Wound Healing, Dressing, and Drains

Wound Healing, Dressing, and Drains
By: Dr. Aidah Abu Elsoud Alkaissi

Wound healing
* Etiology of wounds:
o Surgical: caused by an incision or excision
o Traumatic: caused by an injury (mechanical, thermal, or chemical)
o Chronic:caused by an underlying pathophysiology, such as pressure sores, or venous leg ulcers, over time

Exact biologic process that takes place in orderly sequence
* An exudate containing blood, lymph, and fibrin begins clotting and loosely binds the cut edges together
* Blood supply to the area is increased, and the basic process of inflammation is set in motion
* Leukocytes increase in number to fight bacteria in the wound area and by phagocytosis help to remove damaged tissues
* The served tissue is quickly glued together by strands of fibrin and a thin layer of clotted blood, forming a scab

Wound Healing
* Plasma seeps to the surface to form a dry protective crust
* This seal helps to prevent fluid loss and bacterial invasion
* During the first few days of wound healing, the seal has little tensile (The resistance of a material to a force tending to tear it apart) strength
* After 3-4 days , connective tissue cells (fibroblasts)rapidly proliferate and give strength to the wound by producing collagen, a tough fibrous protein responsible for the structural integrity of the skin
* At the same time small blood vessels regenerate and build new blood channels, granulation tissue (fibrous connective tissue)includes blood vessels and lymphatics that proliferate from the base of the woind
* Rapidly growing and multiple epithelial cells begin to restore the epithelial continuity of the skin
* At this stage the wound appears healed, healing is not complete until the granulation tissue organizes into scar tissue
* By the ninth or tenth day, the wound is moderately well healed and then becomes progressively stronger
* The whole process of repair takes 2 weeks or more depending on factors such as physical condition of the patient, size and location of the wound, and stresses put on the incisional area
* During this time the scar (cicatrix)strengthens as the connective tissue shrinks
* The amount of tissue loss, the existence of contamination or infection and damage to tissue are all factors that determine the type of wound healing that will occur
* Process of healing takes place in one of three ways
o Healing by primary (first) intention
o Healinh by secondary infection (granulation)
o Healing by delayed primary closure (third intention)

Healing by primary (first) intention
* Edges of an incised wound in a healthy person are promptly and accurately approximated
* Contmination is held to a minimum by impeccable (without fault or error) aseptic technique
* Trauma to the wound is minimal
* After suturing , no dead space is left to become site of infection
* Drainage is minimal

Healing by secondary intention (granulation)
* When surgical wounds are characterized by tissue loss with inability to approximate wound edges, healing occurs through secondary intention
* This type of wound is left open and allowed to heal from the inside towaed the outer surface
* In infected wound this process allows the proper cleansing and dressing of the wound as healthy tissue builds up from the inside
* The area of tissue loss gradually fills with granulation tissue (fibroblasts and capillaries)
* Scar tissue is extensive because of the size of the tissue gap that must be closed. Contraction of surrounding tissue also takes place
* Consequently this healing process takes longer than primary intention healing

Healing by delayed primary closure (third intention)
* This healing process takes place when approximation of wound edges is delyed by 3-5 days or more after injury or surgery
* The condition contribute to a decision for a dalyed closure are:
o 1. Removal of an inflamed organ
o 2. Heavy contamination of wound

Factors influencing wound healing
* The patient´s nutritional status and overall recuperative (To return to health or strength; recover) power
* Especially significant is an adequate supply of protein, which is necessary for the growth of new tissues, the regulation of the osmotic pressure of blood and other body fluids and the formation of prothrombin, enzymes, hormones and antibodies
* Vit C which aids connective tissue production and strong scar formation
* Scrupulous aseptic technique must be used to prevent any wound infection-the most common cause of delayed wound healing
* Theories abound as to the genesis of wound infection. Cross – contamination from operating room, post anesthesia care unit and unit personel is believed to be a primary source
* Aseptic principles and maintenance of operating room environmental conditions are significant factors
* Length of time that the wound is open in the operating room has also been mentioned
* The pat own endogenous flora
* Rough handling of tissue causes trauma that cal lead to bleeding and other conditions conducive to the infection
* Other factors pat age, stress level, presxisting condition as diabete, anemia, malnutriion, cancer , obesity, advanced age, cardiovascular, respiratory impairments. Overall physiacal and psychological condition

