An antiemetic should be administered with any intravenous opiate. However, the use of Cycli morph (morphine/cyclizine) is not recommended. Naloxone and equipment for mechanical vent ilatory support MUST be available when morphine (or any other opiate) is administered. Morphine has a duration of action of about 2 hours. CHAPTER 5 Analgesia and anesthesia 370 Pethidine Description Synthetic opioid with a shorter duration of action than morphine. Presentation - 50mg/ml in 1ml and 2ml ampoules for injection - 10mg/ml in 5ml and 10ml ampo ules - Oral pethidine is not suitable for pre-hospital use. Effects - Analgesia - Obstetric analgesia (pethidine does not delay labor) - Atropine like effects \200\224blurred vision, dry mouth. Indications - Moderate pain - Obstetric pain. Dose - 20 \200\22350mg by slow iv injection - 50 \200\223100mg sc or im for obstetric analgesia. Contraindications - Patients taking monoamine oxidase inhibitors - Acute respiratory depres sion - Care in head injury Side-effects - See morphine - There is no evidence to suggest that pethidine has less effec t than morphine on the sphincter of Oddi Notes - Onset within 10 minutes; duration of action 1 \200\2232 hours - Pethidine is associ ated with a greater risk of hypotension because of its alpha blockade, it is NOT RECOMMENDED for pre-hospital use. This page intentionally left blank CHAPTER 5 Analgesia and anesthesia 372 Tramadol Description A synthetic opiate with additional actions (see below). It is a non-se lective OP1 and OP3 receptor agonist, acting mainly at the OP1 receptor. Presentation Tramadol hydrochloride 50mg/ml \200\2242ml ampoule. Effects Tramadol has opioid and non-opioid mechanisms of pain relief. It inhibits reuptake of 5HT and noradrenaline. It inhibits noradrenaline uptake and enhances serotonin release. Indications Moderate to severe pain. Dose 50 \200\223100mg iv every 4 \200\2236 hours. Contraindications See morphine, also epilepsy. Side-effects - Tramadol is claimed to be less likely to cause constipation and respiratory depression than other opioids Confusion, fits, and anaphylaxis - Nausea Pre-hospital use of tramadol is not recommended. USEFUL ANALGESICS: OPIOIDS1 373 Naloxone Description A competitive opiate antagonist. Time to onset 2 \200\2233 minutes. Du ration of action 20 minutes. Presentation - 400 g/ml \200\2241ml ampoule - 400 g/ml \200\2241ml, 2ml, and 5ml pre-fill ed syringe - 1mg/ml \200\2242ml pre-filled syringe Effects Reversal of opioid effects. Indications - Reversal of therapeutic overdose of opiates - Treatment of opiate poisoning ( recreational overdose) - Treatment of unexplained loss/reduction of consciousness. Dose - 0.4mg (400 g) \200\2232mg repeated at intervals, as required, to a maximum of 10mg If naloxone is given to exclude opiates as a cause of loss of conscious- ness, a dose of 10mg should be given Children: iv 10 g/kg, subsequent dose of 100 g/kg if no response. Contraindications Caution in patients who are physically dependant on opiates; will precipi tate pain in patients given opiate for analgesia. Side-effects Nausea and vomiting, tachycardia. Notes Naloxone is short acting. As a result, when long-acting opiates are being reversed, r epeated doses may be needed. Drug abusers may leave the scene after a first dose only to co llapse as the naloxone wears off. In order to reduce the likelihood off this, either the op iate can be reversed only enough to ensure adequacy of respiration before arrival in hospit al, or a similar dose to the intravenous one given above may be given INTRAMUSCULARLY in ad dition. Sudden reversal of opioid overdosage in opioid-dependant patients can produce cardiac arrhythmias, hypotension, and convulsions. CHAPTER 5 Analgesia and anesthesia 374 Treatment of opiate overdosage Opioid overdosage may be absolute (excessive administration) or relative (normal dosage given to compromised patients, commonly hypovolaemic producing excessive plasma levels). The clinical features are: - Sedation - Respiratory depression - Miosis Untreated, overdosage may lead to: - Respiratory arrest - Cardiac arrest Treatments include standard ABC management: - Securing the airway - Supplementary oxygen - Supporting ventilation - Intravenous access - Reversal with Naloxone. USEFUL ANALGESICS: OPIOIDS1 375 Antiemetics Nausea and vomiting are common following opioid administration. Most practition ers give an antiemetic proceeding opioid administration. Symptoms are due to stimulation of the chemoreceptor trigger zone in the fourth ventricle or direct stimulation of the vomiti ng center in the medulla oblongata or the vestibule. For more details, see Chapter 4 (Formulary): Cyclizine, p.319 - Metoclopramide, p.335 - Ondansetron, p.341. CHAPTER 5 Analgesia and anesthesia 376 Other analgesics Mild to moderate pain may be managed by paracetamol and non- steroidal ant i-inflammatory drugs (NSAID). Pre-hospital usage may be limited by the