abnormally high or low WBC
• Sodium: may be decreased
• Urea/Creatinine: may be elevated
• CRP: usually elevated
• CK: may be elevated
• Lactate: usually elevated
• Blood and Tissue Cultures: positive (polymicrobial or monomicrobial)
• Arterial Blood Gas: hypoxemia, acidosis
• Radiography: edema extending along fascial planes/soft tissue gas

Management of Necrotizing Fasciitis

The key principles in the management of necrotizing fasciitis are surgical debridement and empiric antibiotics. Delaying surgical debridement by >12 hours has been shown to be associated with an increased need for future debridement, organ failure and higher rates of mortality. Empiric antimicrobial therapy should be started immediately, as well as fluids for hemodynamic support. Recommended empiric regimens include:

• Vancomycin, linezolid, tedizolid or daptomycin and 
• Piperacillin/tazobactam or a carbapenem and
• Clindamycin (for the antitoxin effects)

 

References:

1. Necrotising Fasciitis. BMJ Best Practice. https://bestpractice-bmj-com.myaccess.library.utoronto.ca/topics/en-gb/821/history-exam
2. Necrotizing Soft Tissue Infections. UpToDate. https://www.uptodate.com/contents/necrotizing-soft-tissue-infections?search=necrotizing%20fasciitis&source=search_result&selectedTitle=1~135&usage_type=default&display_rank=1
3. Necrotizing Fasciitis. Centers for Disease Control and Prevention. https://www.cdc.gov/groupastrep/diseases-public/necrotizing-fasciitis.html

Ischemic Stroke: Secondary Prevention

One day while in Hypertension clinic, I met a patient who was referred from stroke clinic. They had multiple risk factors for a recurrence, including hypertension, dyslipidemia and a significant smoking history. Unfortunately, they had not been treated adequately for these risk factors in the past. Upon reviewing their medications, I noted they were on Aspirin alone for their secondary prevention. This interaction prompted me to review the different options for secondary prevention in stroke.

According to the Thrombosis Canada 2020 guidelines on secondary stroke prevention, in response to ischemic stroke or TIA, there are 10 major factors to consider:

1. Lifestyle Risk Factor Modification – Key behavioural changes to prevent risk of recurrent stroke include eating a balanced diet (fruits, vegetables, fibre, plant-based protein; avoiding saturated fat and cholesterol), limiting sodium intake (<2g daily), increasing exercise (at least 150 minutes per week), weight management (BMI 18.5 – 25) and limiting alcohol consumption (10 drinks per week).
2. Smoking Cessation – There is no clear evidence for the optimal time for nicotine replacement therapy initiation post-stroke. Assess patients’ readiness to change and suggest nicotine replacement when amenable, as it is generally safer than continued smoking. Additionally, prescription of nicotine replacement therapy, varenicline or bupropion may increase patients success in quitting.
3. Blood Pressure Management – Measure BP at each encounter, as hypertension is the most important modifiable risk factor for stroke. <140/90 is the target for all patients after stroke or TIA. <130/80 is the target for patients with diabetes after a stroke. In patients with lacunar stroke, aim for systolic <130.
4. Antithrombotic Therapy – All patients should have antiplatelet therapy in the form of ASA 81mg daily, ASA 25mg and dipyridamole 200mg daily, or clopidogrel 75mg daily, unless there is a contraindication to anticoagulation. Combination therapy, ASA 81mg and clopidogrel 75mg is acceptable for 1 month after stroke or TIA, but should not be continued longer, as it carries an increased risk of hemorrhagic complications. *All stroke patients should be evaluated for atrial fibrillation, which would be an absolute indication for anticoagulation.
5. Lipid Management – Statins are indicated to target LDL <2.0mmol/L or >50% reduction in LDL from baseline; target LDL <1.8mmol/L or >50% reduction in LDL in patients with acute coronary syndrome and coronary disease. If patients do not tolerate statins, or do not meet target, ezetimibe can be considered. Bile acid sequestrants and PCSK9 inhibitors can be considered in addition to statins +/- ezetimibe.
6. Diabetes Management – HbA1c should be targeted to <=7.0%. Refer to Diabetes Canada Guidelines for choice of anti-hyperglycemic agents to achieve target.
7. Sleep Apnea – Obstructive Sleep Apnea (OSA) should be screened for (STOP-BANG questionnaire) and treated, given it is a risk factor for stroke.
8. Management of Carotid Stenosis – Ipsilateral, symptomatic 50-99% internal carotid artery stenosis as measured on CT angiogram in patients with TIA or non-disabling stroke should be referred to neurosurgery/vascular surgery for evaluation. Carotid endarterectomy, if eligible, should occur within 14 days of the onset of symptoms. If stenosis is <50%, surgical management is not indicated.
9. Anticoagulation for Atrial Fibrillation – Investigations for atrial fibrillation should be completed in all patients with stroke (48-hour Holter monitor, loop recorder) and should include prolonged cardiac monitoring in patients >=55 years old.
10. Management of Patent Foramen Ovale (PFO) – Closure of PFO and antiplatelet therapy is recommended for patients 18-60 years old following an ischemic stroke or TIA linked to their PFO.

