SECTION 3 Problems Related to Homeostasis and Protection
12
Inflammation and Healing
Catherine R. Ratliff
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Health Promotion Perfusion
Inflammation Sensory Perception
Nutrition Tissue Integrity
Pain
LEARNING OUTCOMES
1. Describe the inflammatory response, including vascular and 6. Describe the nursing and interprofessional management of
cellular responses and exudate formation. wound healing.
2. Explain local and systemic manifestations of inflammation 7. Explain the etiology and clinical manifestations of pressure
and their physiologic bases. injuries.
3. Describe the drug therapy, nutrition therapy, and nursing 8. Apply a patient risk assessment to measures used to prevent
management of inflammation. the development of pressure injuries.
4. Distinguish among healing by primary, secondary, and 9. Discuss nursing and interprofessional management of a
tertiary intention. patient with pressure injuries.
5. Describe the factors that delay wound healing and common
complications of wound healing.
KEY TERMS
dehiscence, Table 12.9 pressure injury
evisceration, Table 12.9 regeneration
fibroblasts repair
inflammatory response shear
This chapter focuses on inflammation, wound healing, and pressure removes necrotic materials, and sets up an environment suit-
injury prevention and management. Maintaining skin and tissue able for healing and repair. Some use the term inflammation
integrity is a key nursing role. Multiple concepts are closely related to incorrectly as a synonym for infection. Inflammation is always
tissue integrity. Adequate nutrition and perfusion are essential so that present with infection, but infection is not always present with
the body has the needed factors to promote healing when an injury inflammation. An infection involves the invasion of tissues or
occurs. Impaired mobility and sensory perception increase the risk cells by microorganisms, such as bacteria, fungi, and viruses. In
for injury. When an injury does occur, pain and problems regulating contrast, heat, radiation, trauma, chemicals, allergens, and an
temperature and fluid and electrolyte balance are common. autoimmune reaction also can cause inflammation. A person
who is neutropenic may have an infection but not be able to
mount an inflammatory response.
INFLAMMATORY RESPONSE The intensity of the inflammatory response depends on
The inflammatory response is a sequential reaction to cell the extent and severity of the injury and the person’s reactive
injury. It neutralizes and dilutes the inflammatory agent, capacity. The inflammatory response is divided into a vascular
179
,180 SECTION 3 Problems Related to Homeostasis and Protection
PATHOPHYSIOLOGY MAP
Cell injury
Vascular Response Cellular Response
Cell Momentary Chemotaxis Margination and
injury/death vasoconstriction diapedesis of blood
leukocytes
Release of chemical Migration of leukocytes to
mediators (histamine, the site of injury
kinins, prostaglandins)
• Local Neutrophils Monocytes Lymphocytes
vasodilation
• Hyperemia
• Capillary Tissue Macrophages Immune
permeability macrophages response
• Local edema
Phagocytosis
Inflammatory exudates
• Fluid exudate
• Cell exudate
Fig. 12.1 Vascular and cellular responses to tissue injury.
response, cellular response, exudate formation, and healing. Fig. white blood cells (WBCs) to the site of injury. This results in an
12.1 shows the vascular and cellular response to injury. accumulation of neutrophils and monocytes at the site.
Vascular Response Neutrophils
After cell injury, local arterioles briefly undergo transient vaso- Neutrophils are the first WBCs to arrive at the injury site (usu-
constriction. After release of histamine and other chemicals by ally within 6 to 12 hours). They phagocytize (engulf) bacteria,
the injured cells, the vessels dilate. Chemical mediators cause other foreign material, and damaged cells. With their short life
increased capillary permeability and promote fluid movement span (24 to 48 hours), dead neutrophils soon accumulate. In
from capillaries into tissue spaces. At first, this inflammatory time, a mix of dead neutrophils, digested bacteria, and other
exudate is made up of serous fluid. Later, it contains plasma pro- cell debris accumulate as a creamy substance called pus.