route of administrat ion and the adequacy of pain relief. Aspirin, see p.312 Paracetamol, see p.345 Ibuprofen, s ee p.330 Voltarol, see p.323 Compound analgesics, see p.318 OTHER ANALGESICS1 377 Nitrous oxide/oxygen 50:50 (Entonox) Description Entonox is a 50:50 mixture of oxygen and n itrous oxide (N2O). Nitrous oxide is a colorless, sweet-smelling, non-irritant, non-inflamm able gas. It is insoluble in blood, hence its rapid clinical effect, and 15 times more solu ble than nitrogen in plasma. Presentation Various sizes of blue cylinder with a white and blue mantle. Self administered with override valve. Effects Analgesia without loss of consciousness. Indications - Analgesia for moderate pain in fully conscious individuals - Analgesia for sh ort painful procedures - Rapid onset within 60 seconds, analgesic effect for 3 \200\2234 mi nutes. Dose Titrate to effect. Usually self administered using a demand valve. May be overridden b y medical staff. Overdosage does not occur with self admin istration. Contraindications Contraindicated in patients in whom an air-filled cavity exists into whic h nitrous oxide can diffuse. These conditions include pneumothorax (so contraindicated in s ignificant chest injury), the \200\230bends \200\231 (so contraindicated in patients follo wing diving), and open head injuries. Side-effects See above. Notes At temperatures less than \200\2237*C, nitrous oxide/oxygen mixtures will separate. This may lead to inhalation of pure oxygen, with no analgesic effect, followed by pure nitr ous oxide leading to hypoxia. A few shakes of the cylinder will have no effect, on this sep aration. Entonox MUST be kept above \200\2237*C, even if this means transferring it to you r vehicle immediately before departure. CHAPTER 5 Analgesia and anesthesia 378 Ketamine Description A dissociative anesthetic/analgesic in the form of a white crystalloid powder Presentation - 10mg/ml \200\22420ml vial for injection - 100mg/ml \200\22410ml vial for injection. Effects Ketamine has the following features: - It is powerfully analgesic i n subanaesthetic doses - Protective glottal reflexes are relatively preserved - It does not normally cause respiratory depression at conventional doses - It has a long shelf life - I t does not cause hypotension, but ketamine-induced hypertension makes it relatively contraindicated in head injury - It is relatively safe in patients with a full stomach. Indications - Pre-hospital anesthesia for extrication or short procedures Analgesia. Dose Anesthesia: im 5 \200\22310mg/kg (provides 12 \200\22325 min of surgical anesthesia, effective after 4 \200\22315 min) Iv 1 \200\2232mg/kg (provides 5 \200\22310 min of surgical anesthesia, effective after 2 \200\2237 min) Analgesia: ketamine is an effective analgesic when used in subanaesthetic doses by either the intramuscular or iv route Repeat doses may be given as 10 \200\22320mg iv or 20 \200\22350mg im Children: as above Contraindications - Hypertension (including pre -eclampsia) - Head injury (relative, but consider clinical priorities) Side-effects - A sig nificant proportion of patients suffer emergence hallucinations which can be very distressi ng. As a consequence, a benzodiazepine should also be administered to oblate these symptoms . - Tachycardia and hypertension (sympathomimetic effects) - Mild respiratory stimulation a nd bronchodilatation - Cerebral blood flow and intracranial pressure may both be increased - Increased salivation in children Note Analgesia may also be achieved using other routes f or ketamine admini- stration including: - Intramuscular 1 \200\2234mg/kg - Orally 5 \200 \22310mg/kg - Intranasally 6 \200\2238mg/kg Oral or intranasal administration is not recomm ended. The authors prefer to use the preparation 10mg/kg. Carrying three preparations of different strengths risks confusion, particularly if used in a dark, badly lit environment. This page intentionally left blank CHAPTER 5 Analgesia and anesthesia 380 Anesthesia Introduction The administration of drugs to facilitate intubation (rapid sequenc e induction \200\224RSI) should only be undertaken by skilled emergency care practitioners (usually doctors in the UK) who have undergone the necessary training, have the clinical co mpetency, have access to prac- tice the skill, and appropriate clinical indemnity. This pro cedure should not be undertaken by anybody who does not fulfill these criteria. The administration and maintenance of a general anesthetic requires three groups of drugs: - Intravenous anesthetic agents to achieve unconsciousness - Opioid analgesics for the provision of pain relief and to modify the stress response to intubation Muscle relaxants or neuromuscular blocking agents which decrease or abolish muscle tone Before considering sedation or anesthesia, especially in a combative or restless patient, i t is essential to seek and correct: - Hypoxia - Hypovolaemia - Hypoglycaemia Drug abuse, al