In the specific case of an ischemic lacunar stroke, given the presence of cerebral small vessel disease, recommendations are similar, yet continue to be evolving. Hypertension should be managed, but a clear target BP has not been defined. A combination of aspirin and clopidogrel is associated with increased hemorrhagic risk in these patients without corresponding advantages. Statins are effective in treating hyperlipidemia in these patients. Finally, anticoagulant and carotid surgery are not recommended ubiquitously.

This patient was referred to our clinic for hypertension management, so we mainly focused on recommendation 3 by starting a new anti-hypertensive. We were also able to encourage lifestyle modifications in recommendation 1 and validate their decision to quit smoking in recommendation 2.

When providing adequate secondary prevention after a stroke, it is important to take a holistic approach to management. 

-EB-

References:

Thrombosis Canada. Stroke: Secondary Prevention. 2020. Accessible at https://thrombosiscanada.ca/wp-content/uploads/2020/02/Stroke-Secondary-Prevention_26Feb2020.pdf 

Valenti R, Pantoni L. Secondary Prevention After Ischemic Lacunar Stroke. InIschemic Stroke Therapeutics 2016 (pp. 137-146). Springer, Cham.

DASH-ing Towards Lower Blood Pressure

I spoke to a young man in his 40s in the outpatient Hypertension Clinic, he had been seen in the clinic several months prior for resistant hypertension. With many life changes and new stressors, he was having trouble finding the time to eat healthily and exercise, and his blood pressure was rising as a result. At this prior clinic visit, the physician at the time again made a renewed pitch for life-style modifications in addition the the patient's current blood pressure medications. We were now seeing this gentleman following 4 months of these life-style modifications including the DASH diet and exercise.

What is the DASH Diet? 

The DASH diet stands for ‘Dietary Approaches to Stopping Hypertension’. The DASH diet is high in fruits, vegetables and low-fat dairy, and low in snacks, sweets, meats and saturated and total fat. This is not a diet aimed at weight loss, but a diet that focuses on reducing blood pressure.

 

What’s the impact?

Irrespective of sodium intake, the DASH diet has been found to lower blood pressure in both those with high BP and those with normal BP. A further BP reduction is seen when you add on sodium restriction. With the low-sodium DASH diet, the mean fall in systolic BP in one study was 11.5mmHg!

 

Other Lifestyle/Dietary Modifications that can help lower BP:

• Physical Activity: 30-60min most days of the week
• DASH Diet
• Weight loss: losing 10 lbs can lower BP
• Consuming less salt: limit use in cooking and at table, avoid highly processed foods/canned/prepared foods
• Alcohol: limiting alcohol intake to a maximum of 2/day, weekly max:10 for women, and 3/day, weekly max:15 for men
• Smoking: quitting smoking

Some Potential Downsides of DASH Diet Adherence

• Planning that goes into the diet/meal plan
• Those with dietary restrictions may need to make modifications to the diet
• Food list for DASH diet is not comprehensive, can be difficult to determine where some foods fit into the DASH diet
• High fibre foods like fresh fruits and vegetables can lead to increased gas and bloating, reducing the tolerability of the diet for patients, one way to make it more tolerable is slowly introducing high fibre foods (2/3 per week) so the body can adjust

 

Back to our patient: 

Our patient informed us that with dietary modifications and exercise he had lost 38 lbs over 4 months. He found that he was getting light-headed at times, and noted his BP was consistently in the range of 105-110mmHg systolic. We therefore discussed removing one of his blood pressure medications, with the strong likelihood that we would be able to reduce another medication at our next visit.

 

This was a reminder to me that although we talk to patients about their medications at each visit, to make time to discuss non-pharmacologic and lifestyle modifications during appointments, they work!

