Procaine was the first injectable local anesthetic synthesized in 1905. It has a rapid onset of action between 6-10 minutes when used in concentrations between 2-4% for dental procedures. However, it is rapidly metabolized and has a short duration of only 30 minutes, requiring multiple injections. It produces significant vasodilation but lacks efficacy for topical applications due to low concentrations. Overall, procaine was an important early development but has been replaced by safer and longer-acting local anesthetics.
Here are some key resources on pain and anxiety control in dentistry:
- Sturdvent - A leading manufacturer of dental equipment for pain and anxiety control.
- Ada's journal on anxiety and pain control - The American Dental Association's journal focused on non-pharmacological approaches.
- Journal on pain management by the American Society of Endodontists - Focuses on managing endodontic pain.
- Journal on pain control in dentistry - Focused specifically on controlling pain during various dental procedures.
- Pickard's manual of operative dentistry - A comprehensive textbook covering techniques for operative dentistry including pain control.
- Pain control in operative dentistry by Dr Ann Elrich - A
Local anesthetics work by blocking sodium ion channels in nerve cell membranes, preventing the propagation of action potentials and interrupting pain signals. The first local anesthetic was cocaine, discovered in the 1860s. Local anesthetics are classified as esters like cocaine or amides like lidocaine. They take effect by binding to intracellular sodium channels and slowing nerve conduction. The potency of local anesthetics depends on factors like pH, lipophilicity, and protein binding. Different types of nerve fibers vary in their susceptibility to local anesthetic blockade, with small fibers being more easily blocked. Systemic toxicity from overdose can cause central nervous system or cardiovascular effects. Common techniques for local anesthesia include infiltration, topical blocks, nerve blocks, and
General anesthetics are drugs that produce reversible loss of sensation and consciousness. They work by depressing the central nervous system. There are two main types - volatile liquids/gases that are inhaled, and non-volatile drugs given intravenously. Volatile agents include ether, chloroform, halothane and nitrous oxide. Non-volatile agents include thiopental sodium and ketamine. They produce anesthesia through actions on GABA receptors or NMDA receptors in the brain. Ideal anesthetics have properties like potency, ease of use, quick induction/recovery, lack of flammability, muscle relaxation, analgesia and low toxicity.
Control Of Anxiety And Pain In Dentistryshabeel pn
1. The document discusses various theories of pain including specificity theory, pattern theory, and gate control theory.
2. It outlines three phases for controlling pain - before, during, and after dental treatment. Methods discussed for each phase include using local anesthetics, sedation, hypnosis, music, and TENS therapy.
3. Specific techniques for administering local anesthetics safely and effectively are provided. Other non-pharmacological pain control methods like acupuncture and general anesthesia are also mentioned.
General anesthesia involves administering drugs to induce unconsciousness, analgesia, amnesia, muscle relaxation and loss of reflexes. Common general anesthetics are inhaled gases like nitrous oxide or intravenous drugs like propofol and barbiturates. General anesthesia has three phases - induction to put the patient to sleep, maintenance to keep them asleep, and recovery to wake them up. Drugs are chosen based on their properties and safety profile to safely anesthetize patients for surgical procedures.
Local anesthetics work by interrupting pain impulses in a specific region of the body without loss of consciousness. The first local anesthetic introduced was cocaine from coca leaves in the 1860s. Local anesthetics come in two types - amides like lidocaine which are metabolized in the liver, and esters like procaine which are hydrolyzed by plasma enzymes. The mechanism of action involves blocking sodium channels to interrupt nerve impulses. Factors like pH, lipophilicity, and protein binding affect the duration and potency of local anesthetics. Common techniques include infiltration, nerve blocks, and regional blocks like epidurals. Toxicities can occur from overdose and include CNS excitation, depression,
Pain control is important for restorative dental procedures. Various techniques can be used including local anesthesia, sedation, hypnosis and electronic dental anesthesia. Local anesthesia blocks pain pathways using agents like lidocaine with epinephrine. Gentle technique, rubber dam isolation, and pulp protective materials can minimize pain during treatment. Proper case history, motivation and premedication can also help control a patient's pain response.
Here are some key resources on pain and anxiety control in dentistry:
- Sturdvent - A leading manufacturer of dental equipment for pain and anxiety control.
- Ada's journal on anxiety and pain control - The American Dental Association's journal focused on non-pharmacological approaches.
- Journal on pain management by the American Society of Endodontists - Focuses on managing endodontic pain.
- Journal on pain control in dentistry - Focused specifically on controlling pain during various dental procedures.
- Pickard's manual of operative dentistry - A comprehensive textbook covering techniques for operative dentistry including pain control.
- Pain control in operative dentistry by Dr Ann Elrich - A
Local anesthetics work by blocking sodium ion channels in nerve cell membranes, preventing the propagation of action potentials and interrupting pain signals. The first local anesthetic was cocaine, discovered in the 1860s. Local anesthetics are classified as esters like cocaine or amides like lidocaine. They take effect by binding to intracellular sodium channels and slowing nerve conduction. The potency of local anesthetics depends on factors like pH, lipophilicity, and protein binding. Different types of nerve fibers vary in their susceptibility to local anesthetic blockade, with small fibers being more easily blocked. Systemic toxicity from overdose can cause central nervous system or cardiovascular effects. Common techniques for local anesthesia include infiltration, topical blocks, nerve blocks, and
General anesthetics are drugs that produce reversible loss of sensation and consciousness. They work by depressing the central nervous system. There are two main types - volatile liquids/gases that are inhaled, and non-volatile drugs given intravenously. Volatile agents include ether, chloroform, halothane and nitrous oxide. Non-volatile agents include thiopental sodium and ketamine. They produce anesthesia through actions on GABA receptors or NMDA receptors in the brain. Ideal anesthetics have properties like potency, ease of use, quick induction/recovery, lack of flammability, muscle relaxation, analgesia and low toxicity.
Control Of Anxiety And Pain In Dentistryshabeel pn
1. The document discusses various theories of pain including specificity theory, pattern theory, and gate control theory.
2. It outlines three phases for controlling pain - before, during, and after dental treatment. Methods discussed for each phase include using local anesthetics, sedation, hypnosis, music, and TENS therapy.
3. Specific techniques for administering local anesthetics safely and effectively are provided. Other non-pharmacological pain control methods like acupuncture and general anesthesia are also mentioned.
General anesthesia involves administering drugs to induce unconsciousness, analgesia, amnesia, muscle relaxation and loss of reflexes. Common general anesthetics are inhaled gases like nitrous oxide or intravenous drugs like propofol and barbiturates. General anesthesia has three phases - induction to put the patient to sleep, maintenance to keep them asleep, and recovery to wake them up. Drugs are chosen based on their properties and safety profile to safely anesthetize patients for surgical procedures.