teins, primarily albumin. These proteins exert oncotic pressure To keep up with the demand for neutrophils, the bone mar-
that further draws fluid from blood vessels. Both vasodilation row releases more neutrophils into circulation. This results in
and increased capillary permeability are responsible for redness, a high WBC count, especially the neutrophil count. Mature
heat, and swelling at the site of injury and the surrounding area. neutrophils are called segmented neutrophils. Sometimes the
As the plasma protein fibrinogen leaves the blood, it is demand for neutrophils increases to the extent that the bone
activated to fibrin by the products of the injured cells. Fibrin marrow releases immature neutrophils (bands) into circulation.
strengthens a blood clot formed by platelets. In tissues, the clot We call an increased number of band neutrophils in circulation
functions to trap bacteria, prevent their spread, and serves as a a shift to the left. This is common in patients with acute bacterial
framework for the healing process. Platelets release growth fac- infections.
tors that start the healing process.
Monocytes
Cellular Response Monocytes are the second type of phagocytic cells that migrate
Neutrophils and monocytes move from circulation to the site from circulating blood. They usually arrive at the site within 3
of injury (Fig. 12.1). Chemotaxis is the directional migration of to 7 days after the onset of inflammation. On entering the tissue
, CHAPTER 12 Inflammation and Healing 181
TABLE 12.1 Mediators of Inflammation
Mediator Source Mechanisms of Action
Complement components (C3a, C4a, Anaphylatoxic agents generated from complement Stimulate histamine release and chemotaxis
C5a) pathway activation
Cytokines See Table 14.3
Histamine Stored in granules of basophils, mast cells, platelets Cause vasodilation and increased capillary permeability
Kinins (e.g., bradykinin) Produced from precursor factor kininogen because of Cause contraction of smooth muscle and vasodilation. Result in
activation of Hageman factor (XII) of clotting system stimulation of pain
Prostaglandins (PGs) and leukot- Produced from arachidonic acid (Fig. 12.2) PGs cause vasodilation. LTs stimulate chemotaxis
rienes (LTs)
Serotonin Stored in platelets, mast cells, enterochromaffin cells Same as histamine. Stimulate smooth muscle contraction
of GI tract
spaces, monocytes transform into macrophages. Together with
Cell membrane
the tissue macrophages, these new macrophages help with
phagocytosis of the inflammatory debris. Because the area must Inhibited by steroids
be clean so it can heal, they play a key role in the healing pro- Arachidonic acid
cess. Macrophages have a long life span. They can multiply and
Cyclooxygenase pathway
may stay in the damaged tissues for weeks.
When particles are too large for a single macrophage, mac- Inhibited by NSAIDs, ASA Lipoxygenase
pathway
rophages accumulate and fuse to form a multinucleated giant
cell. Collagen encapsulates this giant cell, leading to the forma-
tion of a granuloma. A classic example of this process occurs
in tuberculosis of the lung. While the Mycobacterium bacillus Prostaglandins Thromboxane Leukotrienes
is walled off, a chronic state of inflammation exists. The granu-
loma formed is a cavity of necrotic tissue. Fig. 12.2 Pathway of generation of prostaglandins, thromboxane, and
leukotrienes. Corticosteroids, NSAIDs, and acetylsalicylic acid (ASA) act
to inhibit various steps in this pathway.
Lymphocytes
Lymphocytes arrive later at the site of injury. Their primary role is
related to humoral and cell-mediated immunity (see Chapter 14). role in sensitizing pain receptors to arousal by stimuli that would
normally be painless. PGs stimulate the temperature-regulating
Chemical Mediators area of the hypothalamus, producing a febrile response.
