Acute and Chronic Inflammation

Explore the pathology and physiology of inflammation: a complex immune response triggered by infection, injury, or irritants. Learn how acute and chronic inflammation involve cytokines, immune cells, and vascular changes—impacting healing, pain, and disease progression in clinical care.

Inflammation is a cornerstone concept in pathology and clinical care, influencing the management of a wide spectrum of diseases. For nurses, a strong grasp of inflammation—its mechanisms, genetic underpinnings, clinical manifestations, and nursing implications—is crucial for effective patient care.

Introduction

Inflammation is the body’s complex biological response to harmful stimuli, such as pathogens, damaged cells, or irritants. It is essential for tissue repair and protection but, when uncontrolled or misdirected, can contribute to disease progression and chronic health problems. Nurses, often at the forefront of patient assessment and care, must understand the nuances of inflammation to recognise, manage, and educate patients effectively. Furthermore, advances in genetics have illuminated the role of inherited factors in the inflammatory response, offering new insights into personalised care and risk assessment.

Overview of Inflammation

Definitions

Inflammation is a protective response involving immune cells, blood vessels, and molecular mediators. Its primary purpose is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues, and establish tissue repair. There are two main types:

• Acute Inflammation: A rapid, short-term response to injury or infection, aiming to remove the offending agent and initiate healing.
• Chronic Inflammation: A prolonged, often less intense response that can last for months or years, typically resulting from persistent injury, infection, or immune reactions.

Distinction Between Acute and Chronic Inflammation

Acute and chronic inflammation differ in their time course, cellular composition, causes, and outcomes. Acute inflammation is characterised by redness, heat, swelling, pain, and loss of function—signs familiar to every nurse. Chronic inflammation, on the other hand, is more insidious, often presenting with subtle symptoms but leading to significant tissue damage and systemic effects over time.

Acute Inflammation

Acute inflammation is the body’s immediate and protective response to tissue injury or infection, characterized by redness, heat, swelling, pain, and loss of function. It involves vascular and cellular changes aimed at eliminating the cause and initiating healing

Mechanisms

Acute inflammation unfolds in a series of well-orchestrated steps:

1. Recognition of Injury: Tissue-resident immune cells detect pathogens or damage via pattern recognition receptors (PRRs).
2. Vascular Changes: Local blood vessels dilate (vasodilation), increasing blood flow to the area. Vascular permeability rises, allowing plasma proteins and leukocytes to exit the bloodstream and enter tissues.
3. Leukocyte Recruitment: White blood cells (mainly neutrophils) migrate to the site, guided by chemotactic signals.
4. Phagocytosis and Clearance: Neutrophils and macrophages engulf and destroy pathogens or debris.
5. Resolution: Anti-inflammatory signals promote healing and restoration of normal tissue function.

Causes

• Infections (bacterial, viral, fungal, parasitic)
• Physical agents (trauma, burns, radiation)
• Chemical agents (acids, toxins)
• Immune responses (hypersensitivity reactions)
• Tissue necrosis (infarction, ischaemia)

Genetic Factors in Acute Inflammation

Genetic variations, such as single nucleotide polymorphisms (SNPs), can influence an individual’s acute inflammatory response. Genes regulating cytokines (e.g., interleukin-1, tumour necrosis factor-alpha) may alter the intensity and duration of inflammation. For instance, certain genetic profiles may predispose individuals to exaggerated responses, increasing the risk of complications like sepsis or multi-organ dysfunction.

Clinical Features

• Redness (Rubor)
• Heat (Calor)
• Swelling (Tumour)
• Pain (Dolor)
• Loss of function (Functio laesa)

Systemic manifestations may include fever, malaise, increased heart rate, and elevated white blood cell count (leukocytosis).

Diagnosis

• Clinical assessment: Observation of classic signs and symptoms.
• Laboratory tests: Raised white blood cell count, elevated markers like C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).
• Imaging: Ultrasound, X-ray, or CT scan to identify underlying causes or complications.

Nursing Management

Nurses play a pivotal role in the management of acute inflammation:

• Monitoring vital signs and systemic symptoms.
• Administering prescribed medications (antibiotics, anti-inflammatories, analgesics).
• Applying local therapies (cold compresses, elevation).
• Educating patients and families about symptom monitoring and when to seek further care.
• Preventing complications through prompt intervention and infection control.

Chronic Inflammation

Chronic inflammation is a prolonged, low-grade immune response that persists for months or years, often contributing to tissue damage and the development of chronic diseases like heart disease, diabetes, and autoimmune disorders.

Mechanisms

Chronic inflammation arises when the acute response fails to eliminate the offending agent, or when there is repeated injury. Key mechanisms include:

• Persistent Inflammation: Ongoing recruitment of immune cells, especially macrophages, lymphocytes, and plasma cells.
• Tissue Destruction: Release of enzymes, reactive oxygen species, and inflammatory mediators leads to ongoing tissue damage.
• Attempts at Repair: Fibrosis (scarring) and angiogenesis (formation of new blood vessels) occur alongside tissue destruction.

Causes

• Persistent infections (e.g., tuberculosis, hepatitis)
• Prolonged exposure to toxins (silica, asbestos)
• Autoimmune diseases (rheumatoid arthritis, systemic lupus erythematosus)
• Unresolved acute inflammation

Genetic Factors in Chronic Inflammation

Genetic predisposition is critical in chronic inflammatory diseases. Polymorphisms in genes related to immune regulation, such as HLA (human leukocyte antigen) genes, can increase susceptibility to autoimmune disorders. For example, HLA-DRB1 alleles are strongly associated with rheumatoid arthritis. Additionally, genetic defects in anti-inflammatory pathways may impair resolution, promoting chronicity.

