8.4 Immune, Infectious & Multisystem Conditions

Immune System Review

The immune system has two arms. Innate (natural) immunity is immediate and nonspecific: skin and mucous membranes, neutrophils, macrophages, natural killer cells, complement, and the inflammatory response. Adaptive (acquired) immunity is specific and develops memory:

• Humoral immunity: B lymphocytes produce antibodies (immunoglobulins). IgG is the most abundant and provides long-term memory; IgM appears first in acute infection; IgA protects mucosal surfaces; IgE mediates allergic reactions and parasitic defense.
• Cell-mediated immunity: T lymphocytes — CD4 helper T cells orchestrate the response (the cells HIV destroys) and CD8 cytotoxic T cells kill infected and malignant cells.

Active immunity comes from infection or vaccination (long-lasting); passive immunity comes from transferred antibodies — maternal antibodies or immunoglobulin infusions — and is temporary. Immunocompromised patients (chemotherapy, chronic steroids, transplant, HIV) need protective considerations: strict hand hygiene, no live plants or fresh flowers in neutropenic rooms, avoiding crowds and sick contacts, cooked-food precautions, and no live vaccines (MMR, varicella, intranasal influenza) during significant immunosuppression.

HIV/AIDS

Human immunodeficiency virus (HIV) progressively destroys CD4 helper T cells. Normal CD4 counts run roughly 500-1,500 cells/mm3. AIDS (acquired immunodeficiency syndrome) is diagnosed by a CD4 count below 200 cells/mm3 OR an AIDS-defining (opportunistic) illness, regardless of count. Treatment is combination antiretroviral therapy (ART); the goals are an undetectable viral load, CD4 recovery, and strict adherence — missed doses breed resistance. Untreated persons with sustained undetectable viral loads do not sexually transmit the virus (U=U).

Opportunistic infections by CD4 threshold

Nursing care

Use standard precautions for all patients — HIV is bloodborne, not airborne; add transmission-based precautions only for other indicated organisms. No special room or isolation is required for HIV itself. Teach: never share razors or needles, safe-sex practices, ART adherence, and routine dental care. Support nutrition and skin integrity; assess for depression and stigma. Report fever promptly — in advanced disease even minor infections escalate quickly.

Anaphylaxis

Anaphylaxis is an IgE-mediated type I hypersensitivity reaction causing massive histamine release. Triggers include penicillin and other antibiotics, contrast dye, latex, bee stings, and foods (peanuts, shellfish). Onset is typically minutes after exposure. Signs in priority order:

• Airway/respiratory: stridor, laryngeal edema, wheezing, feeling of throat closure — the most dangerous finding
• Cardiovascular: vasodilation and capillary leak causing hypotension and distributive shock
• Skin: urticaria (hives), flushing, angioedema — often the first sign but not the most dangerous
• GI: cramping, vomiting, diarrhea

Emergency response

1. Stop the exposure (discontinue the IV drug/antibiotic) and call for help / activate the rapid response.
2. Epinephrine 0.3-0.5 mg of 1 mg/mL concentration (1:1,000) IM into the anterolateral thigh (vastus lateralis) — the single most important intervention; it may be repeated every 5-15 minutes. IM thigh absorption beats subcutaneous. Never delay epinephrine to give antihistamines first.
3. Position supine with legs elevated (trendelenburg if tolerated); high-flow oxygen; prepare for airway management.
4. Establish IV access and give rapid isotonic fluids for hypotension.
5. Second-line agents: diphenhydramine and H2 blockers for cutaneous symptoms, albuterol for persistent bronchospasm, and corticosteroids to blunt the biphasic (delayed) reaction.
6. Observe for biphasic recurrence (can occur hours later) and educate on carrying an epinephrine auto-injector and wearing medical identification.

Systemic Lupus Erythematosus (SLE)

SLE is a chronic autoimmune disease in which antinuclear antibodies (ANA positive in nearly all patients) drive immune-complex deposition across organ systems. Hallmark findings: butterfly (malar) rash across the nose and cheeks, photosensitivity, discoid lesions, oral ulcers, nonerosive arthritis, serositis, and renal involvement (lupus nephritis — monitor urine protein and creatinine). Flares are triggered by sunlight, infection, stress, and certain drugs (procainamide, hydralazine). Management centers on hydroxychloroquine for most patients (baseline and periodic retinal exams), NSAIDs for arthralgia, and corticosteroids plus immunosuppressants for flares. Nursing pearls: teach sunscreen and protective clothing, energy conservation, infection vigilance while immunosuppressed, and that women may flare in pregnancy — plan pregnancy with the rheumatologist during remission.

Sepsis: Recognition and the Hour-1 Bundle

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Older framing used the SIRS criteria (systemic inflammatory response syndrome) — two or more of:

• Temperature above 38 C (100.4 F) or below 36 C (96.8 F)
• Heart rate above 90 beats/min
• Respiratory rate above 20 breaths/min (or PaCO2 below 32 mm Hg)
• WBC above 12,000/mm3 or below 4,000/mm3 (or more than 10% bands)

qSOFA (quick Sequential Organ Failure Assessment) is the rapid bedside screen for poor outcomes — one point each for:

1. Respiratory rate 22/min or higher
2. Altered mentation (Glasgow Coma Scale below 15)
3. Systolic blood pressure 100 mm Hg or lower

A score of 2 or more should trigger lactate measurement, cultures, and escalation.

Surviving Sepsis Hour-1 bundle

1. Measure lactate level; remeasure if the initial value is above 2 mmol/L.
2. Obtain blood cultures BEFORE administering antibiotics (do not delay antibiotics more than 45 minutes to get them).
3. Administer broad-spectrum antibiotics within 1 hour of recognition for septic shock (and rapidly for possible sepsis).
4. Rapid 30 mL/kg crystalloid for hypotension or lactate 4 mmol/L or higher.
5. Apply vasopressors if MAP remains below 65 mm Hg during or after fluid resuscitation.

Septic shock

Septic shock is sepsis with vasopressor requirement to maintain MAP 65 mm Hg or higher AND lactate above 2 mmol/L despite adequate fluid resuscitation. Norepinephrine is the first-line vasopressor, ideally through central access; vasopressin is the usual second agent. Additional priorities: source control (drain abscesses, remove infected devices), glucose control (target 140-180 mg/dL), stress-ulcer and DVT prophylaxis, and reassessing fluid responsiveness. Warm extremities and bounding pulses mark early (warm) septic shock; cold, mottled skin marks late decompensation.

Multiple organ dysfunction syndrome (MODS)

MODS is progressive dysfunction of two or more organ systems from uncontrolled inflammation — most often following sepsis, massive trauma, or burns. The lungs fail first (ARDS): refractory hypoxemia requiring mechanical ventilation. The cascade continues with acute kidney injury (rising creatinine, falling urine output), hepatic failure (rising bilirubin, coagulopathy), GI dysfunction (stress ulcers, ileus), hematologic failure (DIC), and cardiovascular collapse. Mortality climbs steeply with each additional failing organ. Nursing care is surveillance and support: strict intake and output, daily weights, trending lactate and organ markers, meticulous skin and line care, and family communication.