cohol, and head injury additionally make the management of these patients hazardous. Intravenous anesthetic agents Unconsciousness is usually achieved rapidly and by one arm to brain circulation time. Consciousness will be regained after bolus injection, unless maint enance anesthetic agents are administered. Drug dosage should be reduced in the hypovolaemi c patient and the elderly. Etomidate is probably the safest induction agent for use in pre-hospital care since it is m ore cardiovascularly stable. In addition, it reduces cerebral oxygen requirement which may have benefit in patients with raised intracranial pressure. The drug profiles of other pote nt anesthetic agents are detailed below. Ketamine may be the drug of choice in hypo- volaem ic/hypotensive patients who are combative or difficult to assess since ketamine administrat ion is associated with an increase in blood pressure alone of all the intravenous induction agents. anesthesia1 381 Etomidate Description A carboxylated imidazole anesthetic induction agent. Presentation 2mg/ml \200\22410ml ampoule for intravenous injection. Effects Induction of anesthesia Indications Anesthesia for: - Intubation - Analgesia - Extrication - Surgical procedures Et omidate causes less hypotension than other commonly used induction agents and is, therefore , probably the drug of choice in trauma. Dose Adults and children, 150 \200\223300 g/kg Contraindications None. Side-effects - Pain on injection (use a large vein, lessened by simultanous administration of an opiate) Involuntary movements (lessened by simultanous administration of an opiate or benzodiazepine) Nausea and vomiting (20% of cases). Notes The major benefit of etomidate is its cardiovascular stability. It is not suitable fo r continuous infusion due to its potential to induce adrenocor- tical function. CHAPTER 5 Analgesia and anesthesia 382 Propofol Description A general anesthetic induction agent. Presentation - Propofol is presented as an emulsion. - 1% propofol (10mg/ml) \200\22420ml a mpoule for IV injection/infusion (1% propofol is also available in 50ml bottles, 50ml pre-filled syringes, and 100ml bottles . 2% propofol (20mg/ml) is available in 50ml vials for IV infusion.) Only one concentration of propofol should be carried and the 1% is recommended. Effects - Induction and maintenance of anesthesia - Anticonvulsant activity. Indications Anesthesia for: - Intubation - Analgesia - Extrication - Surgical procedures Co ntrol of status epilepticus (after other methods have failed) Dose Induction of anesthesia 1.5 \200\2232.5mg/kg (reduce dose in the over 55s) Child: admi nister slowly until anesthesia achieved \200\224over 8 years, usually 2.5mg/kg; under 8 yea rs may need as much as 4mg/kg Maintenance of anesthesia Intermittent doses of 25 \200\22350mg or by iv infusion 4 \200 \22312mg/kg/hr Child: (over 3 years) 9 \200\22315mg/kg/hr Contraindications Hypotension. Side-effects - Hypotension - Nausea and vomiting (less common than with etomidate) - Pain o n injection (may be avoided by adding 20mg of lignocaine to the propofol ampoule) Transient apnoea on induction if injection is too rapid. Notes Induction of anesthesia occurs within 30 seconds of injection. anesthesia1 383 Thiopentone Description A short-acting barbiturate anesthetic agent. Presentation Powder for reconstitution, 500mg vial. Effects - Induction and maintenance of anesthesia - Anticonvulsant activity. Indications Anesthesia for: - Intubation - Analgesia - Extrication - Surgical procedures. C ontrol of status epilepticus (after other methods have failed). Dose Induction of anesthesia 25mg/ml solution, 100 \200\223150mg over 10 \200\22315 seconds (reduce dose and slower injection in elderly or debilitated); further bolus as necessary, after 30 \200\22360 seconds or up to 4mg/kg Child: 2 \200\2237mg/kg Raised intracranial pre ssure, 1.5 \200\2233mg/kg repeated as required Contraindications Porphyria Side-effects - Hypotension - Reduced respiratory rate and tidal volume - Reduced cerebral b lood flow and intracranial pressure - Local tissue damage secondary to extravasation. Notes Induction of anesthesia is rapid but a long half life means that effects may persist for up to 24 hours Ketamine See p.331 CHAPTER 5 Analgesia and anesthesia 384 Muscle relaxants (neuromuscular blocking agents) These drugs facilitate endotracheal intuba tion by abolishing muscle tone and protective laryngeal reflexes. They can be divided into two types, depolarizing and non-depolarizing agents. Depolarizing muscle relaxants: suxamethonium (succinylcholine) Description A depolarizing neuromuscular blocker. Presentation Suxamethonium chloride 50mg/ml \200\2242ml ampoule for iv injection. Effects Neuromuscular blockade. Indications Endotracheal intubation, especially in rapid sequence induction. Dose - Intravenous Initial dose 1mg/kg - Subsequent doses 0.5 \200\2231mg/kg at 5 \200\22310 minute intervals - Neonate