Complications inAnesthesia:A Review of the LiteratureRobert W. Simon, DNP, CRNA, CHSE, CNE
! Identify the most common complicationsassociated with the administration ofanesthesia as reported in various casestudies.LearningObjectives! List the proper steps associated inmanaging these complications.! Discuss current evidence-based practicein relation to managing these events.
CASE STUDY #1As reported by: Leissner KB, Ortega RA, et al.Journal of Clinical Anesthesia
Case Study #1! A 21-year-old male with a past medical history ofasthma and smoking, presented to the operating roomfor an open reduction and internal fixation of afractured mandible he sustained in a bar fight.! After successful iv placement, and induction of generalanesthesia, a pre-formed nasal RAE tube wasadvanced via one of the patient’s nares into theoropharynx.
Case Study #1! Laryngoscopy was performed with a MAC 3laryngoscope blade, and the visualization of the larynxwas described as grade one, according to theCormack and Lehane classification.! The endotracheal tube was then advanced with theaid of a Magill forceps without difficulty.
Case Study #1! After intubation,attempts to ventilate thepatient encounteredhigh airway resistance,and the end-tidalcarbon dioxide tracingshowed an obstructivepattern.
Case Study #1! Breath sounds were distant, and there was little chestmovement.! There was no gastric insufflation with positive pressureventilation.! ETCO2 waveform was still present and still showingobstructive pattern.
Case Study #1! A repeat direct laryngoscopy was performed,revealing that the endotracheal tube was through theglottis.! Also, the patient’s SPO2 was still at his baseline of96-98%
SO WHAT’S THE CAUSE?
Case Study #1! The difficulty in ventilation was assumed to be due tosevere bronchospasm! Treatment was initiated with aerosolized andintravenous bronchodilators.! A suction catheter was inserted into the preformednasal tube but high resistance was encountered at thebend of the tube.
Case Study #1! Desaturation occurred and another repeat directlaryngoscopy again revealed the endotracheal tubepassing through the glottis.! Efforts to treat the presumed severe bronchospasmwere unsuccessful.! Next, a chest x-ray was obtained.
Case Study #1! The oxygen saturation continued to drop, and thepatient suffered a cardiac arrest.! The patient later died due to severe anoxicencephalopathy.
The Cause! When the chest radiograph was reviewed, it showedthat the endotracheal tube was kinked within thetrachea.! The team believed that the shape of the endotrachealtube was the reason for the inabilty to pass thecatheter completely and the maneuver was deemednoncontributory.
Bronchospasm During GA
Bronchospasm During GA! Can present in isolation or as a component of a moreserious underlying pathology such as anaphylaxis.! Characterized by prolonged expiration, wheeze andincreased peak airway pressures during IntermittentPositive Pressure Ventilation (IPPV).
Bronchospasm During GA! Untreated it can cause hypoxia, hypotension andincreased morbidity and mortality.! Suspected bronchospasm during anesthesia should beassessed and treated promptly.! Ongoing management should address the underlyingcause.
Incidence of Bronchospasm! Perioperative bronchospasm in patients with reactive airwaysdisease is relatively uncommon.! In patients with well-controlled asthma and COPD theincidence is approximately 2%.! The overall incidence of bronchospasm during generalanesthesia is approximately 0.2%.! Exposure to tobacco smoke, history of upper respiratory tractinfection (URTI) all increase the risk of bronchospasm duringanesthesia.
Manifestations ofBronchospasm! Bronchospasm during anesthesia usually manifests asprolonged expiration.! An associated expiratory wheeze may be auscultatedin the chest or heard in the breathing circuit.! Wheezing requires movement of gas through narrowedairways and so in severe bronchospasm wheeze maybe quiet or absent.