Local anesthetics work by interrupting pain impulses in a specific region of the body without loss of consciousness. The first local anesthetic introduced was cocaine from coca leaves in the 1860s. Local anesthetics come in two types - amides like lidocaine which are metabolized in the liver, and esters like procaine which are hydrolyzed by plasma enzymes. The mechanism of action involves blocking sodium channels to interrupt nerve impulses. Factors like pH, lipophilicity, and protein binding affect the duration and potency of local anesthetics. Common techniques include infiltration, nerve blocks, and regional blocks like epidurals. Toxicities can occur from overdose and include CNS excitation, depression,
Pain control is important for restorative dental procedures. Various techniques can be used including local anesthesia, sedation, hypnosis and electronic dental anesthesia. Local anesthesia blocks pain pathways using agents like lidocaine with epinephrine. Gentle technique, rubber dam isolation, and pulp protective materials can minimize pain during treatment. Proper case history, motivation and premedication can also help control a patient's pain response.
The document provides a history of anesthetics from primitive techniques to modern discoveries. It discusses Crawford Long using ether anesthesia in 1842, followed by chloroform and nitrous oxide. In 1846, William Morton demonstrated ether anesthesia publicly at Massachusetts General Hospital, considered the beginning of modern anesthesia. The document also describes different types of anesthesia including general, regional, and local, and their mechanisms of action and uses. It discusses various anesthetic drugs and their properties.
THIS ppt explains in brief about general anesthesia for under graduates. It includes brief classification, mechanism of action, side effects of some important drugs. concepts like diffusion hypoxia, second gas effect, balanced anesthesia and pre- anaesthetic medication are discussed.
The document discusses future trends in pain control in dentistry. It covers new local anesthetic drugs like articaine that have a faster onset and longer duration than lidocaine. It also discusses newer drug delivery systems for local anesthesia like electronic dental anesthesia, intra-oral lidocaine patches, and jet injection. Overall, the document focuses on advances in local anesthesia to improve pain management for dental procedures.
This document provides an overview of local anesthesia techniques for pediatric dental patients. It defines pain and local anesthesia, and describes topical anesthetics and the components of local anesthetic solutions. Techniques for mandibular and maxillary anesthesia are outlined, including nerve blocks and infiltration. Supplemental injection methods and maximum recommended doses are also discussed. Potential complications of local anesthesia are reviewed. Finally, some new techniques are mentioned, such as jet injection and computer-controlled delivery systems.
The document discusses the history and current use of spinal, epidural, and caudal anesthesia. It provides details on:
1) The key developments in these techniques from 1885 to present day and their current role in veterinary and human anesthesia.
2) The indications, contraindications, and complications of these regional anesthesia techniques.
3) The local anesthetics, opioids, and other agents used and their mechanisms of action, dosages, durations, and side effects.
4) Techniques for administering spinal, epidural, and caudal anesthesia including needle selection, injection procedures, and postoperative care.
Samya Sayantan presented on anesthetics which are drugs that temporarily depress neuronal function and sensation. Anesthetics are categorized as local or general. Local anesthetics prevent nerve impulses in a specific area without unconsciousness and are used for minor surgeries and pain management. General anesthetics induce reversible loss of consciousness and are administered before, during, or after surgeries using intravenous or inhalational drugs. Both have potential adverse effects from neurological to respiratory depression.
Local anesthesia works by blocking sodium channels in nerve fibers, preventing the propagation of action potentials and sensation of pain. Early local anesthetics included cocaine and procaine. Lidocaine, an amide-type anesthetic, was later developed and causes fewer allergic reactions. The trigeminal nerve provides sensation to the face and can be blocked at its three divisions to provide anesthesia for various procedures. Proper anatomy and technique are required to effectively block branches of the trigeminal nerve while avoiding complications from direct nerve or vascular injection.
Local anesthesia involves applying numbing drugs to specific parts of the body to temporarily block pain sensation during surgery or other procedures. It has a long history dating back to the 1850s with early experiments using cocaine. Local anesthetics work by inhibiting sodium ion channels in nerves, preventing the generation of action potentials. While useful for minor procedures, local anesthetics can cause adverse effects if too much enters the bloodstream, possibly interfering with heart function. Proper administration is important to avoid safety issues.
1. Nicotinic cholinoceptors are located in ganglia and muscles. Drugs can act as nicotinic cholinoceptor agonists or antagonists.
2. Nicotinic cholinoceptor agonists like lobeline and cytisine stimulate respiration by activating carotid body receptors. They are sometimes used to aid smoking cessation.
3. Ganglion blockers like benzohexonium and azamethonium antagonize nicotinic cholinoceptors in ganglia. They cause hypotension by blocking sympathetic ganglia and are used to treat hypertension. Side effects include dry mouth and orthostatic hypotension.
This document summarizes several chronic pain conditions and their treatments. It discusses myofascial pain, intercostal neuralgia, postherpetic neuralgia, complex regional pain syndrome types I and II, cancer pain, and various procedures to treat them. These procedures include trigger point injections, transcutaneous electrical nerve stimulation, spinal cord stimulation, peripheral nerve stimulation, neurolytic blocks, sympathetic nerve blocks, regional anesthesia techniques, and drug therapies. The document provides details on anatomy, signs and symptoms, and techniques for specific procedures to manage chronic pain conditions.
Local anesthetics work by blocking sodium ion channels, preventing nerve impulse propagation. Early agents included cocaine, while modern ones like lidocaine are further classified as esters or amides. Administration can be via local infiltration, nerve block, or regional techniques like epidural or spinal anesthesia. Toxicities include allergic reactions and central nervous system or cardiovascular issues if too much is absorbed systemically. Proper dosage and addition of vasoconstrictors can maximize efficacy and safety.
Local anesthetics work by blocking sodium ion channels, preventing nerve impulse propagation. Cocaine was the first local anesthetic. Esters like cocaine are hydrolyzed while amides like lidocaine are metabolized in the liver. Small unmyelinated C fibers are most susceptible to blockade. Toxicities include allergic reactions, central nervous system excitation or depression, and cardiovascular effects from systemic absorption of excessive doses.
Local anesthetics work by reversibly blocking sodium channels in nerve fibers, inhibiting pain signal conduction. They can provide local anesthesia through infiltration of tissues or regional anesthesia through epidural administration. The two main types are esters and amides, with amides being safer and more commonly used. Potential adverse effects include allergy, toxicity from high doses, and methemoglobinemia. Proper administration techniques and monitoring can help prevent complications.