and infant 2mg/kg, child 1mg/kg Intramuscular Infant up to 4 \200\2235 mg/kg, child up to 4mg/kg, maximum 150mg - Suxamethonium is the mo st rapidly acting neuromuscular blocker (30 \200\22345 seconds), its effectiveness manifest by twitching or fascicula- tion. Recovery occurs in 3 \200\2235 minutes. Total paralysis l asts approximately 4 minutes. Contraindications - Family history of malignant hyperthermia - Low cholinesterase activity (1 in 3000 Europeans have a reduced ability to break down suxamethonium) Suxemethonium may precipitate potassium release and fatal cardiac arrest with delayed admin istration post injury in patients with spinal cord or brain injury or in any other patient with pre-existing muscular dystrophy. Use immediately after injury is not associated with t hese problems. Side-effects - Bradycardia with repeated use - Raised intracranial pressure - Malignant hyp erpyrexia - Muscle pain after use. Notes Suxamethonium is the muscle relaxant of choice in the trauma patient. It does not cro ss the placenta. anesthesia1 385 Non-depolarizing muscle relaxants Description Non-depolarizing neuromuscular blockers which compete with acetyl- choline for receptor sites at the neuromuscular junction Presentation Atracurium Atracurium besylate 10mg/ml \200\2232.5, 5ml and 25ml, ampoules for injection Rocuronium Rocuronium bromide 10mg/ml \200\2245ml and 10ml ampoules for injection Vecuronium Vecuronium bromide powder for reconstitution \200\22410mg vial for injection wit h water Pancuronium Pancuronium bromide 2mg/ml \200\2242ml ampoule for injections Effects Neuromuscular blockade Indications Paralysis at induction and during maintenance of anesthesia Rocuronium is more suitable for intubation cover (see durations of action, below); atracurium is appropriate f or maintenance of paralysis Dose Atracurium (adult and child) Intubation: 300 \200\223600 g/kg by iv injection Mainten ance: 100 \200\223200 g/kg iv as required Rocuronium (adult and child over 1 month) Intubation: 600 g/kg by iv injection Maintenance : 150 g/kg iv (elderly 75 \200\223100 g/kg iv) as required Vecuronium Intubation: 80 \200\223100 g/kg by iv injection Maintenance: 20 \200\22330 g/k g iv as required Child: up to 4 months 10 \200\22320 g with further doses as required to a chieve effect; over 5 months, as adult, reduced dose may be needed for intubation CHAPTER 5 Analgesia and anesthesia 386 Pancuronium Intubation: 50 \200\223100 g/kg by iv injection Maintenance: 10 \200\22320 g iv as required Child: intubation 60 \200\223100 g/kg iv, maintenance 10 \200\22320 g/kg i v as required Neonate: 30 \200\22340 g/kg then 10 \200\22320 g/kg Contraindications Use will be more prolonged in patients with myasthenia gravis and in hypo thermia. Lower doses should, therefore, be used. Side-effects - Histamine release (atracurium, pancuronium) - Tachycardia and hypertension ( pancuronium). Notes Atracurium is the most commonly used competitive neuromuscular blocker in the UK Durations of action - Atracurium: effective within 90 \200\223120 seconds, duration 30 \200 \22340 minutes - Rocuronium: effective after approximately 60 \200\223120 seconds, duration 30 \200\22345 minutes Vecuronium: effective after approximately 3 minutes, duration 25 \200\22340 minutes Pancuronium: effective after 2 \200\2233 minutes, duration 65 \200\223100 minutes Non-depol arizing muscle relaxants can be reversed with anticholinesterases such as neostigmine. Beca use anticholinesterases act at para-sympathetic endings as well as neuromuscular junctions, a parasympatholytic drug, such as atropine, shoud be administered to prevent bradycardia a nd increased bronchial secretions. anesthesia1 387 Rapid sequence induction (RSI) The decision to undertake RSI depends on the clinical compet encies of the attending team. In most patients, the airway can be managed in a stepwise fas hion and adequate ventilation achieved using a two-person bag-valve-mask technique until ar rival in hospital. The indications for RSI in the pre-hospital arena are: Airway protection in acute or impending airway obstruction (for example, unconsciousness, facial burns) Failure to oxygenate the patient by any other measures (for example massive flail chest. To control and optimize ventilation in head injury patients. It is desirable to aim for low normal pCO2 though this is not routinely measured in the pre-hospi tal environment. - To control the aggressive or agitated patient - To control status epilep ticus when other measures have failed RSI involves securing the airway by the use of therap eutic agents and endotracheal intubation. Many trauma patients have a full stomach or decre ased gastric emptying. RSI is designed to minimize the risks of pulmonary aspiration. Ideal ly, full RSI requires four operators: - One person to intubate - One person to provide in-l ine stabilization of the neck - One person to provide cricoid pressure - One person to