Table 12.1 describes inflammatory response mediators. Thromboxane is a powerful vasoconstrictor and platelet-
aggregating agent. It causes brief vasoconstriction and skin pal-
Complement System lor at the injury site and promotes clot formation. It has a short
The complement system is an enzyme cascade (C1 to C9) con- half-life. The pallor soon gives way to vasodilation and redness,
sisting of pathways to mediate inflammation and destroy invad- which is caused by PGs and histamine.
ing pathogens. Major functions of the complement system are Leukotrienes form the slow-reacting substance of anaphy-
enhanced phagocytosis, increased vascular permeability, che- laxis (SRS-A). SRS-A constricts smooth muscles of the bronchi,
motaxis, and cellular lysis. These activities are important medi- causing narrowing of the airway, and increases capillary perme-
ators of the inflammatory response and healing. ability. This leads to airway edema.
Cell lysis occurs when the final components create holes in
the cell membranes and cause targeted cell death by membrane Exudate Formation
rupture. In autoimmune disorders, complement activation and Exudate consists of fluid and WBCs that move from the cir-
the resulting inflammatory response can damage healthy tis- culation to the site of injury. The nature and quantity of exu-
sue. Examples of this include rheumatoid arthritis and systemic date depend on the type and severity of the injury and tissues
lupus erythematosus. involved (Table 12.2).
Prostaglandins and Leukotrienes Types of Inflammation
With cell injury, the arachidonic acid in the cell membrane is The basic types of inflammation are acute, subacute, and chronic.
rapidly converted to produce prostaglandins (PGs), thrombox- In acute inflammation, the healing occurs in 2 to 3 weeks and
ane, and leukotrienes (Fig. 12.2). PGs are considered proinflam- usually leaves no residual damage. Neutrophils are the main cell
matory. They are potent vasodilators contributing to increased type at the site of inflammation. Subacute inflammation has the
blood flow and edema formation. features of the acute process but lasts longer. For example, sub-
Some subtypes of PGs form when platelets are activated. They can acute infective endocarditis has acute inflammation, but it can
inhibit platelet and neutrophil aggregation. PGs have a significant last for weeks or months (see Chapter 40).
12
Inflammation and Healing
Catherine R. Ratliff
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Health Promotion Perfusion
Inflammation Sensory Perception
Nutrition Tissue Integrity
Pain
LEARNING OUTCOMES
1. Describe the inflammatory response, including vascular and 6. Describe the nursing and interprofessional management of
cellular responses and exudate formation. wound healing.
2. Explain local and systemic manifestations of inflammation 7. Explain the etiology and clinical manifestations of pressure
and their physiologic bases. injuries.
3. Describe the drug therapy, nutrition therapy, and nursing 8. Apply a patient risk assessment to measures used to prevent
management of inflammation. the development of pressure injuries.
4. Distinguish among healing by primary, secondary, and 9. Discuss nursing and interprofessional management of a
tertiary intention. patient with pressure injuries.
5. Describe the factors that delay wound healing and common
complications of wound healing.
KEY TERMS
dehiscence, Table 12.9 pressure injury
evisceration, Table 12.9 regeneration
fibroblasts repair
inflammatory response shear
This chapter focuses on inflammation, wound healing, and pressure removes necrotic materials, and sets up an environment suit-
injury prevention and management. Maintaining skin and tissue able for healing and repair. Some use the term inflammation
integrity is a key nursing role. Multiple concepts are closely related to incorrectly as a synonym for infection. Inflammation is always
tissue integrity. Adequate nutrition and perfusion are essential so that present with infection, but infection is not always present with
the body has the needed factors to promote healing when an injury inflammation. An infection involves the invasion of tissues or
occurs. Impaired mobility and sensory perception increase the risk cells by microorganisms, such as bacteria, fungi, and viruses. In
for injury. When an injury does occur, pain and problems regulating contrast, heat, radiation, trauma, chemicals, allergens, and an
temperature and fluid and electrolyte balance are common. autoimmune reaction also can cause inflammation. A person
who is neutropenic may have an infection but not be able to
mount an inflammatory response.
