Unintentional intra-arterial injection: Difference between revisions
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Is often multifactorial and dependent upon type of medication administered. Theories include NE induced vasospasm, crystal formation, venous constriction, lipid solubility, direct cytoxicity, endothelial damage and high osmolality. All pathways suggest the primary mediator of tissue injury is '''thrombosis'''<ref>Sen S, Chini E, Brown M. Complications After Unintentional Intra-arterial Injection of Drugs: Risks, Outcomes, and Management Strategies. Mayo Clinic Proceedings 2005. 80(6):783-795</ref> | Is often multifactorial and dependent upon type of medication administered. Theories include NE induced vasospasm, crystal formation, venous constriction, lipid solubility, direct cytoxicity, endothelial damage and high osmolality. All pathways suggest the primary mediator of tissue injury is '''thrombosis'''<ref>Sen S, Chini E, Brown M. Complications After Unintentional Intra-arterial Injection of Drugs: Risks, Outcomes, and Management Strategies. Mayo Clinic Proceedings 2005. 80(6):783-795</ref> | ||
===Medications known to cause severe injury if administered IA:== | ===Medications known to cause severe injury if administered IA:=== | ||
* Benzodiazepines | * Benzodiazepines | ||
* Barbiturates | * Barbiturates | ||
Revision as of 17:24, 3 June 2016
Background
Accidental intra-arterial cannulation and administration of medications can result in severe pain, paresthesias, swelling. In severe case, direct vascular and tissue injury can progress to compartment syndrome, gangrene and even auto-amputation. This is significant and potentially severe complication of medication administration that every provider should be able to recognize. Must consider this scenario any time patient begins complaining of paresthesias or pain distal to IV site. Self-inflicted cases are also being described in patients with IVDA
Risk Factors
Include:[1]
- Obesity
- Hypotension
- Procedurally difficult situations (ie. agitated patient, back of ambulance)
- Aberrant vascular anatomy
Pathophysiology
Is often multifactorial and dependent upon type of medication administered. Theories include NE induced vasospasm, crystal formation, venous constriction, lipid solubility, direct cytoxicity, endothelial damage and high osmolality. All pathways suggest the primary mediator of tissue injury is thrombosis[2]
Medications known to cause severe injury if administered IA:
- Benzodiazepines
- Barbiturates
- Propofol
- Penicillins
- Amphetamines
- Phenothiazines
- Phenytoin
- Heroin
- Tubocurarine
- Atrcurium
- TPN
- NaHCO3
- Hypertonic Dextrose (D50)
Clinical Features
Differential Diagnosis
Diagnosis
Management
- Maintain catheter in place - to be used for arteriogram and administration of vasodilators
- Thoroughly evaluate medications administered through this catheter
- Evaluate severity of injury (soft compartments, neuro-vascular exam)
- Consider anticoagulation with heparin initial loading dose 60IU/kg
- Treat pain and symptoms
- Hypertonic dextrose - no antidote
- Serial compartment exams
- Pain control
Disposition
See Also
External Links
References
- ↑ Sen S, Chini E, Brown M. Complications After Unintentional Intra-arterial Injection of Drugs: Risks, Outcomes, and Management Strategies. Mayo Clinic Proceedings 2005. 80(6):783-795
- ↑ Sen S, Chini E, Brown M. Complications After Unintentional Intra-arterial Injection of Drugs: Risks, Outcomes, and Management Strategies. Mayo Clinic Proceedings 2005. 80(6):783-795