admi nister drugs and intravenous fluids The stages of RSI can be summarized as: Preparation - Pre-oxygenation - Induction and cricoid pressure - Intubation - Confirmation of endotracheal placement - Failed intubation drills. Preparation - All appropriate kit should be tested and immediately to hand, laid out in a systematic way. Alternative equipment (for example, LMA, needle or surgical airways) should be available in the event of failure to intubate. - All drugs should be drawn up and labeled ready for use. Pre-oxygenation - 12 \200\22315 litres of oxygen using a non-rebreathe mask with reservoir bag should be administered. If ventilation is inadequate, the patient should receive pre-oxygenation using the two-person bag-valve-mask technique. Simple airway adjuncts such as the oropharyngeal or nasopharyngeal airway may help facilitate pre-oxygenation. CHAPTER 5 Analgesia and anesthesia 388 Induction - Induction of anesthesia is achieved using an intravenous induction agent given rapidly without titration. As the induction agent is given, cricoid pressure is applied (see below). - A neuromuscular blocker (usually suxamethonium 100mg) is given immediately after the induction agent. In hypovolaemic/hypotensive patients, the use of ketamine or suxam- ethonium in isolation s hould be considered, adding drugs for sedation later. Cricoid pressure (Sellicks maneuver) - Cricoid pressure is applied as soon as the induction agent is given to reduce the risk of regurgitation and aspiration. Cricoid pressure should only be released when directed to do so by the intubator once the cuff is inflated. Intubation - Manual in-line stabilization of the cervical spine replaces cervical collars and supporting head blocks and straps. Intubation is performed as soon as the muscle relaxant has worked (following muscular twitching if suxamethonium is used). Prolonged attempts at intubation must be avoided, returning to bag-valve-mask ventilation. Longer-acting non-depolarizing drugs should be drawn up and given after successful intubation. A McCoy laryngoscope (straight blade) is preferred by many practitioners. Unless there is a complete view of the whole laryngeal inlet, intubation should be facilitated using a gum e lastic bougie. Confirmation of endotracheal placement Placement should be confirmed by: - Auscultation ove r both axillae and stomach - End tidal CO2 - Observation of the patient \200\231s chest Failed intubation - If there is any doubt about tube placement, it should be withdrawn and the patient ventilated using a two-person bag-valve-mask technique. Following re-oxygenation, further attempts can be undertaken. - If unsuccessful, alternativ e techniques include the use of the laryngeal mask airway (LMA) or intubating laryngeal mask airway (ILMA). - As a last resort, a needle or surgical cricothyroidotomy (cannot intubate, cannot ventilate) should be undertaken. Those practitioners with RSI competence m ust be able to undertake a surgical airway. anesthesia1 389 Local anesthesia An effective local anesthetic block can produce quality analgesia without sedation, nausea and vomiting, or depression of respiration. In excess, or used inappropria tely, their use can have a fatal outcome. Pharmacology Local anesthetic drugs reversibly interrupt axonal conduction by block- ing so dium channels. Their potency is related to lipid solubility and the speed of action is inve rsely proportional to their degree of ionization. The duration of action is related to prot ein binding and the degree of local vasoconstriction. Many local anesthetics act as vasodil ators and efficacy can be enhanced by the addition of adrenaline as a vasoconstric- tor. Ad renaline must be avoided near any end artery. The periphery of a nerve is blocked before it s center part. Therefore, the time to anaesthe- sia is significantly shorter for small nerv es such as digital nerves than larger nerves (for example, the femoral nerve). Complications of local anesthesia: toxicity Toxicity may be absolute, when too much is admi nistered, or relative, when the correct amount has been injected intravascularly or into a highly vascular area leading to systemic absorption. Toxicity can be avoided by ensuring th ere is no aspiration of blood prior to injection and by careful dosage calculation. The features of local anesthetic toxicity are: Perioral numbness with a metallic taste - Light headedness - Tinnitis - Visual disturbances - Slurring of speech - Muscle twitching and convulsions - Coma - Hypotension and bradycard ia - Ventricular arrythmias - Apnoea - Cardiac arrest. The speed of onset will depend on th e mechanism of the toxicity \200\224 clinical features of toxicity will occur within two mi nutes of intravenous injection whereas it may take 30 minutes for the clinical features to develop following an absolute overdosage. Treatment - Stop injecting the local anesthetic - Assess and manage the airway - Assess