PAIN
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- Pain is a normal uncomfortable response to a noxious stimulus or tissue damage that alerts the person to danger.
- OR it can be neuropathic in nature, where pain occurs due to nerve injury without actual tissue damage.
- Chronic pain can lead to…
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- Psychological - depression
- Disuse of limb - wasting, osteoporosis
- Immobility - obesity, metabolic disease
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- 1. Gate Theory -
- non painful input closes nerve gates to painful input in the spinal cord
- This is demonstrated when we rub an area after hitting our leg - the non-painful input closes the painful nerve gates.
- This principle underlies certain pain treatments such as electrostimulation
- 2. Opioid System -
- opioid receptors in spinal cord and brain (mu, delta and kappa) that modulate pain
- When activated, these inhibit the release of substance P, reducing pain
- 3. Descending inhibitory system
- Suggests that chronic pain results from dysfunction in the inhibitory system
- Thus, serotonin reuptake inhibitors can help with pain
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- Femoral nerve block - (-) Quadriceps weakness affecting therapy
- Adductor canal block - (+) no quadriceps weakness
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- Mechanism not well understood, inhibits prostaglandin synthesis
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- Inhibits COX (cyclooxygenase) enzymes which catalyze conversion of arachidonic acid to prostaglandins and thromboxane (anti-inflammatory)
- COX-1 enzymes - present in gastric mucosa, kidney
- COX-2 - active in inflammation
- Thus, newer selective COX-2 inhibitors (e.g., etoricoxib) aim to reduce side effects
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- Mimics endogenous opioid peptides by binding to opioid receptors (specifically mu receptors in the CNS) to reduce pain
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- It functions as a Gamma-Aminobutyric Acid (GABA) mimetic
- Binds to Alpha 2 Delta site in CNS, reducing release of neurotransmitters Glutamate and Norepinephrine
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- Concept was established by Crile in 1913
- Defined as "anti-nociceptive treatment that prevents the establishment of altered central processing of afferent input, which amplifies pain after TKA"
- This approach uses multimodal analgesia administered before pain onset
NERVE PAIN
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- Nociceptive pain caused by actual tissue damage while neuropathic pain results from damage to or pathological change in the nerves.
- Examples - spinal stenosis, radiculopathy, phantom limb pain
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- Stepwise ladder
- Paracetamol
- Tricyclic Antidepressants (TCA) - Amitriptyline. Monitor for cardiac toxicity
- Anticonvulsants - Gabapentin, pregabalin
- Tramadol
- Pain team referral
CRPS
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- Complex Regional Pain Syndrome is syndrome associated with 5 Features PSSAO
- 1. Disproportionate pain (allodynia)
- 2. Swelling
- 3. Stiffness
- 4. Autonomic disturbance - discoloration, trophic changes
- 5. Disuse osteopenia
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- CRPS develops when a persistent noxious stimulus (e.g., distal radius fracture) leads to peripheral and central sensitization, resulting in abnormally heightened sensation including spontaneous pain
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- Type 1 - No nerve injuries or lesions (90%)
- Type 2 - Presence of nerve injury - requires nerve conduction study
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- Acute - localized, painful, warm, dry and red, normal bones
- Subacute (Dystrophic) - becomes cold with muscle wasting, shows osteopenia on X-ray
- Chronic (Atrophic) - less pain but muscle becomes atrophic, skin glossy, severe osteoporosis
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- Budapest Criteria - based on symptoms and signs in 4 categories - sensory, vasomotor, sudomotor, motor
- Sensory = allodynia
- Trophic = reduced ROM, reduced hair
- Vasomotor = Temperature asymmetry
- Edema = swelling, sweating changes
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- CRPS – Based on AAOS CPG (moderate) and RCT by Zollinger et al. 2007, incidence of CRPS 10% in placebo, 2% in vitamin C
- Zollinger - RCT of 416 patients randomized to placebo/200/500/1500mg vitamin C daily. Placebo group 10% vs Vitamin C group 2.4%. Recommended dose is 500mg once daily for 50 days
- Dose = 500mg once daily for 50 days
- Also, avoid tight casts and painful manipulations
zollinger2007.pdf748.6KB
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- Early diagnosis, exclude infection (blood tests)
- Reassure patient
- Refer for physiotherapy - for mobilization
- Refer to Pain clinic - anesthesia for possible sympathetic blockade
Local Anaesthetics
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- All LA produce effects by blocking sodium gated voltage channels, preventing depolarization of the nerve cell and propagation of action potential down the nerve
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- Amides
- Long acting - bupivacaine, ropivacaine
- Short acting - lidocaine
- Vasopressors can be added (e.g., adrenaline) to prolong duration of action
- Esters - cocaine, chloroprocaine, benzocaine - rarely used
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- First, establish a second IV line in the other arm for potential resuscitation, and ensure crash cart is nearby
- Place tourniquet on arm
- Inflate cuff to 100mmHg above patient's SBP
- LA injected - Dose?