Terms

* Keloid
* Proud flesh
* Gangrene
* Adhesions
* Dehiscence
* Evisceration

Wound Classification
* Clean wound
* Clean contaminated wound
* Contaminated wound
* Dirty or infected wound

Dressing
Wound Healing, Dressing, and Drains.ppt

Read more...

Management of Keloids

Management of Keloids
By: Thad Riley
Advisor: Bill Grimes


What is a Keloid?
* Non-cancerous fibrous proliferations that occur in the dermis after trauma or injury to the skin
* Keloids grow beyond the boundaries of the original wound site (vs. hypertrophic scar)
* Etiological factors that determine how a scar becomes a keloid remain unknown

Who and Why?
* Individuals with darker-pigmented skin or who freckle are more predisposed
* Seen largely in Africans, African-Americans, Hispanics, and Asians
* Can be a familial/genetic predisposition
* Can be due to immunological causes
* Bottom line… No one knows!

How? (Pathophysiology)
* A result of an overactive inflammatory response and fibroblast proliferation
* A result of an abnormal collagen deposition in healing skin wounds
* Skin wound tension is a contributing factor in keloid formation
* Individuals with an inflammatory or infectious element are at a predisposition for keloids

Where?
* Anterior Chest
* Mandibular angle
* Shoulder
* Earlobes
* Upper Arms & Upper Back
* Posterior Neck
* Lateral Neck

So…What’s the Problem?

The Problem
* PROBLEM is with the TREATMENT OPTIONS
* The pathophysiology of these scars is so poorly understood that it is basically unknown
* Surgery is the only approved treatment
* A successful surgical protocol for removal of these types of scars is greatly lacking
* Surgical treatments available today only provide temporary relief
* Often grow back and do so in an aggressive manner

Possible Solutions
* Surgical excision alone
* Post-surgical treatment agents:
o Mitomycin C solution
o The dietary compound quercetin
o Imiquimod 5% topical cream
o Intralesional corticosteroid injection
o Topical silicone gel sheets

How they work…
* Mitomycin C solution (MC)
o An anti-neoplastic agent
o Has anti-proliferative effects on fibroblasts, stopping keloid formation
o MC effectively blocks angiogenesis during the healing process of the wound, thus inhibiting keloid development
o MC is widely available and relatively cheap
* The dietary compound quercetin
o most common sources: apples, onions, red wine, and ginkgo biloba.
o has strong anticancer, antioxidant, antiviral, anti-inflammatory, and antimicrobial characteristics
o Inhibit keloid fibroblast proliferation, collagen production, and contraction of keloid derived fibroblasts
* Imiquimod 5% topical cream
o Induces apoptosis in keloidal tissue
* Intralesional corticosteroid injection
o Inhibit fibroblast growth and break down collagen deposition
o postoperative steroid injection is the most common form of keloid treatment
o corticosteroids commonly used include hydrocortisone and dexamethasone.
* Topical silicone gel sheets
o Impermeable to water, reduces hemostasis and therefore, decreases the hyperemia and fibrosis often associated with keloids
o have been used for more than twenty years to help reduce the size of scarring
o efficacy and safety of the silicone gel sheets is well established.