Manifestations ofBronchospasm! Similarly, breath sounds may be reduced or absent.! With IPPV, peak airway pressures are increased, tidalvolumes reduced, or both.! Bronchospasm is not the only cause of wheeze orincreased peak airway pressure
Causes of Wheeze During GA1.Partial obstruction of tracheal tube (including ETTabutting the carina or endobronchial intubation)2.Bronchospasm3.Pulmonary edema4.Aspiration of gastric contents5.Pulmonary embolism6.Tension pneumothorax7.Foreign body in the tracheobronchial tree
Causes of Increased PAP During IPPV!!!Anesthetic equipment!Excessive tidal volume!High inspiratory flow ratesAirway device!Small diameter tracheal tube!Endobronchial intubation!Tube kinked or blocked!Obesity!Head down position!Pneumoperitoneum!Tension pneumothorax!BronchospasmPatient
Occurrences ofBronchospasm! Bronchospasm occurs most commonly andapproximately equally during the induction andmaintenance stages of anesthesia! Less often encountered in the emergence andrecovery stages.! Bronchospasm during the induction stage is mostcommonly caused by airway irritation, often related tointubation.
Causes of Bronchospasm! During the maintenance stage of anesthesia,bronchospasm may result from an anaphylactic orserious allergic reaction.! Drugs! Antibiotics! neuromuscular blockers! Blood products! red blood cells! fresh frozen plasma! Other allergens! latex
Causes of Bronchospasm! Other features of allergic or anaphylactic reactioninclude:! Cutaneous signs! rash! urticaria! angioedema! Cardiovascular signs! tachy/bradycardia! hypotension! circulatory collapse
Differential Diagnoses! When assessing bronchospasm thereare other important differentialdiagnoses and contributing factors toconsider:! Mechanical obstruction! Laryngospasm! Bronchial hyperreactivity! Inadequate depth of anesthesia! Pharmacological! Airway soiling
Mechanical Obstruction! A kinked, blocked (mucous plug, cuff herniation) ormisplaced (endobronchial, esophageal) tracheal tube! Anything that causes occlusion in the breathing circuitcan mimic severe bronchospasm
Laryngospasm! This should be considered and excluded.! In non-intubated patients acute laryngospasm canproduce upper airway noise (usually inspiratory),reduced breath sounds and difficulty in ventilation.! Laryngospasm can present with signs of airwayobstruction including increased respiratory effort,tracheal tug and paradoxical movement of the chestand abdomen (‘see-saw’ respiration).
Bronchial Hyperreactivity! If the patient is known to be at increased risk ofbronchial hyperreactivity the suspicion ofbronchospasm is increased! Main patient groups are those with reactive airwaysdisease, esp. poorly controlled asthma and COPD! Also associated with preoperative exposure totobacco smoke, upper respiratory tract infection (URTI)
Inadequate Depth ofAnesthesia! Certain surgical procedures have highly stimulatingstages that can trigger bronchospasm (andlaryngospasm).! Examples of include anal or cervical dilatation,stripping of the long saphenous vein during varicosevein surgery and traction on the peritoneum.
Pharmacological! Certain volatile anesthetic agents (isoflurane,desflurane) if introduced quickly can triggerbronchospasm.! IV agents including beta-blockers, prostaglandininhibitors (NSAIDs) and cholinesterase inhibitors(neostigmine) are implicated.! Histamine releasing medications
Airway Soiling/ Aspiration! Unexplained bronchospasm, especially in patients withoutincreased risk of airway hyperreactivity, should promptconsideration of airway soiling due to secretions, regurgitationor aspiration.! May occur more with the use of the laryngeal mask airway(LMA)! May also occur with an uncuffed endotracheal tube (ETT) oran inadequately inflated/punctured cuff.! A history of GERD or sudden coughing in a patient breathingspontaneously with an LMA should increase the suspicion ofairway soiling.
PREVENTION OF BRONCHOSPASM!Patients with asthma and COPD should be thoroughly assessedand optimized for surgery.!Wheezing, cough, increased sputum production, shortness ofbreath and diurnal variability in peak expiratory flow rate (PEFR)indicate poor control.!Recent or frequent exacerbations or admission to hospital maybe an indication to postpone non-essential surgery. Patientsshould be encouraged to continue their medication until the timeof surgery.!Preoperative bronchodilators, inhaled or oral corticosteroids,chest physiotherapy and referral to respiratory
! A careful medication history should betaken with particular reference to drugsensitivities.! NSAID-induced bronchospasm in adultasthmatics may be as high as 15% (2010)PREVENTION OFBRONCHOSPASM! All patients should be encouraged to stopsmoking preoperatively. (Six to eightweeks of abstinence before surgery)! URTI in children increases the risk ofbronchospasm and so it may benecessary to postpone surgery until thecomplete resolution of symptoms(approximately 2 weeks)
! Pretreatment with an inhaled/nebulized betaagonist, 30 minutes prior to surgery.! Induction of anesthesia with propofol andadequate depth of anesthesia before airwayinstrumentation reduces the risk ofbronchospasm.PREVENTION OFBRONCHOSPASM! The use of an LMA (in suitable patients) hasbeen shown to reduce the incidence ofbronchospasm compared to trachealintubation.! Regional techniques where appropriate canalso avoid the need for general anesthesia andintubation.
