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Heather Baid

, Fiona Creed

, and Jessica Hargreaves

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date: 05 May 2021

Components of the immune system

Lymphatic system

Lymphatic plexuses

These networks of lymphatic vessels are located in the tissue intercellular spaces that drain tissue fluid into lymph.


These are a collection of lymphatic vessels that originate from lymphatic plexuses along which lymph nodes are located.

Lymph nodes

These small masses of lymphatic tissue collect and filter lymph and transport it to the circulation.

Lymphatic ducts

These larger lymphatic vessels combine to form the ducts that drain lymph from all areas of the body into the venous system for elimination.


This is tissue fluid, which is usually clear and watery, and has the same constituents as plasma. In the presence of infection, foreign proteins are also drained in the lymph from the affected tissue. This stimulates an immunological response, including the formation of specific antibodies and lymphocytes (see Box 13.1 for a definition of lymphoedema).



This produces and secretes antimicrobial proteins and immune cells.

Bone marrow

This produces phagocytes, macrophages, and antigen-presenting cells by a process known as haematopoiesis.


This lymphoid organ is located in the lower part of the neck. It produces mature T cells from immature thymocytes that have migrated from the bone marrow to be released into the circulation.


This lymphoid organ is located in the left upper quadrant region of the abdomen (see Immunology p. [link]). It contains B and T lymphocytes, macrophages, natural killer cells, and dendritic cells.


A pathogen is a disease-causing microorganism (see Box 13.2 for a list of microorganisms).



These are a type of leucocyte, and include basophils, eosinophils, and neutrophils. Through a process of degranulation, antimicrobial cytotoxic chemicals are released from secretory vesicles (granules). Neutrophils are the most numerous granulocyte, and are also able to engulf microorganisms by phagocytosis.

Mast cells

These cells can mediate allergic reactions by releasing inflammatory chemicals such as histamine.


These cells develop into macrophages, which are present in the circulation and in tissues. They coordinate an immune response by signalling to other immune cells and ingesting microorganisms. Macrophages also break down erythrocytes (this occurs without activation of the immune response).

Dendritic cells

These are a type of antigen-presenting cell (APC) located in the lymph nodes, thymus, spleen, and plasma. They are responsible for processing antigens from foreign cells so that they can be recognized by B or T cells in the presence of the major histocompatibility complex (MHC). The latter helps immune cells to distinguish between host and foreign cells.

Natural killer cells

These are responsible for recognizing and killing virus-infected cells or tumour cells. They also contain granules which, when released, can destroy the cell membrane and also coordinate cell apoptosis (programmed cell death). Unlike necrosis, in apoptosis there is no further immune activation.


  • These are large protein molecules called immunoglobulins.

  • Each immunoglobulin has a unique antigen-binding site that allows the antibody to recognize a matching antigen.

  • There are nine classes of human immunoglobulins—IgG (four types), IgA (two types), IgM, IgE, and IgD. Each class has specific functions, including prevention of colonization, allergy response, activation of granulocytes, and antigen receptor.

B cells

  • These produce antibodies in response to antigens (proteins) present on the surface of microorganisms.

  • The antibodies circulate in the blood and lymph, binding to particular antigens and marking them for destruction by other immune cells (e.g. in the spleen).

  • Some antibodies that are bound to antigens activate the complement system to destroy the microorganism.

  • Other antibodies block viruses from entering cells.

T cells

  • There are two types of T cells.

  • T-helper cells (CD4 cells):

    • coordinate immune regulation

    • potentiate the immune response by secreting substances that activate other leucocytes and macrophages

    • signal B cells to make antibodies.

  • T-killer cells (CD8 cells):

    • direct the destruction of virus-infected cells, tumour cells, and parasites

    • have an important role in down-regulation of the immune system.

The immunocompromised patient

The immunocompromised patient exhibits reduced resistance to infection due to an abnormality in the immune system. Causes include:

  • malnutrition (reduces T-cell number, depresses antibody response, zinc deficiency can cause lymphoid atrophy)

  • previous exposure to vaccination or infection (e.g. HIV)

  • autoimmune disorders (e.g. SLE, rheumatoid arthritis)

  • medication:

    • H2 blockers (e.g. ranitidine)

    • antibiotics (e.g. chloramphenicol)

    • cardiovascular drugs (e.g. propranolol)

    • non-steroidal anti-inflammatory drugs (NSAIDs)

    • heparin

    • propofol

    • specific immunosuppressive drugs (e.g. steroids, cytotoxic drugs, monoclonal antibodies)

  • major surgery or trauma (suppresses T-cell production and reduces neutrophil chemotaxis)

  • hypoxaemia (hypoxia stimulates prostaglandin and tumour necrosis factor production)

  • acute or chronic kidney injury (reduced neutrophil activity, inappropriate macrophage activation, impaired macrophage antigen presentation, and defective T-cell function).

