(W400) Saddle Sores in San Antonio - HonakerW400) Sadd… · Saddle Sores in San Antonio: sDTI...

Tuesday, June 9, 2015

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Saddle Sores in San Antonio:

sDTI Update: From Bench To

Bedside- Part 2

Jeremy Honaker MSN, FNP-C, CWOCN

University Hospitals of Cleveland

Department of Dermatology

Cleveland, Ohio

Disclosure• Celleration Inc.

– Educational Grant awarded to Baptist Health

Lexington for research project.

Objective

• Describe the differential diagnosis and

diagnostic methods available for establishing a

sDTI diagnosis, and management options used

to prevent or treat sDTI.


2

What’s in a color?• Non-blanchable Purple (Purpuric dermatoses)

• Extravasation of red blood cells into dermis or

interstitial spaces1

• Process occludes/damages cutaneous

vasculature results in purpuric dermatoses1

Clinical Significance• Palpable purpura1

– Is palpable purpura a key clinical prognosticator for wounds?

– Edema result of inflammation or preceding microvascular ischemia

– May reflect extent of cutaneous hemorrhage

• Two dimensions of palpation3

– Superficial

– Deep

Diascopy


3

History of Present Illnessa) Acute Illness 3, 6, 18-20

1) Sepsis

2) ↓ Mobility

3) Hemodynamic Instability

4) Fall or Trauma

5) Transfer event

6) Surgery

7) Pertinent Labsa) CPK, Hgb, PT, PTTH

Pre-Albumin

8) Past Medical History

9) Hospice/Palliative

care involvement

10) Medications

11) Diagnostic exams

12) Connection between

acute illness history

and lesion

development?

History of Lesion3

a) When did it start?

b) Does it itch, burn, or hurt?

c) Where on the body did it start?

d) How has it spread?

e) Medical device involvement?

Clinical Assessment Guidelines

Clinical Assessment Guidelines

Physical Exam 3, 12-14

a) Type of lesion

a) Size

b) Morphology

c) Location

d) Distribution

e) Multiple lesions

f) COLOR

g) BLANCHABLE

h) PALPABLE

i) Integrity of skin

b) Wound bed status

a) Moisture level

b) COLOR

c) BLANCHABLE

d) PALPABLE

e) Tissue consistency

f) Signs of beginning

necrosis

c) Peri-lesion skin


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Clinical Assessment Guidelines1. Initial Clinical Impression 2,3

2. Darker Skin Tone assessment guide2,3, 12

a) Heightened awareness (epidermal changes)

b) Evaluate peri-lesion skin (tone changes)

c) Palpation

Dark Skin Tone Changes56

Shear/Pressure Mix


5

Purple

lesion

Capillary Malformation

Inflammatory

Medication

Micro-Organisms Pressure/Shear

Skin Failure

Trauma

MicrovascularOcclusion

Coagulopathy

Melanocytosis

Photo Progression of sDTI

Day 1 3 Days Later 10 Days Later

Purple Lesion Differential Dx• Suspected Deep Tissue Injury5

– Etiology: Injury associated with pressure and/or shear

– Lesion Assessment:• Palpable: Yes

– Deep: Induration or Boggy

– Superficial: Elevated

• Irregular, circular, or oval lesion located over bony prominence or under medical device13

• +/− peri-wound erythema

• Tender to touch (Does palpation elicit pain response?)

– Pertinent Medical History6,13-20

• History of unrelieved pressure, recent transfer, compromised host


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Purple Lesion Differential Dx

• Contusion1,21:

– Etiology: Associated with blunt trauma

– Lesion Assessment:

• Palpable: Yes, if hematoma present

• Irregular, Ectopic bruising, Fit shape of device

• Tender to touch

• Typically no erythema in peri-lesion skin area

– Pertinent Medical History:

• Associated with trauma

• Specific area identified with specific event

• Labs

Purple Lesion Differential Dx• Ecchymoses 4,22

– Etiology: Bleeding associated with minor trauma. Underlying coagulopathy or vasculitis.

– Lesion Assessment1,4, 21, 23:• Palpable: No (Unless hematoma present)

• Various locations on body exposed to minor trauma

• Flat, Round or Irregular shaped

• Not tender to touch

• Typically no erythema in peri-lesion skin area

– Pertinent Medical History1,4, 21, 23

• Age, Corticosteroids, Anti-coagulents, recent transportation, Labs.


7


• Emboli 24-26

– Etiology: Microvascular occlusion secondary to thrombosis, plaque, or cholesterol.

– Lesion Assessment:• Palpable: Yes

• Primarily extremities, but may effect trunk/buttocks. 25

• Reticular presentation

• Spontaneous onset, painful, with rapid progression to necrosis

– Pertinent Medical History: • Recent surgical procedure or sepsis

• Look at platelets, PT, PTT


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• Necrotizing Fascitis 22,25

– Etiology: Tissue invasive organisms (Group B Strep)


• Palpable: Unknown

• Perineal area (Fournier’s), trunk, or extremities.

• Rapid onset and deterioration over hours with progression to necrosis

• Foul odor and severe pain associated

• Irregular shape with stellate presentation

– Pertinent Medical History

• S/S of sepsis, May have history of trauma, ↑ CPK and WBC.