! Goal is to provide ongoing therapy andaddress the underlying cause.! Corticosteroids and antihistamines shouldbe given early if the problem is not settlingwith initial measures.SECONDARYMANAGEMENT! Further consideration should be given toallergy/anaphylaxis and a thoroughexamination made for cutaneous andcardiovascular signs.! Review the medication history and considerall drugs given in the perioperative period.
! Examine the patient and reconsider alternativediagnoses such as acute pulmonary edema,tension pneumothorax, pulmonary embolism orforeign body.! If the indication for surgery is not life-threatening,consider abandoning surgery, especially if there isongoing difficulty with ventilation, falling oxygensaturations or hemodynamic compromise.SECONDARYMANAGEMENT! In a non-intubated patient with severebronchospasm, it may be necessary to intubateand mechanically ventilate the lungs whiletherapy is initiated.! Avoidance of histamine release is important andan appropriate muscle relaxant should be used(e.g. rocuronium or vecuronium if available).
CASE STUDY #2As reported by: Jaffe, RA et al.Anesthesiology
Case Study #2! A 54-year-old (160 cm and 90 kg) woman is scheduledfor right front temporal craniotomy for superficialtemporal artery to middle cerebral artery bypass.! PMH: bilateral Moyamoya disease, atrial aneurysm,obstructive sleep apnea, hypertension, andhyperlipidemia.
Moyamoya Disease Defined!The National Institute ofNeurological Disorders and Strokedefines Moyamoya disease as arare, progressive cerebrovasculardisorder caused by blockedarteries at the base of the brain inan area called the basal ganglia.!The name “moyamoya” means“puff of smoke” in Japanese anddescribes the look of the tangle oftiny vessels formed to compensatefor the blockage.!It primarily affects children, but itcan also occur in adults.
Symptoms of MoyamoyaDisease! In children, the first symptom is often stroke, orrecurrent transient ischemic attacks,accompanied by muscular weakness or paralysisaffecting one side of the body, and/or seizures.! Adults usually experience a hemorrhagic strokedue to recurring blood clots in the affected brainvessels.(The National Institute of Neurological Disordersand Stroke)
Case Study #2! All routine preoperative checks were performed on theDrager Apollo anesthesia machine without incident,including the machine’s automated self-test and leaktest.! No abnormalities are found.
Case Study #2! During preoxygenation a normal capnograph tracing isobserved.! The pt is given muscle relaxant and intubated with a7.0 cuffed ett secured at 23 cm at the lip.! Correct position of the Ett is confirmed both by ETCO2and B/L auscultation of breath sounds.
Case Study #2! Subsequently, an abnormalcapnograph waveformwith a single humpmidplateau was noted.! Vitals at this time:! ETCO2 36 mmHg,! tidal volume 513 ml,! peak inspiratory pressure30 cm H2O,! respiratory rate 10,! inspiratory to expiratoryratio 1:4.
Case Study #2! The author notes that:! “There was no obvious cause for this unique waveform,but we thought that it may be related to a leak in thesampling system.”! Tightening the sample line connections resulted in nochange.
Case Study #2! They then replaced theentire sample line with anew 10-foot sample lineand observed thefollowing:
SO WHAT’S THE CAUSE?
It’s A Trap!!! Next, the water trap wasinspected and crackswere seen
Case Study #2! Because a new water trap wasnot available, the crackedwater trap was wrapped with a3M Tegaderm dressing andreinstalled; resulting in a normalappearing waveform.
The Dromedary Sign! This sign occurs as a result of an ‘increaseddyssynchrony between the positive pressure phaseof mechanical ventilation and the arrival of endtidal gas.”! During expiration, negative pressure at the crack inthe water trap allowed room air to dilute thesample leading to a decrease in ETCO2concentration.
