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ANAESTHESIA NEWS
Anesthesia News
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- 2 years, 1 month ago
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ANAESTHESIA NEWS
CAN DEXTOMETOMIDINE BE USED AS PREMEDICATION IN IM ROUTE ? WHAT DOSE ? CAN WE USE PROPOFOL IN INFANTS? THANKS | |
Dr.Palanivel Rajan |
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Dexmedetomedine has shown to be more effective as premedication by intranasal route than intramuscular route. There are not many recent studies on intramuscular dexemedetomedine as premedication. Dexmedetomidine premedication in low dose (1 μg.kg-1) by intramuscular route can induce preoperative sedation and adjuvant anaesthetic effects without clinically significant bradycardia or hypotension. Med Sci Monit. 2014 Dec 18;20:2714-9 For induction of anesthesia, an intravenous dose of 2.5-3.5 mg/kg administered over 20-30 seconds is recommended for children. More rapid administration of propofol is associated with a greater risk for hypotension. The induction dose may be followed by an infusion of 7.5-18 mg/kg/hr (125-300 mcg/kg/min) for maintenance of general anesthesia. In the intensive care setting, lower doses of 1-4 mg/kg/hr should be used, with titration to the desired response. Propofol. In: Olin BR, ed. Drug Facts and Comparisons. St. Louis: Facts and Comparisons. 2000: 990-3. Norreslet J, Wahlgreen C. Propofol infusion for sedation of children. Crit Care Med 1990;18:890-2 Reed MD, Yamashita TS, Marx CM, et al. A pharmacokinetically based propofol dosing strategy for sedation of the critically ill, mechanically ventilated pediatric patient. Crit Care Med 1996;24:1473-81. |
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ADDITIVES TO SAB BUPIVACAINE -ADRENALINE AND MAGNESIUM HOW AND IN WHAT DOSES ARE THEY USED. SOMEANESTHETIS FLUSH SYRINGE WITH ADRENALINE THEN LOAD BUPIVACAINE ANESTHESIA LASTS FOR 6HRS WITHOUT ANY COMPLICATIONS.ARE THESE DRUGS APPROVED TO BE USED IT | |
prema |
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MAGNESIUM SULPHATE IN SPINAL ANAESTHESIA: MgSO4 has been added to spinal bupivaccine in a dose of 50 to 100mg (MgSO4 50% – 0.1- 0.2 ml). It has been shown to increase the duration of sensory block and decrease the postoperative analgesic requirement in the first 24 hours. But the onset of sensory block is delayed compared to plain heavy bupivacaine. BUPIVACANE and ADRENALINE IN SPINAL ANAESTHESIA By reviewing the literature, it is found that 0.2 to 0.4 mg adrenaline can be safely added to prolong the spinal bupivacaine. It is claimed to prolong the sensory analgesic duration by 40 to 50%. The fear of causing intense vasoconstriction and spinal cord ischaemia is unfound. The animal studies had proved that spinal adrenaline doesn’t cause cord ischaemia to that extent of causing neuronal damage. But we don’t know the amount of added adrenaline in rinsing the syringe. And this technique has lost popularity after the free availability of epidural catheters. The sodium meta-bisulphite in some of the adrenaline preparations is found to be safe when given intrathecally in minute quantity. But now preservative free adrenaline is available in the market. Prof.Dr.R.Selvakumar |
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SIR IS SPINAL ANAESTHESIA CONTRAINDICATED IN PATIENTS WITH MULTIPLE SCLEROSIS? | |
sai suraj |
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SPINAL ANAESTHESIA IN MULTIPLE SCLEROSIS: Multiple sclerosis is a degenerative disease of the CNS, characterised by multiple sites of demyelination in the brain and spinal cord. The course of the disease consists of exacerbations and remissions of symptoms. Stress, surgery and fatigue have been implicated in the exacerbation of multiple sclerosis. Spinal anaesthesia which results in high concentration on L.A. in the spinal white matter may produce relapse of the demyelination. Even though direct correlation between local anaesthetics and white mater toxicity is lacking, it is better to avoid spinal anaesthesia in multiple sclerosis. If regional anaesthesia is compulsory