Shock and Anaphylaxis
Introduction:
Shock is a life-threatening clinical syndrome characterized by circulatory failure, inadequate perfusion, and impaired delivery of oxygen and nutrients to tissues. If untreated, it progresses to multi-organ dysfunction and death. Anaphylaxis is a severe, systemic, immediate hypersensitivity (Type I IgE-mediated) reaction that can cause shock through massive vasodilation, bronchospasm, and airway compromise. Both conditions are medical emergencies. For optometry students, awareness is essential because anaphylaxis may occur in the clinic after administration of drugs (local anesthetics, mydriatics, antibiotics) or diagnostic dyes (fluorescein, ICG), and shock may complicate systemic diseases that also have ocular relevance (sepsis, trauma, diabetes, etc.).
Definition
- Shock: A state of systemic hypoperfusion due to reduced cardiac output and/or reduced effective circulating blood volume, leading to cellular hypoxia.
- Anaphylaxis: An acute, severe, generalized allergic reaction mediated by IgE antibodies that results in widespread release of histamine and other mediators, causing vasodilation, bronchospasm, and tissue edema.
Classification of Shock
- Hypovolemic shock: Due to fluid/blood loss (hemorrhage, burns, vomiting, diarrhea).
- Cardiogenic shock: Due to pump failure (myocardial infarction, arrhythmias, cardiomyopathy).
- Distributive shock: Due to systemic vasodilation and maldistribution of blood flow. Includes:
- Septic shock (endotoxins, cytokines from infections).
- Anaphylactic shock (allergic reactions).
- Neurogenic shock (spinal cord injury, anesthesia).
- Obstructive shock: Due to mechanical obstruction of circulation (pulmonary embolism, cardiac tamponade, tension pneumothorax).
Pathophysiology of Shock
- Initial stage: Decreased perfusion → tissue hypoxia → shift to anaerobic metabolism → lactic acidosis.
- Compensatory stage: Tachycardia, vasoconstriction, activation of RAAS and sympathetic nervous system to maintain blood pressure and perfusion.
- Progressive stage: Persistent hypoxia → cellular injury, endothelial dysfunction, capillary leak, organ dysfunction.
- Irreversible stage: Severe multi-organ failure → death despite treatment.
Pathophysiology of Anaphylaxis
- Initial exposure to allergen → IgE antibody production → IgE binds to mast cells and basophils.
- On re-exposure, allergen cross-links IgE on mast cells → degranulation.
- Mediators released: histamine, leukotrienes, prostaglandins, cytokines.
- Results in:
- Vasodilation → hypotension, shock.
- Increased vascular permeability → edema (laryngeal edema dangerous).
- Bronchospasm → wheezing, respiratory distress.
- Skin: urticaria, angioedema.
Clinical Features
Shock (General Features)
- Hypotension (systolic BP < 90 mmHg or MAP < 65 mmHg).
- Tachycardia, weak thready pulse.
- Cold, clammy skin (except in septic/anaphylactic shock where it may be warm initially).
- Oliguria/anuria (reduced urine output).
- Altered mental status (restlessness, confusion, coma).
- Metabolic acidosis (lactic acidosis).
Anaphylaxis (Specific Features)
- Rapid onset (minutes to hours) after allergen exposure.
- Skin: urticaria, itching, flushing, angioedema of lips, tongue, eyelids.
- Respiratory: throat tightness, stridor, wheeze, dyspnea, cyanosis.
- Cardiovascular: hypotension, shock, collapse, arrhythmias.
- Gastrointestinal: abdominal pain, vomiting, diarrhea.
- Ocular: eyelid edema, conjunctival chemosis, redness, tearing.
Investigations
Diagnosis is mainly clinical; investigations support severity and rule out differentials.
- Shock: CBC (hemorrhage, sepsis), blood cultures, ECG, cardiac enzymes, lactate levels, renal/liver function tests, imaging for cause (CT, echo, ultrasound).
- Anaphylaxis: Serum tryptase levels (rise within 2–3 hours); allergy testing later (skin prick, specific IgE assays).
Management
Shock — General Principles
- Ensure airway, breathing, circulation (ABC).
- Oxygen supplementation; intubation if needed.
- IV access, rapid fluid resuscitation with crystalloids (normal saline, Ringer’s lactate).
- Treat underlying cause (antibiotics for sepsis, reperfusion for MI, relieve obstruction).
- Vasopressors (norepinephrine, dopamine) if hypotension persists despite fluids.
- Monitor urine output, lactate levels, hemodynamics.
Anaphylaxis — Emergency Management
- Adrenaline (epinephrine): First-line, life-saving drug. Give 0.3–0.5 mL of 1:1000 (0.3–0.5 mg) intramuscularly into anterolateral thigh, repeat every 5–15 minutes if needed.
- Airway support: oxygen, intubation if airway compromise.
- IV fluids for hypotension.
- Antihistamines (diphenhydramine, chlorpheniramine) for urticaria and itching (adjunct only).
- Corticosteroids (hydrocortisone, methylprednisolone) to prevent late-phase reactions.
- Bronchodilators (salbutamol) for bronchospasm.
- Monitor for biphasic reaction (recurrence after initial improvement).
Prevention
- Identify and avoid known allergens (foods, drugs, insect stings).
- Screen for drug allergies before prescribing.
- In high-risk patients: carry epinephrine auto-injectors (EpiPen).
- Educate healthcare professionals about early recognition and prompt adrenaline use.
- Immunotherapy (desensitization) for selected allergens under specialist care.
Ophthalmic Importance for Optometrists
- Be aware that fluorescein dye, topical anesthetics, antibiotics, and cycloplegics can rarely trigger anaphylaxis in clinics.
