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Veterinary Medicine- Injection reactions
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- 2. INJECTION REACTIONS • Inflammation •Cellulitis • Myositis • Vasculitis /thrombophlebitis • Abscess • Inappropriate route of administration • Intra-arterial injection • Intra-vascular • Extravascular leakage of irritant • Intrarrhachidian cervical injection* • Clostridial myonecrosis • Anaphylaxis • REPORT ADVERSE DRUG REACTIONS!
- 3. INFLAMMATION/INFECTION • Medical terminologyreflects site • Cellulitis • Myositis • Vasculitis • May be inflammatory or infectious • diffuse (cellulitis/infectious cellulitis) • focal (seroma/abscess) • May be life threatening • Therapy • Anti-inflammatory agents: NSAID, topical DMSO • Hot pack • +/- antibiotics
- 4. THROMBOPHLEBITIS • Sequela toIV catheterization and repeated intravascular injections • Prevention is key • Alternate and closely monitor veins • Strict asceptic technique • Recognize high risk patients (severely ill)
- 5. IV CATHETERIZATION Long Term-Polyurethane Short Term- Teflon
- 7. THROMBOPHLEBITIS • Treatment • Restvein • Anti-thrombotics: Aspirin, SQ Heparin (40 IU/kg TID SQ) • Hot pack • Anti-inflammatories: Topical Diclofenamic acid or DMSO • NSAIDS • Antibiotics • Valvular endocarditis is dreaded sequela
- 8. INJECTION ABSCESS • Commonroutes of injection • Which route most associated with abscess formation? • Injection abscess prevention?
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- 12. INJECTION ABSCESS • Findsource • Culture? • Therapy • Lance, drain, and lavage if possible • Anti-inflammatories : NSAID, topical DMSO • Hot pack if can’t be drained • Antibiotics will compromise ability to drain abscess but are indicated if anorexic, febrile and abscess can’t be drained or impinges vital structures
- 14. INTRARRHACHIDIAN CERVICAL INJECTION • Injectionbetween cervical vertebrae that penetrates meninges (intraspinal) • History is critical • Sequelae to incorrect IM injection in neck • Clinical Signs: referrable to NECK PAIN • Reluctant to move • Won’t lower head to eat • improperly called anorexia • Forelimb lameness • usually unilateral on side of injection • Pyrexia • Heat/pain/swelling at injection site are variable
- 15. INTRARRHACHIDIAN CERVICAL INJECTION • Therapy •Antibiotics that cross BBB: • (TMS, Chloramphenicol) • NSAIDs • Topical DMSO • Nursing care • Prognosis: guarded
- 17. INTRA-ARTERIAL INJECTION • Carotidartery • more superficial • near head • caudal 2/3 of the neck • Accidental injection results in • Recumbence within 30 seconds • Seizures, paddling • Blindness • Treatment • Immediately tranquilize with xylaxine (0.44 mg/kg) • Phenobarbitol (5-12mg/kg IV) • Choal Hydrate (to effect) • Supportive care – minimize self trauma • Most animals recover without deficits • Morbidity due to injury • falling or synovial structure laceration
- 18. INTRA-ARTERIAL INJECTION • Oil-BasedIntra-Carotid Injections • Procaine Penicillin, Phenylbutazone, Ceftiofur Crystalline, Diazepam • Higher morbidity, seizure collapse • RAPID DEATH POSSIBLE • If no immediate death, treat as previous slide • Contralateral cortical blindness frequently reported • Cerebral hemorrhage present on necropsy • Water soluable drugs- better prognosis • acepromazine, detomidine, xylazine
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- 27. INAPPROPRIATE INTRA-VASCULAR INJECTION • Drugsthat cannot enter vascular system • can precipitate adverse reactions • Signs are drug dependent • Common with procaine penicillin • after several days of administration (local irritation) • Mistakenly IV • Typically: • excitation, collapse, seizure, paddling • Sudden death possible • Treatment • Immediately tranquilize with xylaxine (0.44 mg/kg) • Supportive care – minimize self trauma • Most animals recover without deficits • Morbidity due to injury • Falling or trauma to synovial structures