because of coexisting illnesses (pulmonary or difficult airway) epidural is better compared to spinal. Because of the fact that the local anaesthetic concentration inside the spinal cord is lower with epidural technique than with subarachnoid block. And another strong reason to avoid neuraxial block in Multiple sclerosis is medico legal. In a progressive neurological illness like Multiple sclerosis, which may coincidentally worsen in the post- operativeperiod and the anaesthetic technique will be blamed. If at all regional anaesthesia has to be contemplated, peripheral nerve block has to be considered as the peripheral nerves are not involved in M.S. Ref: Regional anaesthesia in the patient with pre-existing neurologic dysfunction.-Terese .T.Horlocker , Mayo clinic, Minnesota. |
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WHY IS THERE NO PRESERVATIVE IN BUPIVICAINE HEAVY WHILE IT IS THERE IN BUPIVICAINE PLAIN? | |
Aditya |
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The preservative, Methyl Paraben is added to the multi dose bupivacaine vial as an anti-microbial agent. It doesnot prevent the drug being degraded on prolonged storage or stored in unfavourable climatic conditions. Anti-microbial agent is needed only for multi-dose vials, not for single dose spinal ampoules. That is why bupivacaine heavy is marketed without preservative.
Some additional facts about parabens: Metabolism of parabens results in the formation of PABA derivatives which are potentially allergic products. Often the allergic incidences following amide local anaesthetics are blamed due to its preservatives (parabens) and may be true also. But animal studies and human volunteer studies show that parabens( methyl,ethyl,butyl and propyl) are relatively safe additives. They have been approved by the FDA as standard preservative agents as an anti-microbial agent in many foodstuffs, cosmetics and dermatological preparations (with a safe limit of less than 0.1%). They have not demonstrated any untoward reactions with parabens except some contact dermatitis. If accidental injection of multi dose local anaesthetic agent with paraben in to the thecal sac occurs after an attempted epidural (Total Spinal), the nervous tissue is exposed to the parabens. Even though there is a theoretical possibility of neurotoxicity is there, there is no direct conclusive evidence for the same. It is proved that Rabbit vagus nerve incubation with 0.1% methyl paraben suppresses nerve excitability in a dose dependant manner but does not destroy nervous tissue. Even then FDA did not approve preservative containing local anaesthetic being used in epidural and caudal anaesthesia. Dr.R.Selvakumar |
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HOW DO YOU USE SUGAMADEX? | |
julia oliveira |
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Sugammadex is not available in the drug market because it is not approved by FDA. Here are few interesting facts about Sugammadex.
Sugammadex Is Unique:
Sugammadex is indicated in adults for:
Dosing Recommendations Routine Reversal
Immediate Reversal
Mechanism of Action
FDA Approval Status On September 23, Merck Inc. announced it had received a Complete Response Letter from the U.S. Food and Drug Administration (FDA) informing the company that its resubmitted New Drug Application for sugammadex had been rejected. According to Merck, the FDA raised issues with \\\”operational aspects of a hypersensitivity study\\\” that the FDA had requested in 2008. ASA had previously expressed strong support for the approval of sugammadex in a formal comment letter to the FDA’s Anesthetic and Analgesic Drug Products Advisory Committee. |
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ABOUT THE REASON FOR Y 33% OXYGEN WE USIN IN BOYLES MACHINE .. I SEARCHED IN MANY BOOKS COULDN’T GET EXACT REASON . PLS SAY SIR | |
drsan |
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HEG Boyle designed his anaesthesia machine in 1917. Many modifications have taken place since then. Understanding of gas and agent consumption have paved the way for safe anaesthesia with minimal pollution and cost containment.