Local anesthetics reversibly depress the central nervous system to relieve pain without loss of consciousness. They work by binding to voltage-gated sodium channels in nerve cell membranes, inhibiting the generation of action potentials and reducing nerve excitability. Local anesthetics are classified as amides or esters depending on their chemical structure. Amides are more stable but esters have a faster onset of action. Both types contain an aromatic ring connected by an amide or ester linkage to a hydrophilic amine group, allowing them to penetrate cell membranes. The presence of electron-withdrawing groups on the aromatic ring and lipophilic chains influence their potency and duration. Common applications of local anesthetics include dentistry, dermat
Local anesthetics work by blocking sodium channels in nerves, limiting the propagation of action potentials and producing loss of sensation in a specific area. Early local anesthetics like cocaine and procaine had limitations. Lidocaine, introduced in 1940, was a major improvement as an amide-type local anesthetic with quick onset, duration of hours, and less allergenicity. Factors like lipid solubility, pH, vasoconstrictors, and dosage levels affect the onset and duration of local anesthetics. Regional anesthesia techniques involve anesthetizing broader areas using techniques like topical, field block, and peripheral or central nerve blocks.
Local anesthetics work by blocking sodium channels in nerves, limiting the propagation of action potentials and producing loss of sensation in a specific area. Early local anesthetics like cocaine and procaine had limitations. Lidocaine, introduced in 1940, was a major breakthrough as the first modern local anesthetic due to its quick onset of action, duration of several hours, and minimal allergenicity. The two classes of local anesthetics are esters and amides; amides are preferable due to lower risk of allergic reactions. Factors like lipid solubility, pH, vasoconstrictors, and dosage levels affect the onset and duration of local anesthetics.
The document provides information on pre-anesthetic preparation and medication in veterinary anesthesia. It discusses evaluating animals before anesthesia, including fasting times and physical exams. It also covers the purposes and types of various pre-anesthetic medications like anticholinergics, muscle relaxants, and tranquilizers. The document concludes that there is no single premedication protocol that can be used for all patients.
1. The document discusses clinical pharmacology of anesthetic drugs used for general anesthesia. It describes the components, practical conduct, monitoring, and tools used for general anesthesia.
2. It discusses various drugs used for premedication, induction, maintenance and recovery from anesthesia including opioids, hypnotics, muscle relaxants, inhalational agents, and reversal agents.
3. The document provides details on the pharmacokinetics, pharmacodynamics and side effect profiles of commonly used anesthetic drugs.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
The document provides a history of anesthetics from primitive techniques to modern discoveries. It discusses Crawford Long using ether anesthesia in 1842, followed by chloroform and nitrous oxide. In 1846, William Morton demonstrated ether anesthesia publicly at Massachusetts General Hospital, considered the beginning of modern anesthesia. The document also describes different types of anesthesia including general, regional, and local, and their mechanisms of action and uses. It discusses various anesthetic drugs and their properties.
THIS ppt explains in brief about general anesthesia for under graduates. It includes brief classification, mechanism of action, side effects of some important drugs. concepts like diffusion hypoxia, second gas effect, balanced anesthesia and pre- anaesthetic medication are discussed.
The document discusses future trends in pain control in dentistry. It covers new local anesthetic drugs like articaine that have a faster onset and longer duration than lidocaine. It also discusses newer drug delivery systems for local anesthesia like electronic dental anesthesia, intra-oral lidocaine patches, and jet injection. Overall, the document focuses on advances in local anesthesia to improve pain management for dental procedures.
This document provides an overview of local anesthesia techniques for pediatric dental patients. It defines pain and local anesthesia, and describes topical anesthetics and the components of local anesthetic solutions. Techniques for mandibular and maxillary anesthesia are outlined, including nerve blocks and infiltration. Supplemental injection methods and maximum recommended doses are also discussed. Potential complications of local anesthesia are reviewed. Finally, some new techniques are mentioned, such as jet injection and computer-controlled delivery systems.
The document discusses the history and current use of spinal, epidural, and caudal anesthesia. It provides details on:
1) The key developments in these techniques from 1885 to present day and their current role in veterinary and human anesthesia.
2) The indications, contraindications, and complications of these regional anesthesia techniques.
3) The local anesthetics, opioids, and other agents used and their mechanisms of action, dosages, durations, and side effects.
4) Techniques for administering spinal, epidural, and caudal anesthesia including needle selection, injection procedures, and postoperative care.
Samya Sayantan presented on anesthetics which are drugs that temporarily depress neuronal function and sensation. Anesthetics are categorized as local or general. Local anesthetics prevent nerve impulses in a specific area without unconsciousness and are used for minor surgeries and pain management. General anesthetics induce reversible loss of consciousness and are administered before, during, or after surgeries using intravenous or inhalational drugs. Both have potential adverse effects from neurological to respiratory depression.
Local anesthesia works by blocking sodium channels in nerve fibers, preventing the propagation of action potentials and sensation of pain. Early local anesthetics included cocaine and procaine. Lidocaine, an amide-type anesthetic, was later developed and causes fewer allergic reactions. The trigeminal nerve provides sensation to the face and can be blocked at its three divisions to provide anesthesia for various procedures. Proper anatomy and technique are required to effectively block branches of the trigeminal nerve while avoiding complications from direct nerve or vascular injection.
Local anesthesia involves applying numbing drugs to specific parts of the body to temporarily block pain sensation during surgery or other procedures. It has a long history dating back to the 1850s with early experiments using cocaine. Local anesthetics work by inhibiting sodium ion channels in nerves, preventing the generation of action potentials. While useful for minor procedures, local anesthetics can cause adverse effects if too much enters the bloodstream, possibly interfering with heart function. Proper administration is important to avoid safety issues.
1. Nicotinic cholinoceptors are located in ganglia and muscles. Drugs can act as nicotinic cholinoceptor agonists or antagonists.
2. Nicotinic cholinoceptor agonists like lobeline and cytisine stimulate respiration by activating carotid body receptors. They are sometimes used to aid smoking cessation.
3. Ganglion blockers like benzohexonium and azamethonium antagonize nicotinic cholinoceptors in ganglia. They cause hypotension by blocking sympathetic ganglia and are used to treat hypertension. Side effects include dry mouth and orthostatic hypotension.
This document summarizes several chronic pain conditions and their treatments. It discusses myofascial pain, intercostal neuralgia, postherpetic neuralgia, complex regional pain syndrome types I and II, cancer pain, and various procedures to treat them. These procedures include trigger point injections, transcutaneous electrical nerve stimulation, spinal cord stimulation, peripheral nerve stimulation, neurolytic blocks, sympathetic nerve blocks, regional anesthesia techniques, and drug therapies. The document provides details on anatomy, signs and symptoms, and techniques for specific procedures to manage chronic pain conditions.
Local anesthetics work by blocking sodium ion channels, preventing nerve impulse propagation. Early agents included cocaine, while modern ones like lidocaine are further classified as esters or amides. Administration can be via local infiltration, nerve block, or regional techniques like epidural or spinal anesthesia. Toxicities include allergic reactions and central nervous system or cardiovascular issues if too much is absorbed systemically. Proper dosage and addition of vasoconstrictors can maximize efficacy and safety.