-KD-

 

References: 

1. The Nutrition Source. Diet Review: DASH. Harvard School of Public Health. https://www.hsph.harvard.edu/nutritionsource/healthy-weight/diet-reviews/dash-diet/

2. The DASH Diet to lower high blood pressure. The Heart and Stroke Foundation Canada.https://www.heartandstroke.ca/healthy-living/healthy-eating/dash-diet?gclid=CjwKCAjwmv-DBhAMEiwA7xYrd91WuCqqfiEMnsd2u3pV4kXj9bKph6FTs62xKrDNSbq-fo6Kaia_HhoCVewQAvD_BwE&gclsrc=aw.ds

3. Diet in the Treatment of Hypertension. UpToDate. https://www.uptodate.com/contents/diet-in-the-treatment-and-prevention-of-hypertension?search=DASH%20Diet&source=search_result&selectedTitle=1~28&usage_type=default&display_rank=1#H4

Up All Night: An Approach to Fatigue

One day in GIM clinic, I saw a patient who was referred due to severe fatigue, influencing her daily life. She was unable to work, felt fatigued throughout the day, and these symptoms were negatively impacting his quality of life. Her family physician had completed a robust initial work-up, but I thought fatigue was an interesting chief concern, one with a broad differential and worth exploring further.

Fatigue is a common concern in primary care and can have major impacts on the quality of life of our patients. First, it is critical to distinguish fatigue from sleepiness. Fatigue is more likely when a patient describes non-restorative sleep, mental exhaustion, poor muscle endurance and intensified fatigue with activity. An important cause of fatigue to consider is medications, especially sedative-hypnotics, antidepressants, muscle relaxants, opioids, and antihistamines. It is also critical to take a thorough sleep history, identifying sleep hygiene, disrupted sleep (pain, urination, anxiety), daytime sleeping, exercise, and substance use. Depression may manifest as fatigue, so it is crucial to screen for low mood. As well, screening for constitutional symptoms, such as fevers and weight loss, should be included in the initial history.

Initial laboratory investigations are targeted to investigate secondary causes of fatigue (anemia, hypothyroidism, inflammatory state, liver disease, pregnancy, etc.) and should include CBC, lytes, creatinine, and thyroid function tests. In sexually-active women, it would be important to include a b-HCG test. Further investigations which could be considered are ferritin, iron studies, vitamin B12, and folate levels.

Initial bloodwork for this patient did not yield any indication to her profound fatigue. She is an active smoker with a 50-pack year history, so met criteria for CT thorax to investigate for a lung malignancy. Imaging did not reveal any occult malignancy which would explain her fatigue.

In this instance, the patient also reported a history of feeling fatigued upon waking and requiring naps during the day. Her partner also reported that she snored loudly at night. These symptoms prompted a further history, screening for Obstructive Sleep Apnea (OSA) with the STOP-BANG questionnaire:

• Do you Snore loudly (loud enough to be heard through closed doors or your bed-partner elbows you for snoring at night)?
• Do you often feel Tired, Fatigued or Sleepy during the daytime (such as falling asleep during driving)?
• Has anyone Observed you Stop Breathing or Choking/Gasping during your sleep?
• Do you have or are being treated for High Blood Pressure?
• Body Mass Index more than 35kg/m²?
• Age older than 50 years old?
• Neck size large? (Measured around Adams apple)
• Gender = Male?

A score of 0-2 is correlated with low risk of OSA, 3-4 with a moderate risk of OSA and 5-8 with a high risk of OSA. This patient had a score of 6 (snore, observed, tired, pressure, BMI, age), putting her at high risk for OSA. Her family physician had astutely ordered a sleep study, which demonstrated moderate obstructive sleep apnea.

Treatment for OSA involves behavioural modification and patient education. Patients should be encouraged to exercise, for its benefits in addressing fatigue, as well for the benefits of weight loss. As well, advising patients to avoid sleeping in a supine position and to avoid alcohol, as it can worsen OSA and fatigue. Continuous positive airway pressure therapy is the mainstay of treatment, which acts to prevent upper airway collapse and thereby prevent apnea and hypopnea events. Should patients be unable to use CPAP, they could be offered an oral appliance such as a mandibular advancement splint or tongue-retaining device, however these devices are not as effective as CPAP.