Conservation of mass applies but is not necessary to compute equilibrium conditions. No matter what the starting concentrations of gases in the circuit, the circuit concentration will head toward and eventually reach the concentration of the net flow of gases into the breathing circuit. Net flow is fresh gas flow minus uptake. FGF is comprised of individual flows of oxygen, nitrous oxide, air and vapor Uptake includes oxygen consumption, nitrous oxide uptake, nitrogen uptake and vapor uptake. Oxygen uptake is 200 ml, nitrogen is 0 and nitrous oxide is 100ml/min. carbon dioxide is taken care by circuit design. In practice we have high flow or low flow and air-oxygen or nitrousoxide-oxygen or a combination. 33% oxygen with 66% air gives just above 50% FiO2hence 50% FiO2 is considered safe for low flow anaesthesia. When used with nitrous oxide, 65-70% nitrous oxide is required to get required anaesthetic benefits of the agent. Hence 33% oxygen may be appropriate. At higher the flow lower FiO2 can be used but as we go for low flow higher FiO2 should be used. Suggested reading:TOTALLY CLOSED CIRCUIT NITROUSOXIDE/OXYGEN ANAESTHESIA.F.BARTONANDJ.F.NUNN. Br.J.Anaesth.(1975),47,350 Dr. Prasanta Kumar Dash. |
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SIR CAN U TEL REVERSAL CRITERIA AFTER GA.. | |||||||||||||||
drsan |
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Controversies: |
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MAXILLOFACIAL ANESTHESIA? | |
mostafa |
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For “Anaesthesia and common oral and maxillo-facial emergencies”
Ref: Monica Morosan, Anaesthesia and common oral and maxillo-facial emergencies. For “Oral and Maxillofacial Regional Anesthesia” Ref: Benaifer D. Oral and Maxillofacial Regional Anesthesia. |
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WHAT IS THE ANAESTHETIC MANAGEMENT OF EXPLORATORY LAPAROTOMY WITH UPPER ABDOMINAL INCISION ONLY UNDER EPIDURAL ANAESTHESIA.. | |
drpravin2003 |
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Exploratory laparotomy can be done under lone Epidural anaesthesia in selected cases.( Thin patients, experienced and understanding surgeon). The level of block needed for the upper abdominal surgery shall be from T4 to S5. The lower lumbar and sacral segments have to be blocked for bladder catheterisation and perineal procedures, if any. Otherwise it’s enough to block up to L2. For that, the epidural catheter placement must be done at T8-9 or T9-10. Lower thoracic epidural needle placement is easy when compared to middle thoracic needle entry. It’s necessary to thread the catheter 3 -5 c.m in to the epidural space and not more than that. For an average Indian adult, the 9 or 10 cm mark in the epidural catheter should be at the skin level. Too much threading the catheter will favour its paravertebral entry and result in patchy analgesia.
Test dose with 3 ml of 1.5% Lignocaine with Adrenaline should be done through the catheter. Absence of heart rate increase more than 10 per minute within 10 seconds of test dose administration rules out intravascular placement of epidural catheter. After successful test dosing, the initial dose can be given with 10 � 12 ml of 1.5% Lignocaine with adrenaline (if adrenaline is not contra-indicated). Approximately 1.5 � 2 ml of local anaesthetic solution will be needed per segment to be blocked. I prefer to use Lignocaine as the first dose because of its short onset of action and reduced toxicity.br/> But personally I feel, lone epidural anaesthesia may not be an ideal anaesthetic technique for an exploratory laparotomy .The exaggerated and inevitable B.P fall, uncomfortable patient because of unblocked vagus, intact sensation in the under surface of the diaphragm and moderate abdominal relaxation make epidural as the 2nd choice for the proposed surgery after G.A. I used to tell my P.Gs, Regional anaesthesia for upper abdominal surgery is like travelling in the bus sitting in a lady’s seat. Sometime you may complete the journey without being disturbed. Even if you are not disturbed, you will be tensed up in all the bus stops to see any lady coming towards your seat. Likewise lone epidural anaesthesia may make you and your patient uncomfortable in all stages and may force you to sedate him heavily, losing the advantage of regional Epidural is a nice technique when it is combined with G.A for upper abdominal Dr.R.Selvakumar |