Local anesthetics work by blocking sodium ion channels, preventing nerve impulse propagation. Cocaine was the first local anesthetic. Esters like cocaine are hydrolyzed while amides like lidocaine are metabolized in the liver. Small unmyelinated C fibers are most susceptible to blockade. Toxicities include allergic reactions, central nervous system excitation or depression, and cardiovascular effects from systemic absorption of excessive doses.
Local anesthetics work by reversibly blocking sodium channels in nerve fibers, inhibiting pain signal conduction. They can provide local anesthesia through infiltration of tissues or regional anesthesia through epidural administration. The two main types are esters and amides, with amides being safer and more commonly used. Potential adverse effects include allergy, toxicity from high doses, and methemoglobinemia. Proper administration techniques and monitoring can help prevent complications.
Local anesthetics reversibly depress the central nervous system to relieve pain without loss of consciousness. They work by binding to voltage-gated sodium channels in nerve cell membranes, inhibiting the generation of action potentials and reducing nerve excitability. Local anesthetics are classified as amides or esters depending on their chemical structure. Amides are more stable but esters have a faster onset of action. Both types contain an aromatic ring connected by an amide or ester linkage to a hydrophilic amine group, allowing them to penetrate cell membranes. The presence of electron-withdrawing groups on the aromatic ring and lipophilic chains influence their potency and duration. Common applications of local anesthetics include dentistry, dermat
Local anesthetics work by blocking sodium channels in nerves, limiting the propagation of action potentials and producing loss of sensation in a specific area. Early local anesthetics like cocaine and procaine had limitations. Lidocaine, introduced in 1940, was a major improvement as an amide-type local anesthetic with quick onset, duration of hours, and less allergenicity. Factors like lipid solubility, pH, vasoconstrictors, and dosage levels affect the onset and duration of local anesthetics. Regional anesthesia techniques involve anesthetizing broader areas using techniques like topical, field block, and peripheral or central nerve blocks.
Local anesthetics work by blocking sodium channels in nerves, limiting the propagation of action potentials and producing loss of sensation in a specific area. Early local anesthetics like cocaine and procaine had limitations. Lidocaine, introduced in 1940, was a major breakthrough as the first modern local anesthetic due to its quick onset of action, duration of several hours, and minimal allergenicity. The two classes of local anesthetics are esters and amides; amides are preferable due to lower risk of allergic reactions. Factors like lipid solubility, pH, vasoconstrictors, and dosage levels affect the onset and duration of local anesthetics.
The document provides information on pre-anesthetic preparation and medication in veterinary anesthesia. It discusses evaluating animals before anesthesia, including fasting times and physical exams. It also covers the purposes and types of various pre-anesthetic medications like anticholinergics, muscle relaxants, and tranquilizers. The document concludes that there is no single premedication protocol that can be used for all patients.
1. The document discusses clinical pharmacology of anesthetic drugs used for general anesthesia. It describes the components, practical conduct, monitoring, and tools used for general anesthesia.
2. It discusses various drugs used for premedication, induction, maintenance and recovery from anesthesia including opioids, hypnotics, muscle relaxants, inhalational agents, and reversal agents.
3. The document provides details on the pharmacokinetics, pharmacodynamics and side effect profiles of commonly used anesthetic drugs.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
3. contents
Terms
Pain
Neurophysiology & neuroanatomy
Local anesthesa
History
Classification
Composition
Mode of action
Metabolism
Local Anesthetic agents
3
4. terms
Analgesia: refers to loss of pain sensation without
loss of consciousness.
Regional analgesia: refers to loss of pain
sensation over a portion of anatomy without loss
of consciousness.
Regional anesthesia: refers to loss of all
sensations i.e. pain as well as temperature,
pressure and motor function without the loss of
consciousness.
4
5. terms
Local Anesthesia: Loss of sensation in a
circumscribed area of the body caused by a
depression of excitation in nerve ending or an
inhibition of conduction process in peripheral
nerve.
Malamed
General Anesthesia: A reversible state of
unconsciousness from where a person cannot be
aroused by external stimulus.
Anaesthesia & Analgesia in dentistry
5
6. terms
Nerve block: this method consists of depositing LA
solution within close proximity to a main trunk and thus
preventing afferent impulses traveling beyond that point.
Field block: consisting of depositing LA solution in close
proximity to a large terminal nerve branch so that area to be
anaesthetized is walled off circumscribed to prevent central
passage of afferent impulses.
Local infiltration: small terminal nerve branches in the
area of surgery are flooded with LA solution rendering
them insensible to pain or preventing them from becoming
stimulated and creating an impulse. The incision made in
the same region in which the solution has been deposited.
6
7. terms
Intraligamentary technique: this technique is
injected to provide single tooth anaesthesia and
consists of forcing LA solution under pressure
into periodontal membrane space of teeth.
Topical anaesthesia: it renders the free nerve
endings in accessible structure (intact mucous
membrane, abraded skin, cornea of eye)
incapable of stimulation by the application of a
suitable solution directly to the surface area.
7
8. Pain
An unpleasant sensory & emotional experience
associated with actual or potential tissue damage
or described in terms of such damage
INTERNATIONALASSOCIATION FOR THE
STUDY OF PAIN
An unpleasant emotional experience usually
initiated by noxious stimulus & transmitted over
specialized neural network to CNS where it is
interpreted as such
MONHEIM
8
10. Specificity theory (Von Fray)
late 19th century
A pain centre was thought to exist within the brain,
which was responsible for all overt manifestation
of the unpleasant experience.
10
11. Pattern theory (Goldscheider, 1894)
Central summation and stimulus intensity are
the critical determinants of pain.
Pain results when the total output of cells
exceeds the critical levels.
11
12. Gate control theory (Melzack and Wall, 1965)
Briefly stated this theory postulates the following:
Information about the presence of injury is
transmitted to the CNS by small peripheral nerves.
Cells in the spinal cord, which are excited by these
injury signals, are also facilitated or inhibited by
other large peripheral nerves
Descending control systems originating in the brain
modulate the excitability of the cells
12
13. Therefore, the brain receives information
about injury by way of gate control system,
which is influenced by:
Injury signals
Other types of afferent impulses
Descending control
13
15. A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
Substantia gelatinosa [SG] (located in dorsal horn of
spinal cord) acts as gatekeeper for transmission of pain
impulses
Fast
Slow
15
16. A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
Step 1: without any painful stimulation;
the gate is closed – therefore no pain
transmission
16
17. A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
Step 2: with non-painful stimulation, large
nerve fibers are primarily activated; both the
SG and T cell are activated; activation of SG
closes gate – no pain
O
F
F
17
18. A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
Step 3: with painful stimulation, A-delta & C fibers
are primarily activated; the SG is inhibited and T cell
are activated; inhibition of SG opens gate – pain
transmitted to brain
O
N
18
19. A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
Rubbing the skin stimulates large diameter
nerves, exciting the SG, closing the gate.