and ensure adequate ventilation - Administer 12 \200\22315 litres of oxygen via a non-rebreath e mask and oxygen reservoir Obtain vascular access (if not already in place) - Obtain baseline observations and monitor frequently - Treat convulsions with diazemuls (see p.146) - Treat hypotension by leg eleva tion and bolus fluid therapy. CHAPTER 5 Analgesia and anesthesia 390 Treat life-threatening symptomatic cardiac arrhythmias (cardiac pacing may be required) Consider bretylium for refractory ventricular fibrillation. Hypersensitivity reactions Anaphylactic and anaphylactoid reactions are rare. Treatment fol lows conventional guidelines. Nerve damage Nerves may be traumatized by sharp needles. In conscious patients, injections must be stopped if the patient complains of local severe pain or pain in the distribution o f the relevant nerve. As there is no feedback in the unconscious patient, nerve blocks shou ld be avoided. Altered clinical assessments An effective local block will compromise patient assessment. I t is essential to complete neurological assessment and assessment for compartment syndrome in the relevant areas prior to local block administration. anesthesia1 391 Local anesthetic agents Lignocaine (lidocaine) See also p.332. Description Class Ib anti-arrhythmic and local anesthetic. Presentation for local anesthesia - Lignocaine hydrochloride 1% (10mg/ml) \200\2242ml, 5ml, and 10ml ampoules for injection Lignocaine hydrochloride 2% (20mg/ml) \200\2242ml and 5ml ampoules for injection. Effects Lignocaine blocks sodium channels, reducing the conduction rate and amplitude of ne rve electrical impulses. Indications Local anesthesia for painful procedures. Dose A MAXIMUM safe lignocaine dose for an average adult is 20ml of 1% (200mg) or equivalen t volume of higher concentration solution. This dose can be increased if lignocaine is give n with a vasoconstrictor such as adrenaline. Use of lignocaine with adrenaline may cause ga ngrene if injected into digits or appendages and is NOT RECOMMENDED in pre-hospital care. C hildren (local anesthesia): 3mg/kg Contraindications - Local analgesia: hypovolaemia, complete heart block - Solutions with ad renaline: see notes below. Side-effects - Light headedness followed by sedation, circumoral paraesthesia, and twitching; convulsions in severe cases Convulsions and cardiovascular collapse on intravenous administration. Notes 0.5% lignocaine is available for local anesthetic use. It is not recom- mended in the pre-hospital environment. CHAPTER 5 Analgesia and anesthesia 392 Prilocaine Prilocaine has a similar profile to lignocaine but is slightly less toxic. Dose (adult) - Infiltration: 0.5% up to 80ml - Nerve block: 1% up to 40ml, 2% up to 20ml. Duration of effect 1.5 \200\2233 hours. Bupivicaine A longer-acting local anesthetic usually used for nerve blocks. Bupiva- caine i s more toxic than lignocaine. Dose (adult) - Infiltration: 0.25% up to 60ml - Nerve block: 0.25% up to 60ml, 0.5% up to 3 0ml. Duration of effect 3 \200\2234 hours. anesthesia1 393 Local anesthetic blocks Wound blockade Faced with a painful wound, restricted analgesics, a nd a long transfer time to hospital, local anesthetics can be instilled into the wound or i njected into the sides of the wound for symptomatic relief. Specific blocks Before performi ng a specific block, the procedure should be explained to the patient and consent obtained. Monitoring and intravenous access must be in place. Axillary blocks, wrist blocks (ulnar, median, and superficial branches of the radial nerve) , triple blocks (femoral sciatic and obturator nerves), and foot and ankle blocks (saphenou s, tibial, deep peroneal, superficial peroneal, and sural nerve) are all specialist blocks and are not commonly practiced in pre-hospital care unless by experienced trained personnel in special circumstances. Two blocks in common use, however, are the femoral nerve block and the metacarpal block. Femoral nerve block The femoral nerve block produces analgesia and anesthesia in the anteri or thigh, femur, and hip region. - Place the patient supine with the hip abducted and sligh tly externally rotated (hip flexion risks inadvertent vascular puncture) The key landmark is the femoral artery as it emerges below the inguinal ligament From medial to lateral, the essential anatomy is vein, artery, nerve - Insert a needle appr oximately 1cm lateral to the artery aiming in a cranial direction at a depth of 2 \200\2233.5cm Aspirate to exclude vascular puncture and inject at this point - Instill 10 \200\22315ml of 1% lignocaine or prilocaine The time to onset of a femoral nerve block is 15 \200\22330min utes with a dura- tion of effect of 4 \200\2236 hours. Metacarpal digital nerve blocks The digital nerves lie parallel to the long axis of the met acarpal bones at the level of the distal palmar crease at a depth of 0.5 \200\2231.0cm. - I nsert a 23g needle at the appropriate site and