Nursing the immunocompromised patient

  • Ensure compliance with infection prevention and control measures.

  • Consider isolation, preferably with positive, negative, or laminar flow and high-efficiency particulate air (HEPA) (see Box 13.3).

  • Direct care equipment (e.g. stethoscopes) should be patient-specific.

  • Limit stock to avoid waste.

  • Observe for signs of infection at cannulae sites, wounds, and drains, remove within recommended timescales, and conduct microbial screening (e.g. wounds, blood, skin).

  • Minimize invasive procedures and monitoring.

Human immunodeficiency virus (HIV)

This is a retrovirus (i.e. its genetic material is RNA, not DNA) that causes an autoimmune response in the form of acquired deficiency syndrome (AIDS). Following the initial exposure, viral replication continues with progressive destruction of helper T cells (CD4 lymphocytes). Eventually the rate of production of new CD4 cells cannot match the rate of destruction, and the clinical picture of AIDS develops. Cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.

Admission to the critical care unit

This may be due to:

  • co-infections (e.g. hepatitis B, hepatitis C, TB)

  • acute respiratory failure (e.g. pneumocytis pneumonia)

  • altered conscious level or intractable seizures secondary to neurological manifestations (e.g. CNS toxoplasmosis, CNS lymphoma, cryptococcal meningitis)

  • surgical or medical issues unrelated to the HIV infection.

Complications of HIV infection


Table 13.1 lists the causes of acute respiratory failure. The commonest cause is Pneumocystis carinii.

  • P. carinii is a fungus, transmitted through air, that causes upper and lower respiratory tract infection.

  • The patient presents with fever, tachycardia, and cough.

  • Exertional dyspnoea develops with severe tachypnoea and hypoxia.

  • Pneumatocoeles (air-filled cysts) on chest X-ray predispose to pneumothorax.

  • Treatment is with antibiotics (e.g. high-dose co-trimoxazole), high-dose steroids and, if needed, ventilatory support.

Table 13.1 Causes of acute respiratory failure in HIV disease

Bacterial pneumonia

  • Streptococcus pneumoniae

  • Staphylococcus aureus

  • Haemophilus influenzae

  • Pseudomonas species (e.g. Serratia marcescens)

Atypical pneumonia

  • Mycobacterium tuberculosis

  • Mycoplasma pneumoniae

Fungal pneumonia

  • Pneumocystis carinii

  • Cryptococcus neoformans

  • Histoplasma capsulatum

  • Coccidioides immitis

  • Aspergillus fumigatus

Cytomegalovirus pneumonia

Lymphocytic interstitial pneumonia

Toxoplasma gondii pneumonitis

Non-Hodgkin’s lymphoma and pulmonary Kaposi’s sarcoma


HIV is a neurotrophic virus (i.e. it affects the proteins responsible for growth and maintenance of neurons) that can cause:

  • acute myelopathy

  • encephalopathy

  • meningitis

  • cerebral mass lesions

  • secondary brain infection, such as toxoplasmosis (a parasitic infection).


  • Peritonitis from small bowel or colonic enteritis.

  • AIDS cholangiopathy causing biliary sepsis.

AIDS-related malignancies

  • Kaposi’s sarcoma.

  • Lymphomas.

  • Cervical carcinomas related to human papilloma virus.

  • Hepatitis-B-related carcinomas.

  • Non-Hodgkin’s lymphoma.

Further reading

DeFreitas A et al. Pharmacological considerations in human immunodeficiency virus-infected adults in the intensive care unit. Critical Care Nurse 2013; 33: 46–56.Find this resource:

Prout J and Agarwal B. Anaesthesia and critical care for patients with HIV infection. Continuing Education in Anaesthesia, Critical Care & Pain 2005; 5: 153–6.Find this resource:

Shrosbree J et al. Anesthesia and intensive care in patients with HIV. Trends in Anaesthesia and Critical Care 2011; 1: 153–61.Find this resource:

Systemic lupus erythematosus (SLE)

This is a chronic, potentially fatal autoimmune disease with a high prevalence in young black women. It is termed a connective tissue disorder, and is characterized by the presence of arthritis/arthralgia, vasculitis, and immunological features such as autoantibodies and deposition of immune complex (a network of antigens and antibodies cross-linked to form a large mass that, if trapped in the tissue, can initiate further inflammatory reactions).

Clinical manifestations of SLE

Skin and mucosa

  • Photosensitivity with flushing on the face, and rashes and urticaria on sun-exposed parts of the body.

  • Alopecia (hair loss).

  • Mucosal ulceration conjunctivitis.


