1
The Child with an Alteration in Skin Integrity
Inflammatory Process:
Inflammation: Nonspecific but predictable response of living tissue or the entire body to injury. Injury
can be caused by chemical agents, physical forces, living microbes or pathologic and physiologic stimuli.
• Includes a series of events that are interconnected, one with the other.
• Occurs only in multi-cellular organisms that are capable of mounting a neurovascular and
cellular response to injury.
• Has a protective role and is generally beneficial to the body. However, sometimes the side effects
of inflammation can become noxious and the process uncontrollable.
• Occurs only in living tissue.
• Inflammation is not the same as infection. Infection involves microorganisms
Pathogenesis
Circulatory Changes: Body’s first response to injury. ** Redness and swelling of skin
Mechanical stimuli stimulates nerves signals smooth muscle cells on precapillary arterioles.
Smooth muscle cells act as sphincters, regulating the inflow of blood into the capillaries. Relaxation of
smooth muscle cells blood rushing into the capillaries = redness, swelling & warmth of the tissue.
First response of arterioles to an injurious stimulus is vasoconstriction then vasodilatation flooding of
the capillary network with arterial blood, manifested by redness and mild swelling of the tissue
engorged with bld. Arterial blood = warm & because large qualities pumped to area “warmth” at site or
Hyperemia.
Influx of blood dilates the capillaries, pressure is transmitted to the venules, which also do not have the
capacity to contract the increased pressure in the capillaries & venules forces plasma filtration through
the vessel wall Edema.
Blood flow in dilated capillaries and venules = slow congestion and other hemodynamic changes.
The sludged erythrocytes form stacks impedes circulation even more turbulent flow of blood.
WBCs are marginalized and become attached to the endothelium. Become sticky & adhere to the
endothelial cells lining the capillaries. Adherence of leukocytes to the endothelial cells is one of the most
common triggers for the release of mediators of inflammation.
In acute inflammation most of these cells are polymorphonuclear leukocytes/neutrophils (PMNs).
As the inflammatory process evolves PMNs are joined by monocytes & eosinophils which are in
the exudates in the first 48 hours. As the inflammation proceeds into chronic stages PMNs that
have a
lifespan of 2-4 days become less prominent and are replaced by macrophages, lymphocytes, and plasma
cells.
PMNs that reach the bacteria or other sources of chemotactic substances lose their mobility & act like
scavengers via phagocytosis process. Many PMNs die in the fight with bacteria. Dead & dying
leukocytes + tissue debris + lytic enzymes released from granules formation of viscous yellow fluid
called pus. Inflammations dominated by pus formation are called purulent or suppurative.
Platelets initiate clottingfibrin strands. These strands then anchor the leukocytes to the vessel wall and
prevent them from moving away.
, 2
Mediators of Inflammation
• Most common mediators are biogenic amines (e.g. histamine), peptides (e.g., bradykinin,
complement), and arachidonic acid derivatives (e.g., prostaglandins).
• Are multifunctional and have numerous effects on blood vessels, inflammatory cells, and other
cells in the body.
Most important effects = vasodilatation or vasoconstriction, altered vascular permeability,
activation of inflammatory cells, chemotaxis, cytotoxicity, degradation of tissue, pain, and fever.
Cells of Inflammation:
• PMNs are the first cells to appear in acute inflammation. Account for 60-70% of all WBCs
• Eosinophils – appear 2-3 days after PMNs. Interact with Basophils ** allergic reactions (hay fever
& asthma). Also participate in parasitic infection inflammatory process. Live longer than PMNs,
therefore = chronic inflammation.
• Basophils – participants in inflammatory reactions. Most prominent in allergic reactions mediated
by IgE. Precursors of mast cells.
• Macrophages – Appear at the site of inflammation 3-4 days after the onset of infection or tissue
destruction. Live long so therefore see in chronic inflammation. Capable of phagocytosis and active
in bacterial killing (but not as efficient as PMNs). Also secrete mediators of inflammation (cytokines)
that act locally on other cells and the body as a whole.