depth - Exclude vascular puncture - Instill 3 \200\2235ml of 1% lignocaine or prilocaine The time to onset of action is 3 \200\2235minu tes with a duration of action of 45 \200\22360 minutes. Vasoconstrictors should NEVER be us ed at this site. CHAPTER 5 Analgesia and anesthesia 394 Inguinal ligament External ring Femoral nerve Femoral vein Femoral artery Termination of long saphenous vein Patella Fig. 5.1 The femoral nerve block. Reprinted with permission from Greaves I et al. (2000). T rauma care. Hodder Arnold. This page intentionally left blank CHAPTER 6 Poisoning and substance abuse 396 Approach to the poisoned patient 398 Differential diagnosis of the poisoned patient 400 Sym ptom complexes in poisoning 402 Decontamination 404 Antidotes 406 Poisons 408 Angiotensin c onverting enzyme (ACE) inhibitors 408 Adder bite 409 Alcohol 410 Anticholinergic drugs and agents 411 Anticoagulants 412 Antifreeze 413 Barbiturates 414 Batteries 415 Benzodiazepines 416 Beta blockers 417 Bleach 418 Calcium channel blockers 419 Carbamazepine 420 Carbon mon oxide 421 Chlorine 423 Corrosive substances \200\224acids and alkalis 424 CS gas 425 Cyanid e 426 Detergents and related substances 427 Digoxin and related drugs (cardiac glycosides) 428 Disinfectants 429 Ethanol 430 Ethylene glycol 431 Fungi \200\224poisonous 432 Hypoglyca emic agents 433 Insulin 434 Iron 435 Lithium 436 Mefenamic acid 437 Methanol 438 Chapter 6 APPROACH TO THE POISONED PATIENT1 397 Poisoning and substance abuse Metoclopramide 439 Monoamine oxidase inhibitors (MAOIs) 440 Opiates 441 Organophosphate ins ecticides (including carbamates) 442 Paracetamol 443 Paraquat 444 Pepper spray 445 Petroleu m distillates and turpentine 446 Phenothiazines and haloperidol/droperidol 447 Phenytoin 44 8 Plant toxins 449 Pulmonary irritants 452 Salicylates 453 Serotonin uptake inhibitors \200 \224selective serotonin inhibitors (SSRIs) 454 Snake bite 455 Tetracyclic antidepressants 456 Theophyllines 457 Toiletries and cosmetics 4 58 Tricyclic antidepressants 459 Venomous bites and stings 460 Substance abuse 462 Amphetam ines 463 Amyl nitrate 464 Benzodiazepines 465 Cannabis 466 Cocaine/crack cocaine 467 Ecstas y 469 Gammahydroxybutyric acid 470 Hallucinogenic fungi 471 Ketamine 472 Lysergic acid diet hylamide (LSD) 473 Methanol 474 Opiates 475 Phencyclidine 476 Volatile solvents 477 Common street names for drugs of abuse 478 CHAPTER 6 Poisoning and substance abuse 398 Approach to the poisoned patient In many cases, the toxic agent will not be known and when it is, options for specific treatment are usually limited. Only a very few antidotes are av ailable for pre-hospital use (see pp.406 \200\2237). As a consequence, a generic approach t o the poisoned patient is essential. This will follow the ABCDE sequence: - Airway (with C spine control if there is any possibility of significant trauma) Breathing \200\224with high-flow oxygenation - Circulation Establish intravenous access - Monitor pulse, BP, SaO2, and ECG Disability \200\224establish and record the conscious level using AVPU and DON \200\231T FORGET TO CHECK THE PUPILS! Exposure \200\224as required to exclude other significant injury Airway A patent airway should be established and maintained at all tines. The technique use d will vary according to the patient \200\231s level of consciousness. If the conscious lev el is reduced, an oral or nasopharyngeal airway can be inserted. Intubation may be necessar y. Many patients will also have taken alcohol and will, therefore, be prone to vomit. Appro priate use should be made of the recovery position and working suction MUST be available. Breathing High-flow oxygen should be administered and respiration supported as required. Circulation Intravenous access should be obtained in all but the most trivial of poi- sonin gs. This must not delay transfer of the critical patient. Inadequate circulation may result from a wide range of mechanisms. Wherever possible, arrythmias should be treated in hospit al and rapid evacuation is essential. The arrythmias associated with tricyclic antidepressa nts respond to alkalinization with sodium bicarbonate. If there is no sign of arrythmia or heart failure, judicious administration of intravenous fluids can be used to raise the bloo d pressure. Pulse oximetry, ECG monitor- ing, and blood pressure monitoring should be routi ne. Disability Check AVPU (p.187) and pupils. Assessment of the pupils may provide vital information. Pin point pupils are characteristic of opiate poisoning but also occur in organo- phosphate poisoning (the context may aid in diagnosis). Dilated pupils occur in the anticholinergic syndrome a ssociated with overdose of atro- pine, tricyclic antidepressants and other agents. Assessme nt of the AVPU response will determine the depth of reduction of conscious level. APPROACH TO THE POISONED PATIENT1 399 Dilated pupils - Atropine - Tricyclic antidepressants - Phenothiazines. Constricted