And the Winner is…
* Imiquimod 5% topical cream
Analysis
* 13 keloids from 12 patients were surgically removed
* All keloids were present for at least 1 year and free of any treatment for the past 2 months
* A thin layer of imiquimod 5% cream was applied topically each night for 8 weeks
* 4 week asessments
* At 24 weeks, no keloids had recurred

Pilot study of the effect of postoperative imiquimod 5% cream on the recurrence rate of excised keloids (Berman and Kaufman, 2002 )
* 2 cases of irritation and superficial erosion were reported; resolved with cessation of the cream
* At the 24 week assessment, RECURRENCE RATES of keloids treated with imiquimod 5% cream were LOWER than any previously reported in the literature
* Study did not control for the effects of vehicle application or other potential variables
* Further comparative studies with longer follow-up periods are needed
* Additional studies needed to determine dosing frequency and duration

Pilot study of the effect of postoperative imiquimod 5% cream on the recurrence rate of excised keloids (Berman and Kaufman, 2002 )

Conclusion
* To develop a successful treatment plan for the keloid, two things have to be done:
o 1. Further research to better understand the causes behind keloid formation
o 2. Establish a standard surgical protocol
* In short, the topic of keloids is greatly under-exposed.

References

Management of Keloids.ppt

Read more...

Pathophysiology of Pericardial Disease

Pathophysiology of Pericardial Disease

Pericardium - Anatomy

Normal pericardium is a fibro-serous sac which surrounds the heart and adjoining portions of the great vessels.
The inner visceral layer, also known as the epicardium, consists of a thin layer of mesothelial cells closely adherent to the surface of the heart. The epicardium is reflected onto the surface of the outer fibrous layer with which it forms the parietal pericardium.
The parietal pericardium consists of collagenous fibrous tissue and elastic fibrils.
Between the two layers lies the pericardial space, which contains approximately 10-50ml of fluid, which is an ultrafiltrate of plasma.
Drainage of pericardial fluid is via right lymphatic duct and thoracic duct.

Pericardial Layers:

Visceral layer
Parietal layer
Fibrous pericardium

Function of the Pericardium

1. Stabilization of the heart within the thoracic cavity by virtue of its ligamentous attachments -- limiting the heart’s motion.
2. Protection of the heart from mechanical trauma and infection from adjoining structures.
3. The pericardial fluid functions as a lubricant and decreases friction of cardiac surface during systole and diastole.
4. Prevention of excessive dilation of heart especially during sudden rise in intra-cardiac volume (e.g. acute aortic or mitral regurgitation).

Etiologies of Pericarditis


I. INFECTIVE
1. VIRAL - Coxsackie A and B, Influenza, adenovirus, HIV, etc.
2. BACTERIAL - Staphylococcus, pneumococcus, tuberculosis, etc.
3. FUNGAL - Candida
4. PARASITIC - Amoeba, candida, etc.

II. AUTOIMMUNE DISORDERS
1. Systemic lupus erythematosus (SLE)
2. Drug-Induced lupus (e.g. Hydralazine, Procainamide)
3. Rheumatoid Arthritis
4. Post Cardiac Injury Syndromes i.e. postmyocardial Infarction (Dressler's) Syndrome, postcardiotomy syndrome, etc.

III. NEOPLASM
1. Primary mesothelioma
2. Secondary, metastatic
3. Direct extension from adjoining tumor

IV. RADIATION PERICARDITIS
V. RENAL FAILURE (uremia)
VI. TRAUMATIC CARDIAC INJURY
1. Penetrating - stab wound, bullet wound
2. Blunt non-penetrating - automobile steering wheel accident
VII. IDIOPATHIC

Pathogenesis

1) Vasodilation:
 transudation of fluid

2) Increased vascular permeability
 leakage of protein

3) Leukocyte exudation
neutrophils and mononuclear cells


Pathology
depends on underlying cause and severity of inflammation

serous pericarditis
serofibrinous pericarditis
suppurative (purulent) pericarditis
hemorrhagic pericarditis

Clinical Features of Acute Pericarditis

Idiopathic/viral
* Pleuritic Chest pain
* Fever
* Pericardial Friction Rub
3 component:
a) atrial or pre-systolic component
b) ventricular systolic component (loudest)
c) ventricular diastolic component

* EKG: diffuse ST elevation
PR segment depression

Diagnostic Tests
Echocardiogram: Pericardial effusin
N.B.: absence does not rule out pericarditis
N.B.: Pericarditis is a clinical diagnosis, not an Echo diagnosis!