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65YEAR FEMALE PATIENT POSTED FOR OPEN URETERLITHOTOMY.O/E SHE HAVE ABESNT RADIAL PULSE ON RIGHT SIDE.B.P.NOT RECORDABLE ON RT ARM.LT SIDE ABSOLUTELY NORMAL. ON 2D ECHO THERE IS NO COARCTATION OF AORTA.CHEST X RAY IS NORMAL. WHAT IS THE ANAESTHETIC SIGNIFICANCE ,ANY FURTHER INVESTIGATION AND MANAGEMENT. | |
drpravin2003 |
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Absent radial and brachial pulse may be an incidental finding. Following differential diagnosis call for further investigation
As you have excluded intracardiac pathology by echocardiography, embolic cause is very unlikely. Dr. Prasanta Kumar Dash |
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SIR WHAT ABOUT THE ROUTINE USE OF INTRA THECAL BUPRENORPHINE ?? ANY SERIOUS SIDE EFFECTS ?? CAN THEY BE MANAGED IN ROUTINE POST OPERATIVE WARD OR IN ICU ? THANKS | |
Dr.Palanivel Rajan |
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Even though there are many additives being added to intra-thecal local anaesthetics, Buprenorphine is rarely used as an adjuvant. The reason being its strong affinity to opioid receptors and longer duration of action. Its affinity to µ receptors is high and has a partial antagonistic activity also. The dangerous side effect of any neuraxial opioid is respiratory depression which can occur with Burenorphine also. If it occurs, it will be very difficult to reverse with naloxone. (continuous naloxone infusion is ideal to treat the respiratory depression induced by buprenorphine). For that reason, it is feared and being rarely used.
To be frank, I had used this drug only as an epidural adjuvant in the dose of 150µg(2 – 3 µg/kg). But when I enquired in Trichy where I’m working, I came to know that many Anaesthesiologists use intra-thecal Buprenorphine routinely along with Bupivacaine. They use 60 -90µg along with bupivacaine and claim no side effects. But when I enquired in detail, they couldn’t provide finer details of quality of analgesia and occurrence of side effects. Since they don’t receive any compliant calls from the hospital where they use intra-thecal buprenorphine, they are in a opinion that it is trouble free. They are claiming duration of 36 hours post-operative analgesia. But some other Anaesthesiologists who had used it, stopped now as there was severe itching, nuchal rigidity and urinary retention in some patients.They got an analgesic period of around 12 hours. I conclude that it’s better not to use this drug routinely as an intra-thecal additive as there are better alternative drugs. DR.R. SELVAKUMAR. Further Reading: |
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EVEN AFTER USING APPROPRIATE LMA SIZE AND REQUISITE VOLUME OF AIR FOR LARYNGEAL MASK (CLASSIC ) , SOME TIME , LEAK OF AIR OCCURS WHEN DOING IPPV OR ASSISTED VENTILATION WHAT SHOULD WE DO SIR ? | |
Dr.Palanivel Rajan |
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There are 3 ways of handling this situation.
1) Tug Maneuver: Tug maneuver that I have described is where LMA is inserted till you can push no more and then retracted out gently till you feel there is something holding it back, which is back of the tongue which opposes against the LMA cuff. Perfect alignment of LMA with glottis generally helps. 2) Jaw thrust: It always helps to decrease leak but you will have to keep the jaw thrust all throughout. 3) Side to side movement of the thyroid cartilage helps to displace epiglottis that might be impinging on the grille and causing obstruction and leak. Dr.Pankaj Kundra. |
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WHAT ARE THE DRUGS USED TO ATTENUATE PRESSOR RESPONSE TO LARYNGOSCOPY ,THEIR DOSES AND TIMING OF ADMINISTRATION? | |
ramya |
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Cardiovascular responses to laryngoscopy include hypertension, tachycardia, and dysrhythmias.