pupils - Opiates - Organophosphates. Exposure Exclude or identify injuries due to the overdose or alcohol. Complete exposure of the patient should be avoided in the pre- hospital environment and an exhaustive (and probably fruitless) search for clues should not delay transfer to hospital as long as appropriate attention has been paid to airway and breathing. Nevertheless, some clues such as needle marks from intravenous injection, sores around the mouth (from inhalat ion of chemicals) or burns from caustic substances may be identified. Further information In most cases, time need not be wasted seeking specialist advice. This can be done after arrival in hospital. If transfer is likely to be prolonged or delayed, or the poisoning appears trivial, advice can be sought from the UK National Poisons Advice Ce nter (see box). DON \200\231T EVER FORGET GLUCOSE UK National Poisons Advice Center 0870 600 6266 They will direct the call to the relevant l ocal center CHAPTER 6 Poisoning and substance abuse 400 Differential diagnosis of the poisoned patient In many cases, it will be obvious that a pat ient has been poisoned, and questioning the patient or witnesses, or scene assessment will rapidly confirm this. However, patients with serious suicidal intentions may go to consider able lengths to hide what they have done, or if the patient is unconscious, the clues may b e more subtle. A high index of suspicion is therefore essential. In addition, in some cases , the poison may be unknown or more than one substance may be involved. Mixed overdoses are far from uncommon, and industrial poisonings more often than not involve multiple chemical s which may further react with each other to complicate the clinical picture. Poisoning should be suspected if: The patient \200\231s conscious level is altered - Symptoms occur in an unusual age group - The context suggests prevalence of drug abuse - Bizarre symptom complexes or signs are pre sent - There is obvious reluctance to provide information. Because the symptoms and signs o f poisoning are so varied, and in the majority of cases non-specific, it is equally importa nt not to jump to the conclusion that a patient has been poisoned and to exclude other pote ntially treatable causes. Diagnoses which should be excluded include: Metabolic - Hypoxia - Hypoglycaemia - Electrolyte abnormality. Traumatic - Head injury - Hy potension due to hemorrhage. Neurological - Stroke - Subarachnoid hemorrhage - Post-ictal s tate. DIFFERENTIAL DIAGNOSIS OF THE POISONED PATIENT1 401 CHECK FOR - Pill bottles and medicine containers (take them to hospital) - Signs of alcohol consumption - Medic-Alert bracelet - Injection marks - Paraphernalia of drug abuse - Sig ns of previous self harm - Suicide note (rare). CHAPTER 6 Poisoning and substance abuse 402 Symptom complexes in poisoning There are a number of symptoms or groups of symptoms which t ogether provide useful clues to the likely causative agent. A list of drugs and common recognizable presentations is given below and in Table 6.1: Coma with stable vital signs - Benzodiazepines Hyperthermia - Anticholinergics - Neuroleptics (major tranquilizers/antipsychotics) - Sympa thomimetics - Phencyclidine and hallucinogens - Aspirin. Hypothermia - Sedatives, opiates, alcohol (reduce CNS activity) - Insulin and oral hypoglyc aemics. Hypotension with normal mental state - Calcium channel blockers. Tachypnoea - CNS stimulants - Aspirin - B agonists - Agents causing pulmonary oedema \200 \224including organophosphates, chlorine Agents causing hypoxia \200\224including cyanide, carbon monoxide - Agents causing metaboli c acidosis \200\224including methanol, ethylene glycol. Dilated pupils - Tricyclic antidepressants - Amphetamines (see p.463) - Phenothiazines. Constricted pupils - Opiates - Organophosphates. In many cases it will not be possible to i dentify the agent precisely, so: TREAT THE PATIENT, NOT THE DRUG Table 6.1 Common recognizable presentations Syndrome Causes Symptoms Signs Comments Opioid Opiates Confusion Reduced conscious level Pinpoint pupils Respiratory depression Hypotension Responds to naloxone Cholinergic Organophosphates Sweating, salivation, blurred vision, vomiting, wheeze, diarrhea, muscle cramp Tachycardia, hypo/hypertension, fasciculation, paralysis, respiratory failure, ataxia, fits , coma S Y M P T O M C O M P L E X E S Anticholinergic Atropine Tricyclic antidepressants Phenothiazines Lethargy, confusion, hallucinations, fits, blurred vision, urinary retention, dry mouth, fl ushing Ataxia, cardiac failure, respiratory failure, dry skin, dilated pupils, abdominal distensio n Sympathomimetic Aminophylline Cocaine Amphetamine, Caffeine Phencyclidine Excitation Fits Tachycardia Hypertension I N P O I S O N N G Diazepam Temazepam Coma Vital signs normally stable Hypotension and respiratory depression can occur Benzo diazepine I 1 4 0 3 CHAPTER 6 Poisoning and substance abuse