Blood tests: PPD, RF, ANA
Viral titers
Search for malignancy
Pericardiocentesis:
low diagnostic yield
done therapeutically

Treatment
Pain relief
analgesics and anti-inflammatory
ASA/NSAID’s
Steroids for recurring pericarditis
Antibiotics/drainage for purulent pericarditis
Dialysis for uremic pericarditis
Neoplastic: XRT, chemotherapy

Pericardial Effusion
Normal 15-50 ml of fluid
ETIOLOGY
1. Inflammation from infection, immunologic process.
2. Trauma causing bleeding in pericardial space.
3. Noninfectious conditions such as:
a. increase in pulmonary hydrostatic pressure e.g. congestive heart failure.
b. increase in capillary permeability e.g. hypothyroidism
c. decrease in plasma oncotic pressure e.g. cirrhosis.
4. Decreased drainage of pericardial fluid due to obstruction of thoracic duct as a result of malignancy or damage during surgery.

Effusion may be serous, serofibrinous, suppurative, chylous, or hemorrhagic depending on the etiology.
Viral effusions are usually serous or serofibrinous
Malignant effusions are usually hemorrhagic.


Pathophysiology
Pericardium relatively stiff
Symptoms of cardiac compression dependant on:

1. Volume of fluid
2. Rate of fluid accumulation
3. Compliance characteristics of the pericardium

A. Sudden increase of small amount of fluid (e.g. trauma)
B. Slow accumulation of large amount of fluid (e.g. CHF)

Clinical features
Small effusions do not produce hemodynamic abnormalities.

Large effusions, in addition to causing hemodynamic compromise, may lead to compression of adjoining structures and produce symptoms of:

dysphagia (compression of esophagus)
hoarseness (recurrent laryngeal nerve compression)
hiccups (diaphragmatic stimulation)
dyspnea (pleural inflammation/effusion)

Physical Findings

Muffled heart sounds
Paradoxically reduced intensity of rub
Ewart's sign:
Compression of lung leading to an area of consolidation in the left infrascapular region (atalectasis, detected as dullness to percussion and bronchial breathing)

Diagnostic studies
CXR: “water bottle” shaped heart
EKG:
low voltage
“electrical alternans”
Echocardiogram
Cardiac Tamponade

Fluid under high pressure compresses the cardiac chambers:
acute: trauma, LV rupture – may not be very large
gradual: large effusion, due to any etiology of acute pericarditis

CardiacTamponade -- Pathophysiology
Accumulation of fluid under high pressure:
compresses cardiac chambers & impairs
diastolic filling of both ventricles

 SV venous pressures
 CO systemic pulmonary congestion
Hypotension/shock JVD rales
Reflex tachycardia hepatomegaly
ascites
peripheral edema

Tamponade-- Clinical Features
Symptoms:
Acute: (trauma, LV rupture)
profound hypotension
confusion/agitation
Slow/Progressive large effusion (weeks)
Fatigue (CO)
Dyspnea
JVD
Signs:
Tachycardia
Hypotension
rales/edema/ascites
muffled heart sounds
pulsus paradoxus

Pulsus Paradoxus
Intrapericardial pressure (IPP) tracks intrathoracic pressure.
Inspiration:
negative intrathoracic pressure is transmitted to the pericardial space

 IPP
 blood return to the right ventricle
 jugular venous and right atrial pressures
 right ventricular volume
 interventricular septum shifts towards the left ventricle
 left ventricular volume
 LV stroke volume
 blood pressure (<10mmHg is normal) during inspiration

Pulsus Paradoxus
Exaggeration of normal physiology
> 10 mm Hg drop in BP
with inspiration
Tamponade -- Diagnosis