Result: reduction of pain.
O
F
F
ON
19
20. A-beta fiber
afferents
A-delta and C
fiber afferents
+
-
+
+
-
-
SG T cell
Brain
There are multiple gates in the dorsal horn
of the spinal cord.
Closing one gate reduces some pain
transmission
Relatively impossible to close all gates
20
21. Methods of pain control
Removing the cause
Blocking the pathway of painful impulses.
Raising the pain threshold
Preventing the pain reaction by cortical
depression
21
34. Local anesthesia
Loss of sensation in a circumscribed area of the
body caused by a depression of excitation in nerve
ending or an inhibition of conduction process in
peripheral nerve.
-Malamed 6th Ed
34
43. Injectable
a. Low potency, short duration
Procaine
Chloroprocaine
b. Intermediate potency and
duration
Lidocaine
Mepivacaine
c. High potency, long duration
Tetracaine
Bupivacaine
Surface anesthetic
a. Soluble
Cocaine
Lidocaine
Tetracaine
b. Insoluble
Benzocaine
Butyl aminobenzoate
43
44. According to duration of action
Ultra Short Acting: acting for < 30 mins
e.g Procaine without vasoconstrictor
Short Acting: acting for 45 -75 mins
e.g 4% prilocaine with 1: 200,000 epinephrine
Medium Acting: acting for 90 – 150 mins
e.g. 2% lidocaine with 1: 100,000 epinephrine
Long acting: acting for 180 mins or longer
e.g. 0.5% Bupivacaine with 1: 200,000 epinephrine
44
45. Desirable Properties
Must be reversible
Should not be irritating to tissue
Should not cause any permanent alteration of
nerve structure
Low systemic toxicity
Must be effective-injection/ topical
Onset as short as possible.
Long duration of action
45
46. Composition of LA solution
Local anesthetic agent
Vasoconstrictor
Reducing agent
Preservative
Fungicide
The vehicle
46
48. 2. Vasoconstrictor
This is sometimes included to delay the
removal of the anesthetic from the tissues by
decreasing the blood flow through adjacent
blood vessels
48
49. Advantages
It reduces toxic effects by retarding the
absorption of the constituents.
By confining the anesthetic agent to a
localized area it increases the depth and
duration of anesthesia
It produces a relatively bloodless field of
operation for surgical procedures.
[DCNA2002]
49
50. The choice of selection of
vasoconstrictors depends on:
Length of dental procedures
Requirements for haemostasis
Medical status of a patient
50
51. Vasoconstrictors In
General Use
Adrenaline: a synthetic alkaloid almost identical with
the natural secretion of the adrenal medulla.
Nor-adrenaline: a synthetic substance similar to the
pressor amine secreted in the human body
51
52. Felypressin: is a synthetically produced
polypeptide similar to that secreted from the
human posterior pituitary gland.
Only available in a concentration of 0.03
IU/ml.
Vasoconstrictors In General Use
52
53. Both depth and duration of anesthesia can be
modified by the amount of vasoconstrictor in
solution.
Lidocaine solution containing adrenaline / nor-
adrenaline in concentrations of 1:50,000; 1:
80,000 or 1: 1,00,000
53
54. Dilutions Of Vasoconstrictors
A conc. of 1:1000 means that there is 1 gm of solute
in 1000ml of solution
Therefore 1:1000 ratio means 1000mg in 1000 ml or
1.0mg / ml of solution
To produce a 1:10000 solution a 1:1000 solution of
1ml is mixed with 9 ml of solvent
so 1:10000 is 0.1mg/ml
To produce a 1:100000 solution a 1ml solution of
1:10000 is diluted in 9 ml of solvent
54
55. 3. Reducing agent
Vasoconstrictors are unstable in solution
This results in solution turning brown and
must be discarded
Sodium metabisulphite
It is more readily oxidized
55
56. 4. PRESERVATIVE
Small amount of preservative
Methylparaben have been shown to produce allergic
reactions in sensitized subjects
5. Fungicide
In the past some solutions tended to become cloudy due to
the proliferation of minute fungae
In several modern solutions a small quantity of thymol is
added to serve as a fungicide.
56
57. 6. The vehicle
The anesthetic agent and the additives referred to
above are dissolved in modified ringer’s solution
This isotonic vehicle minimizes discomfort during
injection
57
59. Mode & site of action
Nerve membrane is the site of action of the local
anesthetics.
Altering the basic resting potential of the nerve
membrane
Altering the threshold potential
Decreasing the rate of depolarization
Prolonging the rate of repolarization
59
60. Evolution Of Theories For Mode Of Action
Acetylcholine theory
Calcium displacement theory
Surface charge (repulsion) theory
Membrane expansion
Specific receptor theory
60
64. Class A
Class B
Class C
Class D
Agents acting at receptor
site –external surface.
Agents acting at receptor
site- internal surface.
Agents acting at receptor
independent physico
chemical mechanism.
Agents acting in combn
of receptor and
independent mechanism.
Biotoxin -eg
tetrodotoxin
Quaternary ammonium-
scorpion venom
Benzocaine
Clinically useful agents
–Lignocaine etc
According to biological site and mode of action - MALAMED
64
67. RNH+ displaces calcium ions for the sodium channel receptor site.
↓ which causes
Binding of the local anesthetic molecules to this receptor site
↓ which produce
Blockade of sodium channel
↓ and
Decrease in sodium conduction
↓ which leads to
Depression of the rate of electrical depolarization
↓ and
Failure to achieve the threshold potential level
Lack of development of propagated action potentials
↓ called
Conduction blockade
67
70. BLOOD LEVELS OF LOCALANESTHETICS
ARE INFLUENCED BY THE FOLLOWING
FACTORS
Rate at which the drug is absorbed into the
cardiovascular system
Rate of distribution of the agent from the vascular
compartment to the tissues
Elimination of the drug through metabolism /
excretory pathways.
70
71. METABOLISM / BIOTRANSFORMATION
A significant difference between the two
major types of local anesthetics, the esters
and the amides, is the method by which
they undergo metabolic breakdown.
71
72. ESTERS:
They are hydrolyzed in the plasma by the
enzyme pseudocholinesterase.
AMIDES:
The primary site of biotransformation of
amide agents is the liver.
72
73. EXCRETION
Kidneys
Esters appear only in very small concentrations as
parent compound in urine.
Amides are usually present in the urine as the parent
compound in greater percentage than esters, primarily
because they have a complex biotransformation.