- 28. EXTRAVASCULAR LEAKAGE • Extravascular (perivascular)drug deposition • Causes local irritation and tissue necrosis • Can take several days to fully develop • Phenylbutazone is most common • Drugs with High or low pH more likely to irritate • Prevention is key!!! • Re-evaluate needle placement frequently • During injection and if animal moves • Treatment: ‘dilution is the solution to pollution’ • Locally infiltrate area with saline (10-15mL) • +/- dexamethasone, procaine penicillin • Hot pack • Consider ventral drainage if large volume perivascular
- 29. HYPERSENSITIVITY • State ofexcessive reactivity to an antigen • Allergy often used as synonym • Outcome is deleterious rather than protective • Gell and Coombs Classification: • 4 main types of hypersensitivity (I-IV) • Classification based on: • nature of inflammatory response • tissue damage • Covered in depth next semester
- 30. TYPE I HYPERSENSITIVITY •Initial antigen exposure causes antigen-specific IgE synthesis • IgE binds to mast cells or basophils • Antigen RE-EXPOSURE cross- links surface IgE causing mast cell/basophil degranulation
- 31. INFLAMMATORY MEDIATORS Three Sources: 1.Released from mast cell granules 2. Synthesized upon degranulation 3. Brought in: from chemo-attracted cells Commonly Cited Mediators: -Histamine -Cytokines: TNF, IL-4, IL-5, IL-8, IL-13 -Prostaglandins -Leukotrienes -Enzymes -In reality there are hundreds characterized to date
- 32. INFLAMMATORY MEDIATORS 4 primaryeffects: 1.Chemo-attractants upregulate endothelial adhesion molecules • WBC diapedesis 2.vasoactive dilation, permeability, thrombi formation 3.smooth muscle contraction: • bronchoconstriction (dyspnea) • GI spasm (colic) 4.tissue remodeling, injury, +/- destruction
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- 34. INFLAMMATORY MEDIATOR EFFECTS •Mediators havedefined physiologic effects •Clinical outcome of type I reactions depends upon •Characteristics of individual • amount of IgE present • Individual responsiveness to mediators (varies) •Characteristics of allergen • dose • potency •Site of allergen introduction and degree of dissemination • SYSTEMIC • LOCALIZED
- 35. PHYSIOLOGIC EFFECT OF MEDIATORS •DirectAg introduction to blood or rapid absorption widespread activation of connective tissue mast cells in vessels and systemic anaphylaxis •Ag inhalation upper respiratory: rhinitis lower respiratory: recurrent airway obstruction •Skin Localized injection- wheal and flare Disseminated from GI absorption: urticaria
- 38. PHYSIOLOGIC EFFECT OF MEDIATORS 1.Vasodilation •Localized: erythema • Systemic: hypotension 2.Capillary damage • Thrombi • Increased permeability Edema …signs are site dependent! • Skin: urticaria • GI: Diarrhea, Gastric distention and pain (horses can’t vomit) • Upper respiratory tract : Dyspnea • Systemic: Hemoconcentration, Hypoproteinemia ….continued on next slide
- 39. PHYSIOLOGIC EFFECT OF MEDIATORS 3.Smooth muscle contraction • GI: spasm (Colic) • lung: dyspnea, poor oxygenation, decreased pO2, increased pCO2 4. Complement and coagulation pathway activation • Localized: clotting, tissue disruption • Systemmic: disseminated intravascular coagulation 5. Mucous, gastric acid and catecholamine secretion • Lungs: dyspnea and compromised ventilation • GI: ileus 6. Chemotaxis