Fatigue is a common presenting concern and warrants thorough investigation to rule out serious secondary causes of fatigue, such as malignancy. It is critical to complete a thorough sleep history and consider a diagnosis of OSA in patients who screen positively on the STOP-BANG questionnaire.

 

-EB-

 

References:

Chung F, Abdullah HR, Liao P. STOP-Bang questionnaire: a practical approach to screen for obstructive sleep apnea. Chest. 2016 Mar 1;149(3):631-8.

Qaseem A, Holty JE, Owens DK, Dallas P, Starkey M, Shekelle P. Management of obstructive sleep apnea in adults: a clinical practice guideline from the American College of Physicians. Annals of internal medicine. 2013 Oct 1;159(7):471-83.

Rosenthal TC, Majeroni BA, Pretorious R, Malik K. Fatigue: an overview. American family physician. 2008 Nov 15;78(10):1173-9.

Hypertensive Emergencies: How High is Too High?

Caring for patients in the Hypertension Clinic at Toronto Western I have had the opportunity to talk with my preceptors about the long-term clinical manifestations and complications of high blood pressure. In this blog post, I wanted to explore further what can happen acutely in the case of a hypertensive emergency. 

 

What is a Hypertensive Emergency? 

Hypertensive emergencies don’t refer to a specific elevated blood pressure number, but rather an elevated blood pressure that leads to end organ damage. For each individual patient this can happen at a different number. For example, a patient who regularly has blood pressures of ~180/90, a blood pressure of 200/90 may not trigger a hypertensive emergency. However, a pregnant woman with pre-eclampsia might have a baseline blood pressure of ~110/70, and therefore a blood pressure spike to 165/85 might trigger a hypertensive emergency. Examples of end organ damage include both micro and macrovascular damage. Microvascular complications involving small vessels can include encephalopathy, pre-eclampsia/eclampsia and local inflammatory events. Macrovascular damage can include CHF, MI, aortic dissection, stroke or subarachnoid hemorrhages.

 

What workup should be done in a suspected Hypertensive Emergency? 

Look for the end organ damage.

·      Heart: ECG, CXR, troponin, CT chest with contrast or transesophageal echo

·      Brain: CT or MRI Brain

·      Kidneys: Urinalysis, serum lytes and creatinine

 

When to Suspect Hypertensive Emergencies (not exclusive):

·      Hypertensive Encephalopathy: High blood pressure and…

o   Severe headache +/- vomiting

o   Confusion/altered mental status

o   Seizures

o   Retinal changes

·      Pre-eclampsia/Eclampsia: Pregnant or post-partum + high BP and…

o   Headaches

o   Blurring of vision, flashing lights

o   Pain below the ribs

o   Nausea/vomiting

o   Fluid retention, flash edema

·      CHF: 

o   Dyspnea

o   Peripheral edema

o   Fatigue

o   Weight gain

·      Myocardial Infarction: 

o   Chest pain/chest discomfort/chest pressure

o   Diaphoresis

o   Nausea/vomiting

o   Anxiety

o   Pain in the arm, jaw, abdomen

·      Aortic Dissection:

o   Tearing chest pain, radiates to the back

o   Unilateral arms weakness, pulse deficit, bilateral BPs deficit

o   Stroke symptoms

·      Stroke:

o   Motor or sensory disturbances

o   Speech disturbances

o   Dizziness, diplopia, dysarthria, ‘dystaxia’, dysphagia 

·      Subarachnoid Hemorrhage:

o   Head trauma

o   Meningismus

o   Nausea/vomiting

o   Stroke symptoms

o   Sudden onset headache

 

Approach to Management of Hypertensive Emergencies:

Blood pressure management in the setting of a hypertensive emergency will vary based on the specific hypertensive emergency. For the most part, we don’t want to lower blood pressures too quickly, as end organs and vascular beds have become used to these higher pressures by way of a process called autoregulation. Therefore, we should reduce the blood pressure slowly (~10-20% in the first hour, and then a further 5-15 over the next 23 hours). 

 

Some notable exceptions to this approach are:

o   Ischemic Stroke: in the early stages of an ischemic stroke, we do not want to lower blood pressure too much, as the perfusion of the penumbra (area of the brain at risk for infarct) could be compromised. We therefore don’t typically lower blood pressure unless it is >185/110mmHg (if a candidate for reperfusion), or >220/120mmHg (if not a candidate for reperfusion therapy).

o   Aortic Dissection: in this hypertensive emergency, we want to lower the blood pressure QUICKLY to reduce the shearing forces on the already damaged aorta. The target blood pressure is 100-120mmHg systolic and should be achieved in ~20 minutes.

o   Intracerebral Hemorrhage: this condition is a tricky one, where a balance has to be struck between competing priorities of ensuring that the blood pressure is high enough that the brain is maintaining its perfusion, but not too high so as to induce re-bleeding. A target of ~160 systolic is a reasonable approach, according to AHA guidelines.