Clinical Features

• Less pronounced local signs compared to acute inflammation.
• Systemic symptoms are more common: fatigue, weight loss, anaemia, low-grade fever.
• Organ dysfunction or failure (e.g., liver cirrhosis, chronic kidney disease).
• Development of granulomas in diseases like tuberculosis or sarcoidosis.

Diagnosis

• History and examination: Chronicity of symptoms, systemic features.
• Laboratory investigations: Persistently elevated inflammatory markers (CRP, ESR), presence of specific autoantibodies.
• Imaging: Detection of fibrosis, scarring, or structural changes in affected organs.
• Biopsy: May be required for definitive diagnosis (e.g., liver, kidney, or synovial tissue).

Nursing Management

• Supporting medical management (immunosuppressive therapy, disease-modifying agents).
• Monitoring for complications (organ dysfunction, infection).
• Promoting adherence to long-term therapy.
• Patient education regarding symptom management, lifestyle modifications, and infection prevention.
• Emotional support and counselling as chronic diseases can impact mental health.

Genetics and Inflammation

Role of Genetics in Inflammatory Responses

Genetics plays a significant role in modulating both susceptibility to and outcomes of inflammatory diseases. Inherited differences in immune system genes can explain why individuals vary in their response to the same insult. Key genetic factors include:

• Cytokine gene polymorphisms: Influence the intensity of the inflammatory response.
• HLA gene variants: Predispose to autoimmune and inflammatory diseases.
• Genes affecting cell signalling: Such as those coding for nuclear factor kappa B (NF-κB), a central regulator of inflammation.

Common Genetic Markers

• HLA-DRB1: Associated with rheumatoid arthritis and other autoimmune conditions.
• TNF-α gene polymorphisms: Linked to increased risk of severe sepsis and chronic inflammatory disorders.
• NOD2 gene mutations: Strongly associated with Crohn’s disease, a form of chronic intestinal inflammation.
• IL-6 and IL-1 gene variants: Related to altered cytokine production and inflammatory disease risk.

Implications for Nursing

Understanding genetic influences enables nurses to:

• Identify patients at higher risk of inflammatory diseases.
• Support personalised care, including tailored education and monitoring.
• Collaborate in family screening and genetic counselling referrals where appropriate.

Clinical Implications for Nurses

Assessment and Monitoring

• Conduct thorough patient histories, focusing on risk factors, family history, and symptom progression.
• Regularly assess vital signs, local and systemic signs of inflammation.
• Monitor laboratory markers and report abnormal findings promptly.

Patient Education

• Explain the nature and purpose of inflammation to patients and families in simple terms.
• Educate about medication adherence, potential side effects, and the importance of follow-up appointments.
• Advise on lifestyle modifications to reduce inflammation, such as balanced diet, regular exercise, and smoking cessation.
• Discuss the potential genetic aspects and encourage family members to seek screening if indicated.

Care Planning

• Develop individualised care plans considering the type and stage of inflammation and patient-specific risk factors.
• Coordinate multidisciplinary care, liaising with physicians, physiotherapists, dietitians, and genetic counsellors as needed.
• Document all assessments, interventions, and patient responses accurately.

Case Studies and Practical Applications

Case Study 1: Acute Appendicitis in a Young Adult

• A 22-year-old presents with sudden onset of right lower abdominal pain, fever, and vomiting.
• Assessment reveals tenderness, guarding, and raised white cell count.
• Nursing interventions: Monitor vital signs, administer prescribed antibiotics and analgesics, prepare for possible surgery, educate patient and family about post-operative care.

Case Study 2: Chronic Rheumatoid Arthritis in Middle Age

• A 45-year-old woman reports joint pain and swelling for several months, with morning stiffness lasting over an hour.
• Laboratory tests reveal positive rheumatoid factor and elevated ESR/CRP.
• Nursing interventions: Support adherence to disease-modifying therapy, monitor for complications (e.g., anaemia, infection), educate about joint protection and physiotherapy, offer emotional support.

Case Study 3: Genetic Predisposition and Family History

• A patient with a family history of inflammatory bowel disease (IBD) presents with recurrent abdominal pain and diarrhoea.
• Genetic testing identifies a NOD2 gene mutation.
• Nursing interventions: Educate about genetic risk, support regular screening for family members, reinforce importance of symptom monitoring and early intervention.

REFERENCES

1. Ramadas Nayak, Textbook of Pathology and Genetics for Nurses, 2nd Edition,2024, Jaypee Publishers, ISBN: 978-93-5270-031-8.
2. Suresh Sharma, Textbook of Pharmacology, Pathology & Genetics for Nurses II, 2nd Edition, 31 August 2022, Jaypee Publishers, ISBN: 978-9354655692.
3. Kumar, V., Abbas, A.K., & Aster, J.C. (2020). Robbins and Cotran Pathologic Basis of Disease. 10th Edition. Elsevier.
4. McCance, K.L., & Huether, S.E. (2018). Pathophysiology: The Biologic Basis for Disease in Adults and Children. 8th Edition. Elsevier.
5. Zotova N, Zhuravleva Y, Chereshnev V, Gusev E. Acute and Chronic Systemic Inflammation: Features and Differences in the Pathogenesis, and Integral Criteria for Verification and Differentiation. Int J Mol Sci. 2023 Jan 6;24(2):1144. https://pmc.ncbi.nlm.nih.gov/articles/PMC9862412/
6. Stone WL, Basit H, Zubair M, et al. Pathology, Inflammation. [Updated 2024 Aug 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534820/

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