  • Lupus nephritis (persistent inflammation of the kidney).


  • Anaemia, leucopenia, thrombocytopenia.

  • Venous or arterial thrombi (causing strokes and pulmonary emboli).

  • Prolonged activated partial thromboplastin time.


  • Endocarditis, myocarditis, pericarditis.

  • Cardiac tamponade from pericardial effusions (rare).

  • Chest pain.

  • Arrhythmias.


  • Pleural effusion.

  • Inflammatory pneumonitis.

  • Pulmonary hypertension.

Central nervous system

  • Isolated nerve palsies.

  • Psychosis, personality disorder, dementia.

  • Stroke.

  • Seizures.


  • Peritonitis, pancreatitis.

  • Ascites.

  • Splenomegaly.


  • Steroids and/or immunosuppressive drugs (e.g. azathioprine, cyclophosphamide).

  • Cessation of drugs that may induce SLE (e.g. procainamide, hydralazine, isoniazid).

  • Supportive therapy (e.g. respiratory support, renal replacement therapy).

  • Antibiotics for infections.

  • Plasma exchange or intravenous immunoglobulin may be useful for pulmonary haemorrhage.

  • Long-term anticoagulation (to prevent thrombi and emboli).

Further reading

Demoruelle MK et al. Recent-onset systemic lupus erythematosus complicated by acute respiratory failure. Arthritis Care & Research 2013; 65: 314–23.Find this resource:

Trethewey P. Systemic lupus erythematosus. Dimensions of Critical Nursing 2004; 23: 111–15.Find this resource:

Vasculitic disorders

These are caused by the inflammatory destruction of blood vessels by autoantibodies.

Wegener’s granulomatosis/polyarteritis nodosa

This is a necrotizing vasculitis that affects small and medium-sized vessels. Autoantibodies bind to epithelial cells to form immune complexes, which accumulate in the tissues, leading to inflammation of the vessels. Secondary thrombosis and occlusion of the vessels leads to ischaemia and infarction of multiple organs. Small aneurysms develop in weakened tissue walls. Healing can result in fibrosis.


  • Cold-like symptoms (fever, weight loss, malaise, myalgia).

  • Sinusitis and epistaxis (destruction of nasal cartilage, septal perforation).

  • Pulmonary haemorrhage (due to necrotizing capillaries).

  • Acute kidney injury (secondary to necrotizing glomerulonephritis).

  • Mesenteric artery thrombosis and bowel infarction.

  • Myocardial infarction.

  • Stroke.


  • Immunosuppressive drugs (e.g. corticosteroids, cyclophosphamide).

  • Renal replacement therapy.

  • Balloon dilatation and stent insertion for tracheobronchial stenosis.

Goodpasture’s disease

This is caused by antiglomerular basement membrane (anti-GBM) antibodies binding to the glomerulus and alveolus. Patients present with glomerulonephritis and/or pulmonary haemorrhage (particularly if they are smokers).


  • Immunosuppressive drugs (e.g. corticosteroids, cyclophosphamide).

  • Plasma exchange to remove anti-GBM antibodies.

Anaphylactic and anaphylactoid reactions

These are potentially life-threatening, systemic reactions that occur after re-exposure to an antigen, leading to increased vascular permeability and smooth muscle constriction (see Figure 13.1).

Figure 13.1 Management of a severe anaphylactic reaction (Resuscitation Council (UK) Anaphylaxis Algorithm).

Figure 13.1 Management of a severe anaphylactic reaction (Resuscitation Council (UK) Anaphylaxis Algorithm).

(Reproduced with the kind permission of the Resuscitation Council (UK).)

Anaphylactic reaction: IgE mediated

There is immediate release of inflammatory mediators (e.g. histamine, kinins, leukotrienes) from tissue mast cells and peripheral basophils.

Anaphylactoid reaction: non-IgE mediated

Tissue mast cells are induced to react following complement activation by immune complexes.

Causes of anaphylactic and anaphylactoid reactions

  • Certain foods (e.g. nuts, shellfish, eggs, milk).

  • Venom (e.g. bee sting).

  • Latex.

  • Medication (e.g. vaccine, immunoglobulins, opiates, antibiotics, NSAIDs, dextrans).

  • Radiocontrast media.


These can occur within seconds of exposure. However, the extent of the reaction is variable.

  • Cardiovascular symptoms—vasodilation, myocardial ischaemia, arrhythmias, hypotension, distributive shock.

  • Respiratory symptoms—nasal congestion, upper airway obstruction, stridor, laryngospasm, bronchospasm, pulmonary oedema.

  • Gastrointestinal symptoms—nausea, vomiting, abdominal cramps, diarrhoea.

  • Skin symptoms—flushing, urticaria, pruritus, angio-oedema.