Pain and Palliative Care Anesthesia

Sub-Dissociative Dose Ketamine (SDK) in Pain Management 1. Pharmacology & Mechanism of Action Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist. In sub-dissociative analgesic doses (0.1–0.3 mg/kg IV), ketamine blocks NMDA-mediated central sensitization, wind-up phenomenon, and hyperalgesia without inducing general anesthesia or procedural dissociation. 2. Dosing Spectrum & Clinical Administration Dosing Category Intravenous Dose Range Primary […]

Local Anesthetics in Pain Management: Pharmacology & Safety Protocols 1. Mechanism of Action & Nerve Blockade Local anesthetics prevent conduction of nerve impulses by reversibly binding to the intracellular domain of voltage-gated sodium (Na+) channels. By stabilizing the inactivated state, local anesthetics inhibit rapid depolarization and action potential propagation in peripheral nerve fibers (C >

NEUROPATHIC PAIN  BRIEFThis guide translates Neuropatic pain: Fundamental neurophysiology and pharmacology into structured bedside diagnostic and therapeutic pathways. DEFINITION AND ETIOLOGY Neuropathic pain: Defined by the International Association for the Study of Pain (IASP) as pain caused by a lesion or disease of the somatosensory nervous system .  It is critical to recognize that neuropathic

Nociceptor Classification and Molecular Transduction Clinical Pearls & Key Takeaways •  Temporal Distinction: The dichotomy between ‘first’ and ‘second’ pain is purely a function of conduction velocities between fast myelinated Aδ and slow unmyelinated C fibres. •  Molecular Transduction: TRPV1 acts as a non-selective gating channel responsive to heat and local acidosis, whereas mechanical noxious

Neurotransmitters in Pain Neurotransmitter Role in Pain Modulation Mechanism of Action Glutamate Primary excitatory neurotransmitter; mediates nociceptive signal transmission in the spinal cord and brain. Activates NMDA and AMPA receptors, facilitating excitatory neurotransmission and central sensitization. Substance P Facilitates pain transmission and inflammation by promoting neurogenic inflammation and sensitization. Binds to neurokinin-1 (NK1) receptors; increases

Pain Assessment Tools & Scales 1. Core Principles of Pain Assessment Pain is inherently subjective, making self-reporting the gold standard of pain assessment whenever possible. However, the inability to communicate verbally does not negate the possibility that a patient is experiencing pain. Modern clinical guidelines (such as the PADIS guidelines) emphasize a hierarchical approach to

Referred Pain and Dermatomes  Referred Pain: Pathophysiology & Mechanisms Referred pain is a phenomenon where pain is perceived in an area remote from the site of the actual nociceptive stimulus. This is a highly tested concept across critical care and anaesthesia boards, heavily relying on neuroanatomical principles. The definitive, evidence-based explanation for referred pain is

Central and peripheral sensitization IASP Definitions & Taxonomy The foundation of any pain chapter must align with the International Association for the Study of Pain (IASP) taxonomy. Peripheral Sensitization: “Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields” (Curatolo, 2024). It is clinically associated with primary