INFLAMMATORY RESPONSE The intensity of the inflammatory response depends on
The inflammatory response is a sequential reaction to cell the extent and severity of the injury and the person’s reactive
injury. It neutralizes and dilutes the inflammatory agent, capacity. The inflammatory response is divided into a vascular
179
,180 SECTION 3 Problems Related to Homeostasis and Protection
PATHOPHYSIOLOGY MAP
Cell injury
Vascular Response Cellular Response
Cell Momentary Chemotaxis Margination and
injury/death vasoconstriction diapedesis of blood
leukocytes
Release of chemical Migration of leukocytes to
mediators (histamine, the site of injury
kinins, prostaglandins)
• Local Neutrophils Monocytes Lymphocytes
vasodilation
• Hyperemia
• Capillary Tissue Macrophages Immune
permeability macrophages response
• Local edema
Phagocytosis
Inflammatory exudates
• Fluid exudate
• Cell exudate
Fig. 12.1 Vascular and cellular responses to tissue injury.
response, cellular response, exudate formation, and healing. Fig. white blood cells (WBCs) to the site of injury. This results in an
12.1 shows the vascular and cellular response to injury. accumulation of neutrophils and monocytes at the site.
Vascular Response Neutrophils
After cell injury, local arterioles briefly undergo transient vaso- Neutrophils are the first WBCs to arrive at the injury site (usu-
constriction. After release of histamine and other chemicals by ally within 6 to 12 hours). They phagocytize (engulf) bacteria,
the injured cells, the vessels dilate. Chemical mediators cause other foreign material, and damaged cells. With their short life
increased capillary permeability and promote fluid movement span (24 to 48 hours), dead neutrophils soon accumulate. In
from capillaries into tissue spaces. At first, this inflammatory time, a mix of dead neutrophils, digested bacteria, and other
exudate is made up of serous fluid. Later, it contains plasma pro- cell debris accumulate as a creamy substance called pus.
teins, primarily albumin. These proteins exert oncotic pressure To keep up with the demand for neutrophils, the bone mar-
that further draws fluid from blood vessels. Both vasodilation row releases more neutrophils into circulation. This results in
and increased capillary permeability are responsible for redness, a high WBC count, especially the neutrophil count. Mature
heat, and swelling at the site of injury and the surrounding area. neutrophils are called segmented neutrophils. Sometimes the
As the plasma protein fibrinogen leaves the blood, it is demand for neutrophils increases to the extent that the bone
activated to fibrin by the products of the injured cells. Fibrin marrow releases immature neutrophils (bands) into circulation.
strengthens a blood clot formed by platelets. In tissues, the clot We call an increased number of band neutrophils in circulation
functions to trap bacteria, prevent their spread, and serves as a a shift to the left. This is common in patients with acute bacterial
framework for the healing process. Platelets release growth fac- infections.
tors that start the healing process.
Monocytes
Cellular Response Monocytes are the second type of phagocytic cells that migrate
Neutrophils and monocytes move from circulation to the site from circulating blood. They usually arrive at the site within 3
of injury (Fig. 12.1). Chemotaxis is the directional migration of to 7 days after the onset of inflammation. On entering the tissue
, CHAPTER 12 Inflammation and Healing 181
TABLE 12.1 Mediators of Inflammation
Mediator Source Mechanisms of Action
Complement components (C3a, C4a, Anaphylatoxic agents generated from complement Stimulate histamine release and chemotaxis
C5a) pathway activation
Cytokines See Table 14.3
Histamine Stored in granules of basophils, mast cells, platelets Cause vasodilation and increased capillary permeability
Kinins (e.g., bradykinin) Produced from precursor factor kininogen because of Cause contraction of smooth muscle and vasodilation. Result in
activation of Hageman factor (XII) of clotting system stimulation of pain
Prostaglandins (PGs) and leukot- Produced from arachidonic acid (Fig. 12.2) PGs cause vasodilation. LTs stimulate chemotaxis
rienes (LTs)
Serotonin Stored in platelets, mast cells, enterochromaffin cells Same as histamine. Stimulate smooth muscle contraction
of GI tract
spaces, monocytes transform into macrophages. Together with
Cell membrane
the tissue macrophages, these new macrophages help with
phagocytosis of the inflammatory debris. Because the area must Inhibited by steroids
be clean so it can heal, they play a key role in the healing pro- Arachidonic acid
cess. Macrophages have a long life span. They can multiply and
Cyclooxygenase pathway
may stay in the damaged tissues for weeks.