73
74. Classification: Ester
Prepared by: Alfred Einhorn (1904-1905)
Potency: 1
Toxicity: 1
Metabolism: Hydrolyzed rapidly in plasma, by
plasma pseudocholinesterase.
Excretion: 2% unchanged in urine
90% as para amino benzoic acid
8% as diethylaminoethanol
74
A. Procaine
75. Vasodilatation property: produces the greatest
vasodilatation of all currently employed local
anesthetics.
pKa : 9.1
Onset of action: 6-10 min’s
Effective dental concentration: 2% - 4%
Topical action: not in clinically acceptable
concentrations.
Actions:
It was the 1st injectable local anesthetic to be
synthesized
75
76. Propoxycaine
Classification: Ester
Prepared by: Clinton and Laskowski, 1952
Potency: 7-8
Toxicity: 7-8
Metabolism: Hydrolysed both in plasma and liver
Excretion: Kidneys (almost entirely hydrolyzed)
Vasodilatation property: Present
pKa : Not available
Onset of action: Rapid (2-3 min’s)
Effective dental concentration: 0.4 %
Topical action: Not in clinically acceptable concentrations
76
77. Chloroprocaine
Classification: Ester
Potency: 2
Toxicity: ½ of procaine
Metabolism: by rapid hydrolysis in serum
Excretion: Kidneys
Vasodilatation property: < procaine
pKa : 8.7
Onset of action: Moderate (6-12 min’s)
Effective dental concentration: 2%
Anesthetic ½ life: sec’s to min’s (extremely rapid)
Topical action: not in clinically acceptable
concentrations.
77
78. AMIDES
A. Lidocaine
Classification: Amide
Prepared by: Nils Lofgren, 1943
Introduced in: 1948
Potency: 2 (compared to procaine). Today Lidocaine
is used as standard of comparison.
78
84. Effective dental conc. : 3% without vasoconstrictor
2% with vasoconstrictor
Anesthetic ½ life: approx 90 min’s
Topical anesthetic action: Not in clinically
acceptable concentrations.
Action: Mepivacaine plain is most often
administered in pediatric dentistry and is very
appropriate in management of geriatric patients.
84
86. pKa : 8.1
Onset of action: similar to that of lidocaine but occasionally
requires longer time (6-10 min’s)
Effective dental conc: 0.5%
Anesthetic ½ life: 76 min’s
Topical action: Not in clinically acceptable concentrations
Action:
Lengthy dental procedures (pulpal anesthesia > 90 min’s)
Procedures in which post operative discomfort is
anticipated. Example: - Endodontic surgeries [JOE,2005,AL
READER]
86
88. ARTICAINE
Classification : amide
Prepared by: A. Rusching
Potency:1.5 times that of lignocaine
Toxicity :similar to that of lignocaine
Metabolism :articaine is the only amide type local
anesthetic that causes metabolism in both liver and
plasma
Excretion: via kidneys, 5-10% unchanged, app 90%
metabolites
Vasodilating properties similar to that of lignocaine
88
89. pka-7.8
ph of vaso constrictor containing substance-4.4-5.2
Onset of action: 1-2 mins
Effective dental concentration -4%
Originally known as carticaine and is available in 2
formulations of 4%.
It has been claimed that articaine can better diffuse
through hard and soft tissues than other anesthetics
89
92. Lidocaine: (available in 2 forms)
Lidocaine base
Water-soluble preparation
Benzocaine:
Poorly soluble in water
Poor absorption
Systemic toxic reactions unknown
Prolonged duration of action
Not suitable for injection
Reported to inhibit antibacterial action of
sulfonamides
92
93. EMLA-EUTECTIC MIXTURE OF LOCAL
ANESTHETICS
Recently introduced topical anesthetic agent.
Medical use to achieve anesthesia of skin.
Posses a local anesthetic effect on the oral
mucosa also.
Contents:
Lidocaine 25 mg /ml
Prilocaine 25mg. /ml
93
94. Tetracaine Hydrochloride
Highly water soluble
Applied topically, 5-8 times more potent than cocaine
Slow onset of action (topically)
Duration of action: approximately 45 min’s
Metabolized in Liver and plasma
Injectable: 0.15 % concentration
Topically: 2% concentration.
Rapidly absorbed through mucous membrane
Greater potential for toxicity.
94
99. It is a metallic syringe where the needle is attached to
the barrel of the syringe at the needle adaptor.
The end of the needle then penetrates the barrel of
syringe and pierces the rubber diaphragm on the
cartridge of anesthetic sol.
The screw hub is removable and sometimes
inadvertently discarded with needle when the needle
is removed and discarded.
99
102. Breech – loading, metallic, self aspirating cartridge
102
The self aspirating
syringes obtain the
required negative
pressure for
aspiration by means
of elasticity of the
rubber diaphragm of
the syringe which
directs the needle
into the cartridge
103. 103
Pressure acting directly on the cartridge
through the thumb disk or indirectly through
the plunger shaft stretches the rubber
diaphragm.
When that pressure is released, sufficient
negative pressure is produced with in the
cartridge to achieve aspiration.
The use of self aspirating dental syringe
permits easy, multiple aspirations throughout
the period of local anesthetic deposition.
106. JET INJECTOR
It was introduced by Figge & Scherer in 1947.
Jet injections is based on the principle that liquids
forced through very small openings, called jets, at
very high pressure can penetrate skin or mucous
membrane
106
108. Pressure syringe
These syringes introduced in the late 1970 was
primarily used for periodontal injections
All pressure syringes encase in a glass or metal
container
Help in achieving pulpal anesthesia of a single tooth
108
109. Plastic disposable syringe
Plastic disposable syringes are available in a variety
of sizes and with an assortment of needle gauges.
They are most often employed for intramuscular or
intravenous drugs administration but also useful for
intra oral injections.
109
110. 110
These syringes contain luer – lock screw on
needle attachment but no aspirating tip. These
syringes do not accept the dental cartridges.
The needle, attached to the syringe must be
inserted into a vial or cartridge of local
anesthetic drug and an appropriate volume of
solution removed.
111. Safety syringes
These type of syringes posess “locks” which
prevent the operator from accidental needle pricks
All safety syringes are meant for single use
111
112. In 1997 the first computer
controlled injection system
was introduced into dentistry
Hochman and associates were
the first to demonstrate the
ability of this delivery system
Fukayama and associates in a
controlled study reported less
or no pain on palatal injection
The wand
112
113. The needle
The needle directs the local anesthetic solution
from the dental cartridge into the tissues
surrounding the needle tip.
TYPES OF NEEDLES
•Reusable/Autoclavable
•Disposable
•Winged
113
115. Part of the needle
Bevel
Shank
Hub
1 Bevel Defines the point or tip of the needle
2 Shank Or shaft of the needle consists of the
diameter of the needle lumen and the length of the
shank from it points to the hub.