Classification of inflammation
Acute & Chronic
• Acute = follows sublethal tissue injury
** neutrophils; Quickly resolves – few hours to few days
• Chronic = No exact time when becomes chronic
May become exacerbated or intensification of symptoms
• Extension of an acute illness
• Prolonged healing of an acute inflammation
• Persistence of causative agent
** macrophages = chief cell
Localized or Widespread
• Systemic inflammation = involves multiple organs –Systemic lupus
erythematosus, rheumatoid arthritis
General Therapeutic Management & Nursing Care for Integumentary Alteration
Diagnostic Evaluation
History & Subjective Symptoms
1. Pruritus
, 3
2. Anesthesia
3. Hyperesthesia or hypo
4. Paresthesia
Condition may remain localized or migrate, constant or intermittent, or may be aggravated by a specific
activity, such as exposure to sunlight.
Determine if child has allergic condition (e.g., asthma or hay fever) or hx of previous skin disease.
Atopic dermatitis often = from allergies, frequently begins in infancy.
Questions:
• When lesion or symptom first appeared
• Whether it occurs with ingestion of a food or other substance, including med
• Whether related to activity (e.g., contact with plants, insects, or chemicals).
Other Findings: Lesion Characteristics
• Erythema
• Ecchymoses (bruises)
• Petechiae
• Primary lesions
• Secondary lesions
• Distribution pattern
• Configuration and arrangement (discrete, clustered, diffuse, or confluent)
Laboratory Studies:
• If skin problem related to system disease (e.g., collagen or immunodeficiency disease
(e.g., Lupus) = Lab studies focus on identifying condition.
• Miscroscopic examinations
• Cultures
• Biospsy
• Cytodiagnosis
• Patch testing
• Wood light examination
• Allergic skin testing
• Blood counts & sedimentation rates, CRP…..
• Immunoglobulin E (IgE)
• Potassium hydroxide (KOH) prep – reveals fungal infections
General Therapeutic Management – (Review related pages in Hockenberry textbook)
Goal: To prevent further damage, eliminate the cause, prevent complications, and provide relief of
discomfort.
Most common causative agent of dermatitis in infants, children, & adolescents = environmental factors
(soaps, bubble baths, wet diapers….) and the natural elements (dirt, sand, heat….). May also occur from
home remedies & meds.
The Child with an Alteration in Skin Integrity
Inflammatory Process:
Inflammation: Nonspecific but predictable response of living tissue or the entire body to injury. Injury
can be caused by chemical agents, physical forces, living microbes or pathologic and physiologic stimuli.
• Includes a series of events that are interconnected, one with the other.
• Occurs only in multi-cellular organisms that are capable of mounting a neurovascular and
cellular response to injury.
• Has a protective role and is generally beneficial to the body. However, sometimes the side effects
of inflammation can become noxious and the process uncontrollable.
• Occurs only in living tissue.
• Inflammation is not the same as infection. Infection involves microorganisms
Pathogenesis
Circulatory Changes: Body’s first response to injury. ** Redness and swelling of skin
Mechanical stimuli stimulates nerves signals smooth muscle cells on precapillary arterioles.
Smooth muscle cells act as sphincters, regulating the inflow of blood into the capillaries. Relaxation of
smooth muscle cells blood rushing into the capillaries = redness, swelling & warmth of the tissue.
First response of arterioles to an injurious stimulus is vasoconstriction then vasodilatation flooding of
the capillary network with arterial blood, manifested by redness and mild swelling of the tissue
engorged with bld. Arterial blood = warm & because large qualities pumped to area “warmth” at site or
Hyperemia.
Influx of blood dilates the capillaries, pressure is transmitted to the venules, which also do not have the
capacity to contract the increased pressure in the capillaries & venules forces plasma filtration through
the vessel wall Edema.
Blood flow in dilated capillaries and venules = slow congestion and other hemodynamic changes.
The sludged erythrocytes form stacks impedes circulation even more turbulent flow of blood.
WBCs are marginalized and become attached to the endothelium. Become sticky & adhere to the
endothelial cells lining the capillaries. Adherence of leukocytes to the endothelial cells is one of the most
common triggers for the release of mediators of inflammation.
In acute inflammation most of these cells are polymorphonuclear leukocytes/neutrophils (PMNs).