Purple Lesion Differential Dx• Ecythma Gangrenosum 22,26,27

– Etiology: Vessel invasive microorganisms (Pseudomonas)



• Grouped closely together on buttocks or extremities

• Purple lesions that become vesicles that when unroofed reveal necrotic center

• Punched out appearance

• Quick onset


• Immunocompromised, elderly, cancer patients, children, diabetes

• Labs: CBC, Culture wounds


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B. Ecthyma gangrenosum: Presentation in a normal neonate

Ganesh Athappan MD, Athira Unnikrishnan MD, Satish Chandraprakasam MD

Dermatology Online Journal 14 (2): 17. 2008

A. Bacterial Infections

James, William D, MD, Andrews' Diseases of the Skin: Clinical Dermatology, Chapter 14, 247-286

Copyright © 2011 © 2011, Elsevier Inc. All rights reserved.

B


• Multi-factorial ulcerations– Etiology: Unknown. Affects mixed small medium

vessels

– Lesion Presentation• Palpable: Unknown

• Grouped

• Gradual onset

• Purple that progress to necrosis

• Perineal, buttocks and thigh locations

– Pertinent Medical History:• Syndrome of obesity, renal failure, incontinence and

immobility


10

• Pyoderma Gangrenosum 22,28,29

– Etiology: Auto immune associated dysfunction

– Lesion Assessment: • Palpable: Yes

• 4 P’s (Painful, Purpuric, Purulent, & Pathergy)

• Extremities or trunk (area exposed to trauma)

• Rapid progression of days

• Oval to irregular in shape

– Pertinent Medical History• Hx of Inflammatory bowel disease, arthritis, hematologic

dyscrasias, malignant disease

• Diagnosis of exclusion


• Coumadin Necrosis 22, 26, 30

– Etiology: Medication induced paradoxical occlusive thrombi in cutaneous and SQ tissue.

– Lesion Assessment• Palpable: Yes

• Early red, painful plaques develop in adipose rich areas (breast, buttocks, hips)

• Plaques ulcerate or develop into necrotic areas

• Only one or two areas involved

– Pertinent Medical History• 3 to 5 days after coumadin initiated.

• Protein C & S deficiency



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• Calciphylaxis 22, 26, 31

– Etiology: Calcification of arterioles and arteries of the deeper dermis and SQ tissue

– Lesion Assessment: • Palpable: Yes

• Irregular shape with reticular presentation

• Very painful with Rapid onset

• Location to extremities, but can occur in buttocks

– Pertinent Medical History:• End Stage Renal Disease and associated with obesity and

diabetes

• Elevated Ca and Phosphorus levels.



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• Vasculitis22,26, 32, 33

– Etiology: Vessel damage secondary to immune complex deposition and activation of inflammatory cascade.

– Lesion Assessment• Palpable: Yes

• Extremities and dependent areas with Grouped/geographic distribution

• Polymorphous and palpable (SQ edema)

– Pertinent Medical History• Development associated with infection and/or medication

• Associated with fever, athralgias, myalgias, and malaise


Cutaneous Vasculitis

Shinkai, Kanade, Dermatology, 24, 385-410.e2

Copyright © 2012 © 2012, Elsevier Limited. All rights reserved.


• Trombley Brennan Terminal Tissue Injury34

– Etiology: Unknown but precedes death



• Trunk, extremities, or bony prominence involvement

• Butterfly/linear presentation

• Spontaneous development

• Presentation similar to bruise


• Precedes death by hours to days


13

Differential Dx tips

1. History, History, History

2. Clinical Assessment (Good biopsy)

3. Interpretation (How does it apply to this

patient)

4. Timed reassessment

5. No silver bullet

Standard Guidelines• Clinical Guidelines9, 19, 35, 36

– Therapeutic Support Surface Selection

– Incontinence Management

– Repositioning Schedule/Protect vulnerable pressure points

– Modalities to reduce shear/friction

– Systemic Support

Treatment options

• Non-contact Low Frequency Ultrasound– Mechanism of Action 37-45

• ↑ Nitric Oxide through ↑ eNOS

• ↑ VEGF

• Suppresses Inflammatory Response

• Stimulates Cell Survival

• Soft Silicone border dressing46-47

– Prevention and Treatment

– Mechanism of Action

• Absorbs friction/shear

• Protects


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Diagnostic Test

• Ultrasound48

– Intermediate vs. High Frequency

– Discontinuous fascia and heterogenous hypoechoic areas

observed at first examination may predict deteriorations

– Limitations: Experienced Clinician, Cost, and Availability

– Maybe a reliable diagnostic tool for ruling out deep tissue

injury57

Diagnostic Test• Thermal Imaging System

• Monitors Thermal Intensity gradiency49

• Physiologic View of Tissue49

• A 1.5°C increase/decrease suggestive for a “at risk” area50-51

• Limitation: More research needed to identify specificity.

• Farid thermography study findings52:

– Pressure related intact discolored area of skin (PRIDAS)

• Warm PRIDAS and Blanchable erythema: Did not progress

• Cool PRIDAS and non-blanchable erythema: 65.4% progress to necrosis

Diagnostic Labs

• Serum CPK53

• Blood level CPK20

• Hypoxia Inducible Factor 1-alpha54

• Northwestern University Study55


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Summary

• Check List

– Know the patient history (peri-hospitalization)

– Recognize clinical differences

(History/Presentation) between sDTI and other

purple lesions.

– History and Morphology can guide backing into a

differential diagnosis

– Assessment findings dictated by time course of

lesion

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