3 Hub It is a plastic or metal piece through which
the needle is attacked to the syringe.
115
116. Length
Needles are available in two lengths
Long-32 mm
Short-20mm
Care and handling
Needles must never be reused
Needles should be changed after several penetrations
Needles should be covered with protective sheath
It should be properly disposed
116
119. CARTRIDGE
The dental cartridge is a glass cylinder that contains,
among other ingredients, the local anesthetic drug.
The dental cartridge is commonly referred to as
“CARPULE”.
119
120. Components
Cylindrical glass tub
Rubber stopper
Aluminium cap
Rubber diaphragms
Rubber stopper:- Is located at the end of the cartridge
that receives the harpoon of the syringe. The harpoon is
imbedded in the plunger by gentle finger pressure on the
thumping of the syringe. The rubber plunger occupies
little more than 0.2 ml of the volume of the entire
cartridge.
120
121. Aluminium Cap :- Is located on the opposite end of
the cartridge from the rubber plunger. It fits tightly
around the neck of the glass cartridge, holding the
thin rubber diaphragm in position.
Rubber diaphragm:- Is a permeable membrane
through which the cartridge end of the needle
penetrates. When properly prepared, the hole made
by the needle is centrically located and hound,
forming a tight seal around the needle.
121
122. Care While Handling Cartridges
Some local anesthetic cartridges come vacuum sealed in a tin
container of fifty cartridges. The glass dental cartridge should
not be autoclaved.
The seals on the cartridge cannot withstand the extreme
temperatures of autoclaving, and the heat labile
vasoconstrictors will be destroyed in the process.
The cartridges are moistened with (not immersed) wither 91%
is isopropyl or 70% ethyl alcohol. There must be no alcohol
present around the cartridge.
122
123.
124. Seminar / table clinic
TECHNIQUES OF MAXILLARY
ANESTHESIA
Dr. Sangam Mittal
Dr. Niti Shah
125. Techniques
Three major types of local anesthetic injection can be
differentiated
Local infiltration
Field block
Nerve block
126. Local Infiltration
Small terminal nerve endings in the area of dental
treatment are flooded with local anesthetic
solution
127.
128. Field block
Local anesthetic solution is deposited near the
larger terminal nerve branches so the
anesthetised area will be circumscribed,
preventing the passage of impulses from the
tooth to the C.N.S.
Incision (or treatment) is made into an area
away from the site of injection of the anesthetic
eg. maxillary injections administered above the
apex of the tooth
129.
130. Nerve block
Local anesthetic is deposited close to a main
nerve trunk, usually at a distance from the site
of operative intervention
Post sup alv., inf. Alv. and nasopalatine
137. Signs & symptoms
Subjective : Feeling of numbness in the area of
administration
Objective: Use of EPT with no response from
tooth
Absence of pain during treatment
138. Failures of anesthesia
Needle tiip lies below the apex
Needle tip lies too far from the bone
141. Area anaesthetized:
Maxillary 3rd, 2nd & 1st molar (except mesio-buccal root
of 1st molar
Bone & periodontium over these
142. Indication:
Treatment of 2 or more molars required
Supra-periosteal injection – ineffective
Acute inflammation
Contra-indication:
Pt with bleeding disorders
164. Signs & symptoms
Subjective : Tingling and numbness
Subjective & Objective: numbness in the teeth &
soft tissues along the distribution of ASA & MSA
nerves
Objective: Use of EPT with no response from tooth
Absence of pain during treatment
165. Failures of anesthesia
Needle contacting bone below the infraorbital
foramen
Needle deviation medial or lateral to the
infraorbital foramen
185. Signs & symptoms
Subjective : Numbness in anterior portion of the
palate
Objective: Absence of pain during treatment
186. Failures of anesthesia
Unilateral anesthesia
Inadequate palatal soft tissue anesthesia in the
area of the maxillary canine and first premolar.
191. Signs & symptoms
Subjective : Numbness on the palatal tisses
Subjective: Numbness of the teeth and asso soft
tissues
Objective: Use of EPT
Objective: Absence of pain during treatment
201. Maxillary nerve block – Extra Oral
Areas anaesthetised
Anterior temporal & zygomatic region
Lower eyelid
Side of nose
Anterior cheek
Upper lip
Maxillary teeth / alveolar bone & overlying structures
– 1side
Hard & soft palate
Tonsils – parts of pharynx
Nasal septum – floor of nose
202. Indications
Extensive surgery – 1 half of maxilla
Others blocks not possible
Therapeutic purposes
Technique
Mid point of zygomatic process
Needle gently contact lateral pterygoid plate
Maximum length of 4.5cms directed slightly upward & forward
Note:
In final position – internal maxillary artery – inferior to needle
Temporal vessels on either sides
Posteriorly foramen ovale with mandibular nerve & foramen
spinosum with middle meningeal artery
Anteriorly pterygomaxillary fissure
203.
204. Seminar / table clinic
MANDIBULAR INJECTION TECHNIQUE
Dr. Sangam Mittal
Dr. Niti Shah
217. Signs & symptoms
Subjective : Tingling and numbness of the lower lip
Subjective: Tingling and numbness of the tongue
Objective: Use of EPT with no response from tooth
Absence of pain during treatment
226. Area anesthetized
All mandibular hard and soft tissue upto mid line
Anterior 2/3rd of the tongue
227. Indications
Multiple procedures on mandibular teeth,
Buccal soft tissue anaesthesia from third molar to midline
Conventional inferior alveolar nerve block is
unsuccessful
Contraindications
Infection or acute inflammation in the area of infection
Patients with restricted mouth opening
228.
229.
230.
231.
232. Signs & symptoms
Subjective : Tingling and numbness of the lower lip
Subjective: Tingling and numbness of the tongue
Objective: Use of EPT with no response from tooth
Absence of pain during treatment
235. Area anesthetized
Mandibular teeth to the midline
Body of mandible & inferior portion of ramus
Mucous membrane ant to mental foramen
Anterior 2/3rd of tongue & floor of the oral cavity
236.
237.
238. Signs & symptoms
Subjective : Tingling and numbness of the lower lip
Subjective: Tingling and numbness of the tongue
Objective: Use of EPT with no response from tooth
Absence of pain during treatment
239. Failure of anesthesia
Almost always present because of falure to
apprecate the flarng nature of the ramus
Needle insertion point too low
Underinsertion or overinsertion of the needle
258. Indication for the PDL injection
The need for anesthesia of one or two mandibular
teeth
Treatment of isolated teeth
Treatment of children
Its use as a possible aid in the diagnosis
Nerve block is contraindicated
As an adjunctive technique after nerve block
anesthesia
259. CONTRA-INDICATION TO THE PDL
INJECTION
Infection or severe inflammation at the injection
site.