! Because of the cracks in the water trap,the positive pressure exerted by theventilator contributes to an increase indead space in the sample line as well.TheDromedarySign! Therefore, the transit time delay causedby the additional dead space in thesample line combined with a crackedwater trap resulted in the appearance ofthe Dromedary sign.
Case Study #3As reported by: Kinghorn, K. MD; et. alAnesthesiology
Case Study #3!A 60-yr-old, 104-kg, 71-inch-tall manpresented for a left total kneearthroplasty for degenerative jointdisease.!Medical history: hypertension,chronic obstructive pulmonarydisease, gout, and a 40-pack-yearsmoking history.!Home medications: naproxen,atenolol, and allopurinol.!Naproxen had been discontinued 1week before surgery.
Case Study #3Results ofpreoperative neurologicexam werenormal.Examinationby theorthopedicsurgeonnoted theabsence ofa valgusdeformity orflexioncontracture.
Case Study #3! Before placement of theblocks, 100 mcg fentanyland 2 mg midazolam wereadministered intravenously.! In the preoperative holdingarea, sciatic and femoralnerve catheters wereplaced for postoperativepain management.
Case Study #3! The patient was transferred to the operating room,where a subarachnoid block was performed forsurgical anesthesia using a 25-gauge Whitacre pencilpoint spinal needle through which 1.2 ml hyperbaricbupivacaine (0.75%) was injected.! A T10 level of anesthesia was attained. The patient waspositioned supine for surgery, and a tourniquet wasapplied to the left thigh.(Kinghorn; et. Al2012)
Case Study#3! Before surgicalincision, thetourniquet wasinflated to apressure of 250mmHg. The surgerywas completeduneventfully.! Total tourniquet timewas 46 min.
! In the recovery room, infusions in eachcatheter were begun immediately aftersurgeryCaseStudy #3! The catheters were test dosed with nointravenous symptoms, and bupivacaine(0.25%) infusion was begun in eachcatheter at a rate of 7 ml/h.
POD 1! On the morning of postoperative day 1, the local anestheticinfusions were discontinued, and both catheters wereremoved! On the afternoon of postoperative day 1, physical exam bythe hospital’s pain service was noted a left lower extremitymotor strength score of 3 of 5 (Medical Research Councilscale) and an absence of ankle dorsiflexion! The patient reported no pain or tenderness.! No ecchymosis was seen at the sites of nerve block injection
! The patient reported pain on the plantarsurface of the left foot, pain over theposterior left thigh, and a left foot dropwas noted.POD #2! The patient continued physical therapyfor the remainder of his inpatient stay andwas discharged home on postoperativeday 4, without improvement in motorexamination.
Case Study #3! An outpatient appointment was made with neurologyduring the week after discharge, but the patient failedto appear.! Despite several telephone call reminders, he did notfollow up.
Case Study #3! Three and one half weeks later, the patientpresented to the emergency departmentreporting pain and weakness in the left leg andfoot.! Physical exam revealed a warm left lowerextremity with mild swelling, absent dorsiflexion,and decreased sensation over both the medialand lateral aspect of the foot.
Case Study #3! A complex regional pain syndrome type one wasconsidered; gabapentin was prescribed, andplans were made for the patient to follow up witha neurologist the next week! At the neurologist’s appointment, the patient stillhad unresolved lower extremity symptoms, theplantar surface foot pain had been replaced bynumbness over the dorsum of the foot andoccasional shooting pains up the posterior aspectof the leg and thigh
! Decreased sensation to pinprick on thedorsum of the foot, weakness of both footdorsiflexion (score 0 of 5) and plantarflexion (score 3 of 5), mild weakness (score4of 5) of the hamstrings, and absence ofthe left ankle deep tendon reflex.At theNeurologist’s! Electrodiagnostic testing demonstratedabsent left sural and superficial peronealsensory responses, and absent leftperoneal (extensor digitorum brevis andtibialis anterior recording) and tibial motorresponses.! The right sural sensory response wasnormal.
Case Study#1! There was no sciaticnerve abnormality,but there was anabnormal signal inthe mid- to distalfemur that wasconsistent with abone infarct
! Foot drop is a term that aptly describesthe most striking physical finding ofperoneal nerve injury.Foot Drop! Compensation for weakness of footdorsiflexion results in the characteristichigh-stepping gait used to preventtripping over the toes.