- Dose = 3mg/kg
- Cuff should remain inflated for MINIMUM 20-25min post injection, MAXIMUM 60-90min
- Deflate briefly for 10s, then reinflate. If no signs of toxicity after 45s, deflate again for 5-10s. Repeat once more before permanent removal
- This allows gradual release of local anaesthetic into systemic circulation at intervals, preventing toxicity from sudden large bolus release
- Monitor for toxicity signs - headache, dizziness, cardiovascular collapse, seizures
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- Infection decreases pH → less effective
- Infection increases blood supply → LA cleared from area before taking effect
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- Get help from emergency medicine or anaesthesia colleagues
- ACLS - SLE
- ACLS - bag valve mask, low-dose epinephrine, amiodarone for arrhythmias
- S - seizure suppression with benzodiazepines
- L - Lipid emulsion therapy with 20% intralipid
- ECMO
General Anaesthetics
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- Triad of analgesia, amnesia, and muscle relaxation
- Balanced anaesthesia involves combining drugs in smaller doses to minimize side effects
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- 3 main classes of drugs:
- Inhalational induction agents - isoflurane, sevoflurane, desflurane
- Intravenous induction agents - midazolam, ketamine, propofol, etomidate [TIVA: total intravenous anaesthesia]
- Paralytics - neuromuscular blockers
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- Non-depolarizing - blocks binding of acetylcholine to nicotinic receptors at post-synaptic membrane [competitive inhibitors], e.g., atracurium, rocuronium
- Depolarizing - depolarizes the post-synaptic membrane (causing initial fasciculations followed by a second phase), e.g., suxamethonium
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- Neostigmine - antagonist to acetylcholinesterase. Prevents breakdown of acetylcholine, leading to increased acetylcholine at neuromuscular junction
BLOOD REPLACEMENT
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- Whole Blood [no more]
- Shelf life 1 month
- Packed Cells
- Obtained via centrifugation
- Shelf life 35 days
- Platelet Concentrate
- Shelf life 5 days
- Fresh Frozen Plasma
- Unconcentrated source of all clotting factors without platelets
- Cryoprecipitate
- Concentrated clotting factors containing factors 8, 13, fibrinogen, and von Willebrand factor
DVT/ TXA
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- Intrinsic and Extrinsic pathways
- https://www.youtube.com/watch?v=s4FoSf6Yi_s
- Draw intrinsic pathway: Factor 12 (activated by damaged endothelial tissue) ➔ 11 ➔ 9 ➔ 10 ➔ 2 (Prothrombin) ➔ Fibrinogen
- Add factors 8 and 5
- Draw extrinsic pathway: Factor 3 (tissue factor released from damaged tissue) ➔ 7
- Common pathway involves factors 10, 5 and 2 (aka thrombin) [2 × 5 = 10]
- Thrombin (factor 2) converts fibrinogen (factor 1) to fibrin to form the clot.
- The intrinsic and extrinsic pathways converge into the common pathway, which involves factors 10, 5 and 2 (aka thrombin). Thrombin converts fibrinogen to fibrin to form a clot. The intrinsic pathway involves factors 12, 11 and 9, while the extrinsic pathway involves factors 3 and 7.
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- Extrinsic pathway = PT and INR
- Intrinsic pathway = PTT
- Platelet function = Bleeding Time
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- Stasis, Coagulopathy, and Endothelial damage
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- Clot dissolution is performed by plasmin
- Plasminogen is converted to plasmin by Tissue Plasminogen Activator (TPA)
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- Prevents clot breakdown and reduces bleeding
- Acts as an antifibrinolytic by preventing the conversion of plasminogen to plasmin, which in turn prevents clot dissolution
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- Can be active or passive
- Passive = provides a structural matrix for platelet aggregation, e.g., Gelfoam, alginate
- Active = contains clotting factors, e.g., Floseal, Tisseel
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- Floseal = thrombin (factor 2) + gelatin
- Tisseel = thrombin + fibrinogen
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- Based on NICE guidelines 2018 (https://www.nice.org.uk/guidance/ng89/chapter/recommendations#interventions-for-people-having-orthopaedic-surgery)
- Elective TKR. Total 14 days. Choose either:
- LMWH for 14 days OR
- Aspirin 75 or 150mg for 14 days OR
- Rivaroxaban
- Elective THR. Total 28 days. Choose either:
- LMWH for 10 days followed by aspirin 75/150mg for 28 days OR
- LMWH for 28 days OR
- Rivaroxaban
- Hip Fracture. Choose either:
- LMWH starting 6-12 hours after surgery
- Continue until patient is adequately mobile
- Consider preoperative dose if surgery is delayed. Give last dose >12 hours before operation for LMWH
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- AAOS guidelines - against routine post op Duplex US (strong evidence)
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- 5 main groups - warfarin, heparin, NOAC, platelet inhibitors, and dabigatran
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- Affects factors 2/7/9/10. Check PT/INR
- Reversal via Vitamin K, FFP (contains all clotting factors) or Cryoprecipitate (contains fibrinogen, vWF, Factors 8, 13)
- Half-life - 5 days
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- LMWH (aka Clexane) = Enoxaparin (works on 10a + 2a)
- Short 12-hour half-life
- Unfractionated Heparin
- MOA: binds to antithrombin 3
- Fondaparinux
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- Direct Factor 10 inhibitors: apixaban, rivaroxaban, edoxaban
- Direct thrombin (Factor 2 inhibitor): dabigatran
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- Aspirin = inhibits COX that produces prostaglandins
- Plavix = inhibits ADP binding to platelets receptor
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- Previous DVT
- Malignancy
- On oral contraceptive pills
- Pregnancy
- Congenital thrombophilia
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- Clinical - check for calf suppleness; ultrasound lower limbs
- Signs of PE - tachycardia, hemoptysis
- Well's criteria for PE: history of cancer, immobilization, previous PE
- Well's Criteria ➔ if > 4 points, PE likely ➔ Consider CT angiogram
- If < 4 points, PE unlikely ➔ do D-dimer
- If D-dimer positive ➔ CT angiogram
- If D-dimer negative ➔ stop workup
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- Albumin
- Bilirubin
- Coagulopathy
- Distension
- Encephalopathy
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- Increased bleeding risk — managed with tranexamic acid and cell saver
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