Primary teeth, when permanent tooth bud is
present is present
260. Advantages
Prevents anesthesia of lip, tongue, and other
soft tissue
Minimum dose of local anesthetic necessary
An alternative to partially successful regional
nerve block
Rapid onset
Less traumatic
261. Disadvantages
Proper needle placement is difficult to achieve
Leakage of local anesthetic solution
Excessive pressure or overly rapid injection
A special syringe may be necessary
Excessive pressure can produce focal tissue damage
Post injection discomfort may persist
The potential for extrusion of a tooth exists
262.
263.
264.
265. Signs & symptoms
Subjective : No adequate sign is present
A. ischemia of soft tissue at the injection site.
B. resistance to injection of solution
Objective: use of EPT with no response
268. Indication
When both pain control and
haemostasis are desired for soft tissue
and osseous periodontal treatment
Contraindication
Infection or severe inflammation at
the injection site
269.
270.
271. Signs and symptoms
No objective symptoms. The anesthetized area
is too circumscribed.
There is absence of pain during the treatment.
Subjective Resistance to the injection of solution
is felt.
273. INTRAOSSEOUS INJECTION
It has been in use since the start of twentieth
century.
The technique traditionally was a two-step
procedure used to deliver anesthetic into the
cancellous bone near the apex of the targeted
tooth.
274. Nerves Anesthetized :Terminal nerve endings at
the site of injection and in the adjacent soft and
hard tissue.
Areas Anesthetized : Bone, soft tissue, and root
structure in the area of injection
275. Indication : Pain control for dental treatment on
single or multiple teeth in a quadrant.
Contraindication : Infection or severe
inflammation at the injection site.
276. Lateral perforation
1.At a point 2mm apical to the intersection of lines
drawn horizontally along the gingival margins of
the teeth and a vertical line through the
interdental papilla.
2.The site should be located distal to the tooth to be
treated, if possible
283. INTRAPULPAL INJECTION
Nerves Anesthetized
Terminal nerve endings at the site of injection in the
pulp chamber and canals of the involved tooth.
Areas Anesthetized
Tissues within the injected tooth
284. Indication
When pain control is necessary for pulp
extirpation or other endodontic treatment in the
absence of adequate anesthesia from other
techniques
Contraindication
None.
285.
286. Signs and Symptoms
Subjective: There are no subjective symptoms
that can ensure adequate anesthesia. The area is
too circumscribed.
Objective The endodontically involved tooth
may be treated painlessly.
292. Definition
An anaesthetic complication may be defined as any
deviation from the normal expected pattern during
or after securing regional anaesthesia
Local
Systemic
298. Prevention
Correct gauge – 25 gauge
Long needles – prevent penetration till hub
Not to insert a needle into soft tissue to its
hub
Do not bend needles
299. Management
Patient – not to move
Fragment visible – remove it
Fragment not visible – inform patient
Radiograph suggested
300.
301. Persistent anaesthesia / paresthesia
Causes
• Direct trauma to nerve
• LA solution containing neurotoxic substance –
alcohol
• Injection of wrong solution
• Hemorrhage / infection – near to nerve
302. Problem
Persistent anaesthesia – usually rare
Biting / thermal / chemical insult – without patient
awareness
When lingual nerve is involved – taste impaired
304. Management
Usually resolve in 8 weeks
Periodic recall & check up of patients
Persistence – consult neurosurgeon
Recall patient every 2 months for check up
323. Management
Immediate – apply firm pressure
Inf. Alveolar Nerve Block – medial aspect of ramus
Infra orbital, Mental, Incisive block – directly over
foramen
PSA – pressure on soft tissue with finger as posteriorly
as tolerated by patient
Patient to be reviewed after 24 hours
330. Infection
Comparatively rare complication
Instrument needle solution to be as aseptic as
possible
Area & operative hands – cleaned
Avoid passing needle through infected area
Use disposable syringes
331. Edema
Causes
Trauma during injection
Infection, hemorrhage
Allergy (Angioedema)
Injection of irritating solution
333. Prevention
Proper care & handling of armamentarium
Atraumatic injection technique
Complete medical evaluation prior to injection
334. Management
Trauma – resolve in few days without therapy
Hemorrhage – resolve slowly over 7-14 days
Allergy – life threatening
Total airway obstruction – Tracheostomy /
Cricothyroidectomy
341. overdose
Overdose reactions are those clinical signs and
symptoms that manifest as a result of an
absolute or relative over - administration of a
drug, which leads to elevated blood levels of
the drug in its target organs
344. Causes of toxicity
Biotransformation usually slow
Drug – slowly eliminated by kidney
Too large a total dose
Absorption from injection site – rapid
Accidental intra-vascular injection
Drug Formulaton MRD (mg/kg)
Articaine With epinephrine -- 7.0
Lidocaine Plain 300 4.4
With epinephrine 500 7.0
Mepivacaine Plain 400 5.7
With epinephrine 400 5.7
Prilocaine Plain 600 8.8
With epinephrine 600 8.8
345. Symptoms
Central Nervous System
0.5 – 4 µg / ml
> 4.5 µg / ml
> 7.5 µg / ml
Cardiovascular system
Less sensitive
1.8 µg / ml – 5 µg / ml
5 - 10 µg / ml
> 10 µg / ml
347. Definitive Care
Reassure the patient
Administer oxygen
Montor & record vital signs
Establish IV infusion (optional)
Permit the patient to recover
Consider emergency medical assistance
349. Definitive Care
Protect patient’s arms, legs & hand
Loosen tight clothes
Summon emergency medical assistance
Continue basic life support
Administer an anti-convulscant
350. Idiosyncrasy
“It is an adverse response that is neither an overdose
nor an allergic reaction”
Treatment – symptomatic ..remember ABC’s!
351. Syncope
“Transient loss of consciousness that is caused due to
cerebral ischemia (neurogenic shock)”
356. Sodium bisulfite allergy
Antioxidant for vasoconstrictor
Bronchospasm
LA solution without a vasopresson should be
used
357. Prevention
Questionnaire
Are you allergic or made sick by penicillin, aspirin,
codeine or any other medications?
Have you ever had asthma, hay fever, sinus trouble?
Describe exactly what happened?
What treatment was given?
What was the time consequence of events?
358. Prevention
Questionnaire
Were the services of emergency medical
personnel necessary?
What drug was used?
What volume of the drug was administered?
Did the local anesthetic contain a
vasoconstrictor?
Details of the doctor?
359. Allergy testing
No form : 100 % reliable
Skin testng : primary mode
Intracutaneous injections : most reliable
0.1 ml test sol into patients forearm
360. Signs And Symptoms Of Allergy
Dermatological reactions
Urticaria
Angioedema
Respiratory reactions
Bronchospasm
Laryngeal edema
Generalised anaphylaxis