Foot Drop! Weakness of foot eversion and toe extension is alsopresent.! This clinical picture can be caused by a lesionanywhere along the course of the L5 nervefascicles, from the anterior horn cells to theperoneal nerve itself.! Damage to the sciatic nerve can result in footdrop if there is injury to the lateral trunk becausethis trunk becomes the peroneal nerve.
Foot Drop! Peroneal nerve injury causing foot drop is a wellknown complication of total knee arthroplasty.! Injury in this setting can be caused bycompression, ischemia, traction, crush, orlaceration.! The incidence of this injury based on more recentobservations is estimated to be 0.79%
Nerve Injury Etiology! Most commonly suggested risk factors is a valgusdeformity of the joint greater than or equal to 10degrees! Intraoperative correction of the deformity results intraction on the nerve.
! preoperative flexion contracture of the knee alsoincreases stretch on the nerve after surgery and isa predisposing factor.! baseline neuropathy increases risk, andpreoperative neurologic evaluation has beenrecommended so that surgical technique can beadjusted if a known underlying neuropathy ispresent
Other PredisposingFactors 1.Tourniquet time longer than 120 min2.Rheumatoid arthritis3.constrictive dressings4.postoperative bleeding,5.previous lumbar laminectomy.6.tourniquet pressures greater than 400 mmHg
! The numerous factors that influence therisk of nerve injury after knee arthroplastycan make the determination of a singlecause of injury challenging.CaseStudy #3! It is likely that a combination of thesefactors explains the much higherincidence of nerve injury after total kneearthroplasty than is associated withregional nerve block or tourniquet usealone
! Like other peripheral nerve blocks, cancause neurologic injury from needletrauma, intraneural injection of localanesthetic, neuronal ischemia, andneurotoxicity of local anesthetic.SciaticNerveBlockade! True symptoms of neuropathy, (allodynia,hyperpathia, and hyperesthesia) must bedistinguished from perceived nerve injuryresulting in paresthesia.
! Lack of pain on injection is not a reliableindicator of safetySciaticNerveBlockade! Resistance on injection has beensuggested to be more indicative ofintraneural placement of the needle.
! An epidural in place has been implicatedas a risk factor for peroneal nerve injuryafter total knee arthroplasty.InSummary! It has been proposed that the sensoryand proprioceptive deficits of thistechnique may result in patient toleranceof either unsafe leg position or overlyconstrictive dressings.! Epidural anesthesia is also suspected ofdelaying the diagnosis of nerve injury ofother etiologies.
CaseStudy #4As reported by: Gilles A.Orliaguet, M.D., Ph.D; etalAnesthesiology
! A 10-month-old boy (8.5 kg body weight)was taken to the operating room (at11:00 PM), without premedication, foremergency surgery of an abscess of thesecond fingertip on the right hand.CaseStudy #4! Past medical history: unremarkableexcept for an episode of upperrespiratory tract infection 4 weeks ago.! The mother volunteered that he wasexposed to passive smoking in the home.
Case Study #4! Preoperative evaluation was normal (85/50 mmHg,heart rate 115 beats/min, [SpO2] 99% on room air).! The procedure was expected to be very short, andgeneral anesthesia with inhalational induction andmaintenance, without tracheal intubation
! The pt was induced by a resident under the directsupervision of a senior anesthesiologist withinhaled sevoflurane in a 50/50% mixture of oxygenand nitrous oxide.CaseStudy #4! Two min after loss of eyelash reflex, a first episodeof airway obstruction with inspiratory stridor andsuprasternal retraction was successfully managedby jaw thrust and manual positive pressureventilation.! An IV line was obtained while the child wasmanually ventilated.! Anesthesia was then maintained by facemaskwith 2.0% expired sevoflurane in a mixture ofoxygen and nitrous oxide 50/50%.
! About 5 minutes into the case; aninspiratory stridulous noise was notedagain.CaseStudy #4! Manual facemask ventilation becamedifficult with an increased resistance toinsufflation and SpO2dropped rapidlyfrom 98% to 78%, associated with adecrease in heart rate from 115 to 65beats/min.! Laryngospasm was immediatelysuspected.