 

What is Used to Lower Blood Pressure in Emergencies?

The classes of drugs used in hypertensive emergencies are beta-blockers, vasodilators and calcium channel blockers. Depending on the hypertensive emergency in question one of these medications (or a combination of these antihypertensives) can be used.

 

~KD~

 

References:

1.    Hypertensive Emergencies. Emergency Medicine Cases. https://emergencymedicinecases.com/episode-41-hypertensive-emergencies/

2.    Evaluation and Treatment of Hypertensive Emergencies in Adults. UpToDate. https://www.uptodate.com/contents/evaluation-and-treatment-of-hypertensive-emergencies-in-adults?search=hypertensive%20emergencies&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H1

How Low Can You Go? - Orthostatic Hypotension

One day in clinic, I was scheduled to see a patient with a chief concern of dizziness, syncope and gait imbalance. He had a history of orthostatic hypotension and was being investigated for the underlying etiology. While the patient did not attend his appointment, I though it was an interesting case and a topic I didn’t have much exposure to.

Upon standing, much of our circulating blood volume pools in the lower extremities and splanchnic circulation. As such, decreased venous return leads to decreased cardiac output and blood pressure. In response, baroreceptors in the carotid sinus and aortic arch are activated, generating increased sympathetic outflow and decreased vagal tone. By increasing peripheral resistance, venous return and cardiac output, this baroreflex response helps to maintain blood pressure with positional change. Without an adequate baroreflex response and subsequent sympathetic vasoconstriction, orthostatic hypotension and associated cerebral hypoperfusion occur in response to this autonomic failure.

Orthostatic hypotension is defined as a reduction in systolic BP by at least 20 mmHg or a reduction in diastolic BP by at least 10 mmHg in the first 3 minutes of standing after lying down or sitting. This diagnosis should be considered in any patient presenting with falls, pre-syncope, syncope and dizziness. Prevalence increases with age, as changes of aging are associated with diminished baroreflex response. This presentation can be quite debilitating if not treated, as orthostatic hypotension can limit a patient's mobility, independence and quality of life.

The differential diagnosis for orthostatic hypotension is quite broad, but by considering the work-up for this condition, we can organize our thoughts. When considering the diagnosis of orthostatic hypotension, it is critical to assess intravascular volume status by examining the vitals, JVP, and mucous membranes. Volume depletion can cause orthostatic hypotension, and if symptoms resolve after volume correction, a diagnosis has been made. If the patient is volume replete, consider non-neurogenic causes, including cardiac (CHF, MI, myocarditis, pericarditis, arrhythmia), endocrine (adrenal insufficiency, diabetes insipidus) or infectious (sepsis) etiologies. Another important category to consider is medication side-effect. Medications which can cause orthostatic hypotension include antihypertensives (diuretics, calcium channel blockers), alpha-adrenoreceptor blockers and atypical antipsychotics. If this approach has yielded no diagnosis, consider neurogenic causes which include multiple system atrophy, alcoholic polyneuropathy, diabetic neuropathy and multiple sclerosis.

Treatment of orthostatic hypotension can be very challenging. In addition to treating the underlying cause, some initial non-pharmacologic interventions include encouraging hydration (drinking 2-2.5 litres/day) and increasing intake of salty foods (up to 10g of sodium/day). We can also counsel patients to perform gradual movements with postural change, to allow time for autonomic adaptation. As well, we can prescribe compression stockings and an abdominal binder to reduce peripheral venous pooling.

The only pharmacologic treatment approved for use in orthostatic hypotension is midodrine, a peripheral, selective, direct alpha-adrenoreceptor agonist. Fludrocortisone has also been used, for its mineralocorticoid properties to increase plasma volume. Other agents which may be considered are recommended based on data from small, single-centre trials and include pyridostigmine, desmopressin acetate and erythropoietin.

This diagnosis is an interesting one which requires careful consideration of the pathophysiology responsible.  Overall, the aim of treating orthostatic hypotension is to manage symptoms, through non-pharmacologic and pharmacologic treatment.