As the inflammatory process evolves PMNs are joined by monocytes & eosinophils which are in
the exudates in the first 48 hours. As the inflammation proceeds into chronic stages PMNs that
have a
lifespan of 2-4 days become less prominent and are replaced by macrophages, lymphocytes, and plasma
cells.
PMNs that reach the bacteria or other sources of chemotactic substances lose their mobility & act like
scavengers via phagocytosis process. Many PMNs die in the fight with bacteria. Dead & dying
leukocytes + tissue debris + lytic enzymes released from granules formation of viscous yellow fluid
called pus. Inflammations dominated by pus formation are called purulent or suppurative.
Platelets initiate clottingfibrin strands. These strands then anchor the leukocytes to the vessel wall and
prevent them from moving away.
, 2
Mediators of Inflammation
• Most common mediators are biogenic amines (e.g. histamine), peptides (e.g., bradykinin,
complement), and arachidonic acid derivatives (e.g., prostaglandins).
• Are multifunctional and have numerous effects on blood vessels, inflammatory cells, and other
cells in the body.
Most important effects = vasodilatation or vasoconstriction, altered vascular permeability,
activation of inflammatory cells, chemotaxis, cytotoxicity, degradation of tissue, pain, and fever.
Cells of Inflammation:
• PMNs are the first cells to appear in acute inflammation. Account for 60-70% of all WBCs
• Eosinophils – appear 2-3 days after PMNs. Interact with Basophils ** allergic reactions (hay fever
& asthma). Also participate in parasitic infection inflammatory process. Live longer than PMNs,
therefore = chronic inflammation.
• Basophils – participants in inflammatory reactions. Most prominent in allergic reactions mediated
by IgE. Precursors of mast cells.
• Macrophages – Appear at the site of inflammation 3-4 days after the onset of infection or tissue
destruction. Live long so therefore see in chronic inflammation. Capable of phagocytosis and active
in bacterial killing (but not as efficient as PMNs). Also secrete mediators of inflammation (cytokines)
that act locally on other cells and the body as a whole.
Classification of inflammation
Acute & Chronic
• Acute = follows sublethal tissue injury
** neutrophils; Quickly resolves – few hours to few days
• Chronic = No exact time when becomes chronic
May become exacerbated or intensification of symptoms
• Extension of an acute illness
• Prolonged healing of an acute inflammation
• Persistence of causative agent
** macrophages = chief cell
Localized or Widespread
• Systemic inflammation = involves multiple organs –Systemic lupus
erythematosus, rheumatoid arthritis
General Therapeutic Management & Nursing Care for Integumentary Alteration
Diagnostic Evaluation
History & Subjective Symptoms
1. Pruritus
, 3
2. Anesthesia
3. Hyperesthesia or hypo
4. Paresthesia
Condition may remain localized or migrate, constant or intermittent, or may be aggravated by a specific
activity, such as exposure to sunlight.
Determine if child has allergic condition (e.g., asthma or hay fever) or hx of previous skin disease.
Atopic dermatitis often = from allergies, frequently begins in infancy.
Questions:
• When lesion or symptom first appeared
• Whether it occurs with ingestion of a food or other substance, including med
• Whether related to activity (e.g., contact with plants, insects, or chemicals).
Other Findings: Lesion Characteristics
• Erythema
• Ecchymoses (bruises)
• Petechiae
• Primary lesions
• Secondary lesions
• Distribution pattern
• Configuration and arrangement (discrete, clustered, diffuse, or confluent)
Laboratory Studies:
• If skin problem related to system disease (e.g., collagen or immunodeficiency disease
(e.g., Lupus) = Lab studies focus on identifying condition.
• Miscroscopic examinations
• Cultures
• Biospsy
• Cytodiagnosis
• Patch testing
• Wood light examination
• Allergic skin testing
• Blood counts & sedimentation rates, CRP…..
• Immunoglobulin E (IgE)
• Potassium hydroxide (KOH) prep – reveals fungal infections
General Therapeutic Management – (Review related pages in Hockenberry textbook)
Goal: To prevent further damage, eliminate the cause, prevent complications, and provide relief of
discomfort.
Most common causative agent of dermatitis in infants, children, & adolescents = environmental factors
(soaps, bubble baths, wet diapers….) and the natural elements (dirt, sand, heat….). May also occur from
home remedies & meds.
