The case for multimodal emergency analgesia
Pain management is among the most important tasks of the emergency physician (EP). Pain is a primary presenting complaint in the majority of emergency department (ED) patients and EP’s are expected to possess a mastery of pain management well beyond that of most other types of physicians.1,2 Commonly encountered painful conditions range from major burns to acute fractures to vascular headaches to cancer pain to chronic lumbar back pain. Additionally, minor surgical procedures, fracture reductions, and many other invasive procedures are both commonplace in ED practice and often very painful. The wide range of painful conditions among the highly variable ED patient population presents both a challenge and an opportunity for optimal pain management.
The physical and emotional impacts of untreated pain in the emergency department are significant and potentially long lasting. A humanistic approach demands attention to the personal suffering and the associated fear and anxiety of uncontrolled pain. From a physiologic standpoint, severe pain has been convincingly linked to a systemic stress response, in turn associated with delirium, hyperglycemia, immunosuppression, hypercoagulable states,and ultimately increased morbidity and mortality. Long-term sequelae include delays in physical recovery, chronic pain syndromes such as complex regional pain syndrome (CRPS), and psychological disorders such as post-traumatic stress disorder (PTSD).3-6
Although emergency physicians traditionally focus on diagnosis and treatment of acute life-threatening conditions, the morbidity associated with uncontrolled pain has too often been overlooked. Although the undertreatment of pain, or oligoanalgesia, is prevalent in the ED, the armamentarium of available agents and modalities for emergency pain management is large and ever-growing, empowering the EP to effectively manage all types of pain across a wide spectrum of patients. This chapter reviews the current state-of-the-art of ED pain management, with an emphasis on integrating peripheral nerve blocks into a multimodal approach.
The neurobiological basis of multimodal pain management The experience of pain is produced and maintained through a complex set of mechanisms throughout the peripheral and central nervous systems. Mounting evidence suggests thatacute pain management should simultaneously target the multiple pathophysiologic targets that exist along the entire pain pathway. Practically, multimodal analgesia involves combining medications with different and complimentary mechanisms of action in a tailored approach based on both the type of pain and the type of patient. Goals include rapid and effective acute pain management, prevention of short term suffering and pain-induced physiological derangements, and the reduction of long-term sequelae such as chronic pain.
Acute tissue damage produces pain via the direct opening of synaptic ion channels sensitive to mechanical and thermal stimuli, and by the release of tissue chemical mediators such as prostaglandins that sensitize afferent nociceptive fibers. Once activated, afferent C-fibers reflexively amplify the local tissue through antidromic signaling in which collateral afferents release sensitizing neurohormonal chemical mediators into the tissue adjacent to the injury site. The combination of direct mechanical disruption and the development of “sensitizing soup” around the sensory afferent culminates with membrane depolarization and transduction of an impulse through the peripheral nerve toward the central nervous system.
Nerve block anatomy A peripheral nerve is composed of efferent and afferent axons of various types. Each axon (and its schwann cell myelin sheath depending on the fiber type, is suspended in a delicate connective matrix termed the endoneurium. Bundles of axons and their endoneurium are organized into fascicles by an encasing squamous epithelial sheath termed the perineurium. The macroscopic peripheral nerve is formed by the epineurium’s connective tissue that bundles fascicles together into a distinct cord-like structure. The peripheral nerves often travel in a fascial plane or “gliding sheath” that allows musculoskeletal freedom of movement while minimizing mechanical stress on the nerve itself. A regional block is placed by perineural injection of local anesthetic inside this sheath. After perineural injection, local anesthetic then diffuses inward from the epineurium towards the axonal membrane itself where it its direct action takes place. Diffusion of local anesthetic along the tissue concentration gradient results first in blockade of the exposed, outermost mantle fascicles that typically innervate the most proximal anatomic regions. Block recovery results from diffusion of the local anesthetic out of the nerve as well as absorption by the vascular bed. Due to the increased vascularity of the nerve central core, recovery typically progresses in reverse fashion with the most distal anatomic areas regaining function first.
Further reading
Cousins, Michael J. Cousins and Bridenbaugh's neural blockade in clinical anesthesia and pain medicine. 4th Ed. Lippincott Williams & Wilkins, 2012.
Hadzic, Admir. Regional Anesthesia and Acute Pain Management. McGraw-Hill Medical, 2007.
Gregoretti, Cesare, et al. "Regional anesthesia in trauma patients."Anesthesiology Clinics 25.1 (2007): 99-116.