- Recognize ocular signs (eyelid swelling, chemosis, conjunctival redness) as possible indicators of systemic anaphylaxis.
- Optometrists should be trained in emergency management: administer intramuscular adrenaline promptly, call for emergency help, and support airway/breathing.
- Patients with known severe allergies should be advised to carry epinephrine auto-injectors and inform their eye care provider in advance.
Allergy
Introduction:
Allergy is an exaggerated immune response to otherwise harmless environmental substances known as allergens. It is mediated by immune mechanisms, usually IgE antibodies, and manifests in various organs such as the skin, respiratory tract, gastrointestinal tract, and eyes. Allergic diseases are highly prevalent and significantly affect quality of life. For optometry students, understanding allergy is vital because the eye is a common target organ — allergic conjunctivitis, keratoconjunctivitis, and drug-induced hypersensitivity are frequent conditions encountered in eye care practice.
Definition
An allergy is a hypersensitivity reaction initiated by immunological mechanisms, often IgE-mediated (Type I hypersensitivity), against environmental antigens such as pollen, dust mites, animal dander, foods, drugs, or occupational exposures.
Classification of Allergic Reactions (Gell & Coombs)
- Type I (Immediate, IgE-mediated): Rapid onset (minutes), involves mast cell degranulation. Examples: allergic rhinitis, asthma, urticaria, anaphylaxis, seasonal allergic conjunctivitis.
- Type II (Cytotoxic): IgG/IgM antibodies directed against cells → complement-mediated lysis. Examples: autoimmune hemolytic anemia, ocular cicatricial pemphigoid.
- Type III (Immune complex-mediated): Antigen-antibody complexes deposit in tissues → inflammation. Examples: systemic lupus erythematosus, vasculitis, peripheral ulcerative keratitis.
- Type IV (Delayed-type, T-cell mediated): Develops over 24–72 hours. Examples: contact dermatitis (from topical drugs, preservatives), phlyctenular keratoconjunctivitis, tuberculin reaction.
Pathophysiology of IgE-Mediated Allergy
- Sensitization phase: Initial allergen exposure → activation of B-cells → production of IgE antibodies → IgE binds to mast cells and basophils.
- Early (immediate) phase: On re-exposure, allergen cross-links IgE → mast cell degranulation → release of histamine, leukotrienes, prostaglandins → vasodilation, itching, edema, bronchospasm.
- Late phase: Recruitment of eosinophils, basophils, and T-cells → sustained inflammation and tissue damage.
Common Allergic Disorders
- Respiratory: Allergic rhinitis, asthma.
- Skin: Urticaria, angioedema, eczema (atopic dermatitis).
- Systemic: Anaphylaxis (severe, generalized allergy).
- Ocular:
- Seasonal allergic conjunctivitis (SAC).
- Perennial allergic conjunctivitis (PAC).
- Vernal keratoconjunctivitis (VKC).
- Atopic keratoconjunctivitis (AKC).
- Contact allergy to topical drugs, preservatives, or cosmetics.
Ocular Allergy — Clinical Features
- Intense itching (hallmark symptom).
- Redness, watering, burning, photophobia.
- Conjunctival chemosis (swelling).
- Stringy mucous discharge (especially in VKC).
- Giant papillae on tarsal conjunctiva in VKC/AKC.
- Corneal involvement in severe VKC/AKC — punctate keratitis, shield ulcers, scarring.
- Eyelid dermatitis in contact allergy or atopic keratoconjunctivitis.
Investigations
- Clinical diagnosis based on history and symptoms (itching, seasonality, exposure to allergens).
- Skin prick testing — to identify specific allergens.
- Serum IgE levels (total and specific).
- Conjunctival scrapings — eosinophils in severe allergic conjunctivitis.
Management
General Measures
- Avoidance of known allergens (dust control, pollen avoidance, pet dander, cosmetics).
- Use of protective glasses in windy/pollen seasons.
- Cold compresses and artificial tears to reduce irritation.
Pharmacotherapy
- Topical antihistamines: Olopatadine, azelastine, ketotifen — relieve itching and redness.
- Mast cell stabilizers: Sodium cromoglycate, lodoxamide — prevent mast cell degranulation, useful for long-term control.
- Dual-action agents: Combine antihistamine + mast cell stabilization (e.g., olopatadine).
- Topical lubricants: Dilute allergens, relieve dryness.
- Topical corticosteroids: For severe VKC/AKC; short-term use under supervision to avoid complications (glaucoma, cataract, infection).
- Topical immunomodulators: Cyclosporine, tacrolimus in steroid-resistant chronic cases.
- Systemic therapy: Oral antihistamines for generalized allergy; systemic steroids only in severe cases.
Immunotherapy
- Allergen-specific immunotherapy (subcutaneous or sublingual) can provide long-term desensitization in severe cases, especially allergic rhinitis with ocular involvement.
Complications of Ocular Allergy
- Persistent corneal involvement leading to scarring, thinning, and visual loss (especially in VKC/AKC).
- Secondary infections due to chronic rubbing.
- Side effects from prolonged steroid use: glaucoma, cataract, superinfection.
- Reduced quality of life from chronic discomfort and vision fluctuation.
Ophthalmic Importance for Optometrists
- Itching is the cardinal sign of ocular allergy — differentiates it from infective conjunctivitis (more discharge) or dry eye (grittiness).
- Recognize severe forms (VKC, AKC) that may cause vision-threatening complications and refer to ophthalmologists for corneal care.
- Educate patients on allergen avoidance, proper use of eye drops, and risks of unsupervised steroid use.
- Provide supportive therapy (lubricants, cold compresses) and prescribe safe topical antihistamines/mast cell stabilizers where permitted.