- 40. TYPE I EQUINE HYPERSENSITIVITY Exactrole of IgE mediated hypersensitivity in horses becomes sketchy: • reagents for equine IgE research have limited availability • Systemic anaphylaxis • Many urticarial reactions • Local anaphylaxis • Insect and parasite hypersensitivities • Atopic dermatitis • Feed Hypersensitivity • Respiratory manifestations • Atopic respiratory disease • Inflammatory Airway disease • Recurrent Airway obstruction
- 41. SYSTEMIC ANAPHYLAXIS (FAIRLY COMMON) •Anaphylactic Shock • Onset within 30 min of Ag exposure (hours if Ag is metabolite) • Immunologic vs Non-immunologic triggering • Most common antigens are biologics: • Sera, vaccines (IgE-Driven) • Therapeutics less common • small simple molecules • Often via direct activation of Complement-kinin system • Structurally related compounds can cross react • Disease can be localized or systemic • Localized reaction can progress to life threatening systemic RXN
- 42. SYSTEMIC ANAPHYLAXIS • Anydrug, via any route, at any time • Longer duration, higher dose increases risk • Atopic individuals higher risk (IL-4, IL-13/Th2) • Examples: • thiamine, vitamin E, Selenium • anthelmintics • penicillin, TMS, chloramphenicol, aminoglycosides, tetracyclines • halothane, guaifenesin
- 43. SYSTEMIC ANAPHYLAXIS LUNGS andGI are target organs in horse!! • Vasodilation Erythema, Hypotension • Capillary damage Edema, Hypovolemia, Hypotension • Smooth muscle contraction lung: dyspnea GI: cramping (Colic) uterus: abortion • Mucous secretion Dyspnea +/- Diarrhea • Chemotaxis Induration • Perpetual Cycle LATE PHASE REACTION
- 44. ANAPHYLAXIS • Differentials: • Druginteractions • Inappropriate route • Others specific to signs demonstrated • Colic differentials • Respiratory disease • Other (uriticaria differentials…etc) • Diagnostics • Signs and history • CBC and serum biochemistries are variable • ECG: can develop signs of hypoxemia • prolonged QRS, ST depression
- 45. TREATMENT EARLY INTERVENTION ISKEY • Not all reactions require therapy • Sudden Dyspnea and hypotension warrant aggressive therapy • monitor less severe reactions closely • Goals: • counteract mediators • maintain respiratory and CV stability
- 46. TREATMENT • Remove antigen!!!! •Place IV catheter • Assure airway – tracheotomy may be required • GLUCOCORTICOIDS *hallmark of Rx* • Prednisolone sodium succinate • 0.25-1.0 mg/kg • IV fluids: shock volumes • Oxygen • Cardiac monitoring • Epinephrine…with caution • Antihistamines, NSAIDS
- 47. EPINEPHRINE THERAPY IN HORSES •Why? sympathetic stimulant: α1, α2, β 1, β2 • KNOW how the drugs work • Excitement • IV admin to standing horse is ill advised • IM (10-20 ug/kg = 5-10 ml of 1:1000) • If dyspnea or hypotension are mild • IV (3-5 ug/kg = 1.5-2.25 ml of 1:1000) • If severe dyspnea or hypotension • Endotracheal if no venous access • Repeat every 15 minutes until hypotension improves • Refractory cases may need epinephrine or norepinephrine CRI
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Editor's Notes
- #4 Most commonly Jugular, other places- RLP sites. Septic vs non-septic
- #5 Long Term- Polyurethane Short Term- Teflon
- #14 Intra-ra-kid-ean
- #17 Water soluable drugs- better prognosis (acepromazine, detomidine, xylazine) Oil-Based Drugs- rapid death possible (procaine penicillin, Ceftiofur crystalline- Exceed, diazepam)
- #18 Water soluable drugs- better prognosis (acepromazine, detomidine, xylazine) Oil-Based Drugs- rapid death possible (procaine penicillin, Ceftiofur crystalline- Exceed, diazepam)
- #19 Alcohol, hold off
- #41 Can be activation of IgE (larger molecules, previous sensitization) or- direct activation of complement-kinin system by some part of the drug (usually smaller molecules)