EKG: low voltage, sinus tachycardia,

electrical alternans
Echocardiography
pericardial effusion
(r/o other etiologies in dif dx)
RA and RV diastolic collapse

Right Heart Catheterization
Catheterization Findings:
Elevated RA and RV diastolic pressures
Equalized diastolic pressures
Blunted “y” descent in RA tracing
y descent: early diastolic filling (atrial emptying)
 BP and Pulsus paradoxus
Pericardial pressure = RA pressure

Jugular venous pressure waves

Normal JVP contours
(1) A-wave
1) results from ATRIAL contraction
2) Timing - PRESYSTOLIC
3) Peak of the a-wave near S1
(2) V-wave

1) results from PASSIVE filling of the right atrium while the tricuspid valve is closed during ventricular systole (Remember the V-wave is a "V"ILLING WAVE)

2) Large V-waves on the left side of the heart may be seen with mitral regurgitation, atrial septal defect, ventricular septal defect. The v-wave in the jugular venous pulse reflects right atrial events. To see the v-wave on the left side of the heart Swan-Ganz monitoring is needed

3) timing - peaks just after S2

(3) X-descent

1) results from ATRIAL RELAXATION

2) timing - occurs during ventricular systole, at the same time as the carotid pulse occurs

(4) Y-descent

1) results from a FALL in right atrial pressure associated with opening of the tricuspid valve

2) timing - occurs during ventricular diastole

(5) Generalizations

1) the A-wave in a normal individual is always larger than the V-wave

2) the X-descent is MORE PROMINENT than the Y-descent
RA Pressure Tracing

a wave: atrial contraction
v wave: passive filling of atria during
ventricular systole with mv/tv closed
y descent: early atrial emptying with mv/tv
open (early passive filling of ventricle)

Tamponade:
blunted y descent (impaired rapid ventricular filling due to compression by high pericardial pressure)

Tamponade -- Treatment
Pericardiocentesis
Pericardial Window
Balloon Pericardiotomy
Pre-pericardiocentisis
Post-pericardiocentesis
Constrictive Pericarditis
Late complication of pericardial disease
Fibrous scar formation
Fusion of pericardial layers
Calcification further stiffens pericardium
Etiologies:

Pathophysiology
Rigid, scarred pericardium encircles heart:

Systolic contraction normal
Inhibits diastolic filling of both ventricles

 SV venous pressures
 CO systemic pulmonary congestion
Hypotension/shock JVD rales
Reflex tachycardia hepatomegaly
ascites
peripheral edema
Physical exam
Kussmaul’s sign
Diagnosis
CXR: calcified cardiac silhouette
EKG: non-specific
CT or MRI: pericardial thickening

Cardiac Catheterization
Prominent y descent: “dip and plateau”:
rapid atrial emptying rapid ventricular filling then abrupt cessation of blood flow due to rigid pericardium

Elevated and equalized diastolic pressures (RA=RVEDP=PAD=PCW)
Constriction vs. Restriction

Similar presentation and physiology, important to differentiate as

constriction is treatable by pericardiectomy

Majority of diseases causing restriction are not treatable
Constrictive Pericarditis
TAMPONADE
Low cardiac output state
JVD present
NO Kussmaul’s sign
Equalized diastolic pressures
RA: blunted y descent
Decreased heart sounds

CONSTRICTION

Low cardiac output state
JVD present
Kussmaul’s sign
Equalized diastolic pressures
RA: rapid y descent
Pericardial “knock”
Constriction vs. Tamponade Summary
TAMPONADE
Pulsus paradoxus:
Present
Echo/MRI:
Normal systolic function
Large effusion
RA & RV compression
Treatment:

Pericardiocentesis
CONSTRICTION
Pulsus paradoxus:
Absent
Echo/MRI:
Normal systolic function
No effusion
Pericardial thickening
Treatment:
Pericardial stripping

Pathophysiology of Pericardial Disease.ppt

Read more...