! Despite a jaw thrust maneuver, positivepressure ventilation with 100% O2, andadministration of two bolus doses (5 mg) ofIV propofol (0.6 mg/kg), the obstructionwas not relieved and SpO2 decreased to52%.CaseStudy #4! A 0.2-mg IV bolus dose of atropine wasinjected and IV succinylcholine was givenat a dose of 16 mg, followed by trachealintubation.! Thereafter, surgery was quickly completed,while tracheal extubation andpostoperative recovery were uneventful.
! Laryngospasm is an anestheticemergency that is still responsible forsignificant morbidity and mortality inpediatric patients.Laryngospasm! Frequent complication that occurs withvarying frequency dependent on multiplefactors.
Laryngospasm! According to recent research, childrenare more prone to laryngospasm thanadults, with laryngospasm being reportedmore commonly in children (17.4/1,000)than in the general population
! Many factors may increase the risk oflaryngospasm.! These risk factors can be related to the:RiskFactors1.Patient2.Procedure3.Anesthesia
! Personal history! Male! Upper respiratory tract infection presentthe day of surgery or within the past 2weeksPatientRiskFactors! Wheezing at exercise or more than threetimes in past 12 months! Nocturnal dry cough! Eczema present or in the past 12 months! Family history! History of at least two family membershaving asthma, atopy (rhinitis, eczema),or smoking
! Age.PatientRiskFactors! Young age is one of the most importantrisk factors.! The highest incidence (more than 2%)was found in preschool age groups.
Upper Respiratory TractInfection.! Upper respiratory tract infection is associated with atwofold to fivefold increase in the risk of laryngospasm.! Children with URI are prone to develop airway (upperand bronchial) hyperactivity that lasts beyond theperiod of viral infection.! Whereas epithelial damage heals in 1–2 weeks, virusinduced sensitization of bronchial autonomic efferentpathways can last for up to 6–8 weeks.
SmokeExposure! Household exposure to tobacco smokewas shown to increase the incidence oflaryngospasm from 0.9% to 9.4% inchildren scheduled for otolaryngologyand urologic surgery.
! The highest incidence of laryngospasm isfound in procedures involving surgery andmanipulations of the pharynx and larynx.ProcedureRelatedRiskFactors! The incidence of laryngospasm, aftertracheal extubation, has already beenreported to exceed 20% and be as highas 26.5% in pediatric patients who haveundergone tonsillectomy.! Urgent procedures also carry a higher riskof laryngospasm than electiveprocedures.
! Insufficient depth of anesthesia is one ofthe major causes of laryngospasm.! Any stimulation in the area supplied by thesuperior laryngeal nerve, during a lightplane of anesthesia, may producelaryngospasm.AnesthesiaRelatedRisk Factors! Common triggers of reflex laryngealresponse during anesthesia are secretions,blood, insertion of an oropharyngealairway suction catheter, and laryngoscopy.! Inexperience of the anesthetist is alsoassociated with an increased incidence oflaryngospasm and perioperativerespiratory adverse events.
! Some factors are associated with a lowerrisk of laryngospasm:! IV inductionA LowerRisk! Airway management with facemask,! inhalational maintenance of anesthesia.! Induction and emergence fromanesthesia are the most critical periods
! Identifying and removing the offendingstimulus,Prevention ofLaryngospasm! Applying airway maneuvers to open theairway,! Administering anesthetic agents if theobstruction is not relieved.
! A detailed history should be taken toidentify the risk factors.! For children with URI, cancellation ofelective procedures for a period of 4–6weeks was traditionally the rule.PreoperativeManagement! However, children younger than 3 yr maydevelop 5–10 URI episodes per year.! Thus, the potential window for safeadministration of general anesthesia isfrequently very short.
! Rescheduling patient 2–3 weeks after anURI episode appears to be a safeapproach.PreoperativeManagement! Premedication with anticholinergicagents may decrease secretions but hasno demonstrated influence on theincidence of laryngospasm.
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adequate depth of anesthesia before airway instrumentation reduces the risk of bronchospasm. ! The use of an LMA (in suitable patients) has been shown to reduce the incidence of bronchospasm compared to tracheal intubation. ! Regional techniques where appropriate can also avoid the need for general anesthesia and intubation.