In children, bradycardia may occur, but hypoxemia must always be considered as the primary cause. In healthy patients these responses are generally well tolerated; however, in patients with limited coronary or myocardial reserve, myocardial ischemia or failure may follow. The patient with a vascular lesion at risk such as an intracranial vascular anomaly or trauma of the thoracic aorta may also suffer serious sequelae. The clinician must be careful so as not to over treat these responses and create more difficulties than the responses themselves. Because the MAC for endotracheal intubation is about 30 percent higher than MAC for surgical incision, a relatively deep level of anesthesia must be established. Because deep anesthesia may not be tolerated by many patients, drugs that tend to block the response to airway instrumentation or antihypertensives may be used. Thiopentone, Propofol and Etomidate are ineffective in eliminating hemodynamic response to Laryngoscopy and intubation. In general patients with difficult laryngoscopy or intubation or both have higher pressure response. Hypertensive patients have more chance of pressure response. Direct laryngoscopy is associated with more pressure response than video laryngoscopy Narcotics are one option as an adjunct to blunt pressure response. Fentanyl has been best studied and requires a dose of at least 3 to 4 micro gm/kg to be effective. Alfentanil has a more rapid onset of action and is effective for this purpose, and remifentanil is also likely to be similarly effective at a dose of 25-50 micro gm/kg. Lidocaine reduces anesthetic requirements by 30 percent with a 1.5 mg/kg IV bolus that is minimally depressive to the cardiovascular system. Intravenous lidocaine may be used to supplement the narcotic effect on hemodynamics. A variety of antihypertensive agents have also been used to diminish the blood pressure and heart rate responses to intubation. These include adrenergic blockers, phentolamine, nitroprusside, clonidine, captopril, nitroglycerin, and hydralazine,but their relative efficacy is not established. 1-1.5mg/kg esmolol bolus is superior to IV high-dose lidocaine or low-dose fentanyl in preventing the tachycardia associated with intubation. Combination of lignocaine and Esmolol is effective and safe in obstetrics anaesthesia. Other drugs not commonly used include oral gabapentin, oral clonidine and IV dexmeditomedine. Dysrhythmias during or immediately following laryngoscopy and intubation generally resolve with adequate ventilation, and establishment of adequate anesthetic depth. Dr. Prasanta Kumar Dash |
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SIR, WHAT WILL HAPPEN IF WE REVERSE IMMEDIATELY AFTER GIVING NDP RELAXANT T4/T1 STILL 0 | |
bhavani |
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Neuromuscular blocking agents have long been used as adjuncts to general anesthetics in order to facilitate endotracheal intubation, or to provide muscle relaxation to facilitate mechanical ventilation and surgery. Nondepolarizing neuromuscular blocking agents act primarily by competitive inhibition of acetylcholine binding to the postjunctional nAChR.
Spontaneous recovery of neuromuscular function following administration of a nondepolarizing neuromuscular blocking agent involves diffusion of the relaxant away from the nAChR and the motor endplate, as well as its elimination from the body. Recovery is facilitated in the presence of anticholinesterases, which increase acetylcholine concentration at the motor endplate. Recovery is also influenced by depth of neuromuscular block at the time of antagonism, the clearance and half-life of the relaxant used, and any factors that affect neuromuscular blockade. The speed of antagonism of residual block is related to the depth of block at the time of administration of the anticholinesterase. Deeper levels of neuromuscular block require a longer time for the return of twitch strength to acceptable levels. The speed of antagonism of block by either tubocurarine or pancuronium depends on the dose of neostigmine administered: larger doses of anticholinesterase are required for more complete and faster recovery of neuromuscular function. Following neostigmine antagonism of profound pancuronium induced neuromuscular block there is an initial period of rapid but incomplete antagonism, which peaks within 10 minutes. Further recovery of neuromuscular function occurs relatively slowly; this second, slower stage of recovery appears to depend on the clearance of the relaxant. In the case of long-acting relaxants, with clearance values of 1.5–3.0 mL/min/kg and elimination half-lives of 1.5–2 hours, little drug is eliminated during the