-EB- 

References:

Bradley JG, Davis KA. Orthostatic hypotension. American family physician. 2003 Dec 15;68(12):2393-8.

Figueroa JJ, Basford JR, Low PA. Preventing and treating orthostatic hypotension: as easy as A, B, C. Cleveland Clinic journal of medicine. 2010 May;77(5):298.

Freeman R. Neurogenic orthostatic hypotension. New England Journal of Medicine. 2008 Feb 7;358(6):615-24.

What’s in a Name? A Refresher on Dermatologic Morphology

I had the opportunity during this selective to join an outpatient dermatology clinic. We managed patients with a variety of skin concerns from acne to basal cell carcinomas. I was reminded of the unique terminology used to describe various lesions and skin concerns that are used in dermatology. This post will contain a brief review on the terms used to describe dermatologic lesions.

 

How do describe a lesion:

1. Primary Morphology
2. Size
3. Demarcation
4. Colour
5. Secondary Morphology
6. Distribution

 

Primary morphology describes the general size classification, as well as whether the lesion is palpable (so you must feel the lesion!).

-       Flat Lesions (non-palpable):

o   Macule: flat (not palpable), smaller than 1 cm in size (think of a freckle)

o   Patch: flat (not palpable), larger than 1 cm in size (think of a flat birth mark)

-       Raised Lesions (palpable):

o   No deep component – confined mostly to the epidermis

§  Solid:

·      Papule: raised/solid swelling, smaller than 1 cm in size (think a mole)

·      Plaque: raised/solid swelling, larger than 1 cm in size (think of psoriasis)

§  Pus Filled:

·      Pustule: a raised swelling, smaller than 1cm in size, that is filled with pus (think of pimples)

·      Abscess, Faruncle, Carbuncle: a raised swelling, larger than 1 cm in size, named depending on the skin affected

§  Fluid Filled:

·      Vesicle: a raised fluid filled swelling, smaller than 1cm in size that is filled with fluid (think of a small blister)

·      Bulla: a raised, fluid filled swelling, larger than 1 cm (think of a large burn blister)

o   Deep Component – proliferation of cells in the mid-to-deep dermis

§  Nodule: has both a raised and deep component, smaller than 1 cm

§  Tumour: has both a raised and deep component, larger than 1 cm

 

2. Size: a self-explanatory part of the description, but try to be precise here, track down your ruler!

3. Demarcation: when we are looking at demarcation, we want to decide how well circumscribed the lesion is. If the lesion blends in with the surrounding tissue it is not well demarcated, if there is a clear border between the surrounding skin and the lesion is is well demarcated.

4. Colour: what colour is the lesion, is it skin-coloured, red, black? Are there multiple colours or is it all the same colour? 

5. Secondary Morphology: a description of other changes associated with the primary lesion, Examples:

• Scale: excess keratin deposits from keratinocyte over-activity
• Crust: dried blood, serum, or pus
• Excoriations: superficial skin scratches
• Fissures: deep line/break in skin
• Erosions: break in skin at level of epidermis (doesn’t usually scar)
• Ulceration: break through in skin through to the level of the dermis (secondary to rubbing of skin) - usually scars
• Atrophy: thin skin from aging, sun exposure, inappropriate activity, topical steroids
• Lichenification: thickened skin with increased skin markings, usually from chronic rubbing

6. Distribution: where is the lesion? On the face, back, hands? 

 

Example: Try describing the following lesion, using the principles described above. (answer found below references).

 

So, what’s in a name? When it comes to describing dermatologic morphology, a lot!

 

-KD-

 

References:

 

1. Approach to the Dermatologic Patient: Description of skin lesions. Merck Manual.https://www.merckmanuals.com/en-ca/professional/dermatologic-disorders/approach-to-the-dermatologic-patient/description-of-skin-lesions

2. Approach to the clinical dermatologic diagnosis. UpToDate. https://www.uptodate.com/contents/approach-to-the-clinical-dermatologic-diagnosis?search=dermatology%20morphology&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2#H4

3. Image: Medical News Today. https://cdn-prod.medicalnewstoday.com/content/images/articles/323/323152/psoriasis-on-persons-elbow.jpg

 

Answer:  Plaque, approximately 3cm x 2cm, well demarcated, pinkish red, with overlying silvery scale on the extensor surface of the elbow. What is it? Psoriasis!