When particles are too large for a single macrophage, mac- Inhibited by NSAIDs, ASA Lipoxygenase
pathway
rophages accumulate and fuse to form a multinucleated giant
cell. Collagen encapsulates this giant cell, leading to the forma-
tion of a granuloma. A classic example of this process occurs
in tuberculosis of the lung. While the Mycobacterium bacillus Prostaglandins Thromboxane Leukotrienes
is walled off, a chronic state of inflammation exists. The granu-
loma formed is a cavity of necrotic tissue. Fig. 12.2 Pathway of generation of prostaglandins, thromboxane, and
leukotrienes. Corticosteroids, NSAIDs, and acetylsalicylic acid (ASA) act
to inhibit various steps in this pathway.
Lymphocytes
Lymphocytes arrive later at the site of injury. Their primary role is
related to humoral and cell-mediated immunity (see Chapter 14). role in sensitizing pain receptors to arousal by stimuli that would
normally be painless. PGs stimulate the temperature-regulating
Chemical Mediators area of the hypothalamus, producing a febrile response.
Table 12.1 describes inflammatory response mediators. Thromboxane is a powerful vasoconstrictor and platelet-
aggregating agent. It causes brief vasoconstriction and skin pal-
Complement System lor at the injury site and promotes clot formation. It has a short
The complement system is an enzyme cascade (C1 to C9) con- half-life. The pallor soon gives way to vasodilation and redness,
sisting of pathways to mediate inflammation and destroy invad- which is caused by PGs and histamine.
ing pathogens. Major functions of the complement system are Leukotrienes form the slow-reacting substance of anaphy-
enhanced phagocytosis, increased vascular permeability, che- laxis (SRS-A). SRS-A constricts smooth muscles of the bronchi,
motaxis, and cellular lysis. These activities are important medi- causing narrowing of the airway, and increases capillary perme-
ators of the inflammatory response and healing. ability. This leads to airway edema.
Cell lysis occurs when the final components create holes in
the cell membranes and cause targeted cell death by membrane Exudate Formation
rupture. In autoimmune disorders, complement activation and Exudate consists of fluid and WBCs that move from the cir-
the resulting inflammatory response can damage healthy tis- culation to the site of injury. The nature and quantity of exu-
sue. Examples of this include rheumatoid arthritis and systemic date depend on the type and severity of the injury and tissues
lupus erythematosus. involved (Table 12.2).
Prostaglandins and Leukotrienes Types of Inflammation
With cell injury, the arachidonic acid in the cell membrane is The basic types of inflammation are acute, subacute, and chronic.
rapidly converted to produce prostaglandins (PGs), thrombox- In acute inflammation, the healing occurs in 2 to 3 weeks and
ane, and leukotrienes (Fig. 12.2). PGs are considered proinflam- usually leaves no residual damage. Neutrophils are the main cell
matory. They are potent vasodilators contributing to increased type at the site of inflammation. Subacute inflammation has the
blood flow and edema formation. features of the acute process but lasts longer. For example, sub-
Some subtypes of PGs form when platelets are activated. They can acute infective endocarditis has acute inflammation, but it can
inhibit platelet and neutrophil aggregation. PGs have a significant last for weeks or months (see Chapter 40).