first 10 minutes after neostigmine administration, as this 10-minute period represents only about one-10th of one half life. Consequently, during antagonism of long-acting relaxants the return of neuromuscular function to normal depends almost entirely on the antagonistic effect of the anticholinesterase. For relaxants with shorter half-lives (2–20 minutes), a larger fraction of the relaxant is eliminated during the 10-minute period following administration of the anticholinesterase. Therefore, antagonism of residual blockade in the latter represents a combination of the pharmacodynamic effect of the anticholinesterase and the pharmacokinetic effect of clearance of the relaxant. The net result is that antagonism of residual effect is more rapid and more complete with shorter-acting relaxants than with long-acting relaxants. This result in a higher incidence of residual weakness in the recovery room following the administration of long-acting nondepolarizing neuromuscular blockers compared with intermediate-acting drugs. Administration of doses of neostigmine greater than 2.5 mg is associated with an increased incidence of postoperative nausea and vomiting. In order to decrease the incidence following the administration of anticholinesterases, waiting for a greater degree of spontaneous recovery of neuromuscular function and then administering neostigmine – 2 mg or less – should be effective. There is a limit to the depth of neuromuscular blockade that can be effectively antagonized by anticholinesterases. Anti- cholinesterases administered at any point after the administration of a nondepolarizing neuromuscular blocker will shorten the time required for recovery of neuromuscular function compared to spontaneous recovery. Recovery to clinically acceptable levels of neuromuscular function, however, occurs more quickly if the anticholinesterase is administered once a significant amount of spontaneous recovery has occurred and more acetylcholine receptors are available. In the case of neostigmine, the maximal effect of the anticholinesterase is observed approximately 7 minutes after its administration. Further recovery of neuromuscular function depends on ongoing elimination of the relaxant from the neuromuscular junction and the body. Reference: Dr. Prasanta Kumar Dash |
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1.WHAT TO DO WHEN GET VENOUS OR ARTERIAL BLOOD ON ASPIRATION DURING SUPRACLVICULAR APPROCH OF BPB. 2. WHAT TO DO WHEN BE UNABLE TO FIND ANY PARSTHESIA 3. CAN EFFECTIVE BLOCK BE ACHIEVED BY PUSHING A LARGER(DILUTED) VOLUME OF LOCAL ANAESTHETIC AGENT JUST AROUND FIST RIB?( IN A CONDITION WHEN ITS DIFFICULT TO GET PARSTHESIA) | |
alokmadhavi |
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1. If you review the anatomy carefully, it will be found that subclavian vein is placed behind the clavicle, medial to the subclavian artery. So, when we are trying for the supraclavicular block, mostly we will enter into the artery, not the vein.
If arterial puncture occurs, you need not feel panicky. At least we can be sure that the nerves are close by. Withdraw the needle and apply pressure over the puncture site not allowing a haematoma to develop. Now redirect the needle little laterally. Invariably you will get the paraesthesia. If haematoma develops, it will confuse the aspiration test. Blood will appear in the syringe even if the needle is not in the vessel. And also, the haematoma may make the block patchy. 2. If paraesthesia is not obtained, the success rate of the plexus blocks decreases. As the sheath containing the plexus crosses the 1st rib in a narrow area, it is possible that we may end up outside the sheath even though the needle is on the rib. (Now a days the existence of a complete sheath covering the brachial plexus is being questioned – Ref: The sheath of the brachial plexus: fact or fiction? Even then deposition of drug as close to the plexus is advisable.) So it is better to get paraesthesia or conducted pulse of the subclavian artery on your needle.( Even though I still practice the paraesthesia technique, experts say eliciting paraesthesia is not advisable as it may injure the nerves permanently). 3. Increasing the volume by diluting the drug will not increase the success rate. Success depends upon the placement of solution as close to the plexus as possible. In fact using higher volume sometimes results in ascend of solution high up causing phrenic nerve blockade. Some tips for the successful block: 1. Proper positioning Ref: The Sheath of the Brachial Plexus: Fact or Fiction? Anesthesiology: September 2006 – Volume 105 – Issue 3 – pp 563-565 |
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