Anaphylaxis during general anaesthesia
	Death or permanent disability from anaphylaxis in anaesthesia may be avoidable if the reaction is recognised early and managed optimally
	Recognition of anaphylaxis during anaesthesia is usually delayed because key features such as hypotension and bronchospasm more commonly have a different cause.
	If anaphylaxis is suspected during anaesthesia, it is the anaesthetist’s responsibility to ensure the patient is referred for investigation.
	Anaphylaxis is a severe, life-threatening, generalized or systemic hypersensitivity reaction.
	The following guidelines to be applied in suspected anaphylactic reactions associated with anaesthesia. 2007 Scandinavian Clinical Practice Guidelines, the 2008 Resuscitation Council UK guidelines and the British Society for Allergy & Clinical Immunology (BSACI) guidelines.
	Causes
	Individuals with a history of atopy, asthma or allergy to some foods appear to be at increased risk of latex allergy.
	Patients with asthma or taking b-blocking drugs may suffer a more severe reaction.
		Antibiotics
		Chlorhexidine
		Dextran
		Gelatins
		Hydroxyethylstarch (HAES)
		Iodinated contrast media
		Ketamine
		Natural rubber latex
		Local anaesthetics
		Midazolam
		Neuromuscular blocking agents (NMBAs) - The quaternary ammonium ion is identified as the allergenic epitope, and is shared by all NMBAs, morphine, pholcodine and other morphine/codeine analogues.
		Opioids - Morphine, codeine and meperidine
		Propofol
		Thiopental
	Symptoms and diagnosis
	Cutaneous symptoms, such as flushing, urticaria and oedema, are common, but, during anaesthesia, these are usually hidden by surgical drapings.
		Hypotension and tachycardia
		Severe arrhythmias and cardiovascular collapse if not recognised and treated.
		Bronchospasm
		Cardiovascular collapse
		Bronchospasm
		Transient
		Asthmatics
		Cutaneous Rash
		Erythema
		Urticaria
		Angioedema
		Generalised oedema
		Pulmonary oedema
	Classification of clinical manifestations of anaphylaxis during anaesthesia
	Class Clinical manifestations I Generalised cutaneous signs: erythema, urticaria with or without angioedema II Moderate multiorgan involvement with cutaneous signs, hypotension and tachycardia, bronchial hyperreactivity (cough, ventilatory impairment) III Severe life-threatening multiorgan involvement that requires specific treatment: collapse, tachycardia or bradycardia, cardiac arrhythmias, bronchospasm; the cutaneous signs may be absent or occur only after the arterial blood pressure recovers IV Circulatory or respiratory arrest V Death due to a lack of response to cardiorespiratory resuscitation
	Scandinavian Society of Anaesthesiology and Intensive Care Medicine (SSAI ) Guideline on treatment of anaphylactic reactions during anaesthesia
	Primary treatment Dosage Stop administration of suspected substance   Call for help and inform the surgeon   Trendelenburg position   Maintain airway and give oxygen FiO2 1.0 Adrenaline Adults: Use diluted adrenaline i.v. maximum concentration 0.1 mg/ml Mild to moderate reaction: 0.01–0.05 mg i.v.   Circulatory collapse: 0.1–1.0 mg i.v.   i.v. infusion starting at: 0.05–0.1 μg/kg/min   Without i.v. access: 0.5–0.8 mg i.m. Titrate dose to response Children: If large doses are needed, use i.v. infusion Mild to moderate reaction: 0.001–0.005 mg/kg i.v.   Circulatory collapse: 0.01 mg/kg i.v.   Without i.v. access: 0.005–0.01 mg/kg i.m. Fluid therapy Adults: NaCl 9 mg/ml, Ringer’s acetate or colloids 20 ml/kg, more may be needed   Children:   20 ml/kg, more may be needed Secondary treatment   Corticosteroids Adults:   Hydrocortisone 250 mg i.v. or Methylprednisolone 80 mg i.v.   Children:   Hydrocortisone 50–100 mg i.v. or Methylprednisolone 2 mg/kg i.v. Antihistamines Adults:   H1 antagonist, e.g. Clemastin 2 mg or Deksklorfeniramin 10 mg or Promethazin 50 mg given i.v.   H2 antagonist: consider Ranitidine 50 mg i.v.   Children:   e.g. Clemastin 0.0125–0.025 mg/kg or Deksklorfeniramin 5 mg or Promethazin 0.3–1.0 mg/kg given i.v./i.m. Nebulised β2-agonist may be used for symptomatic treatment of bronchospasm, but is not first-line treatment   Lack of response to adrenaline   Noradrenaline i.v. infusion starting at: 0.05–0.1 μg/kg/min Vasopressin Increments of 2–10 IU i.v. until response Glucagon Increments of 1–2 mg i.v. until response (If lack of response to large doses of adrenaline in patients on β-blockers)
	BSACI guidelines for the investigation of suspected anaphylaxis during general anaesthesia
	SUSPECTED ANAPHYLACTIC REACTIONS ASSOCIATED WITH ANAESTHESIA
	The Association of Anaesthetists of Great Britain and Ireland and British Society for Allergy and Clinical Immunology
	Scandinavian Clinical Practice Guidelines on the diagnosis, management and follow-up of anaphylaxis during anaesthesia†
	GUIDELINES
	Suspected Anaphylactic Reactions Associated with Anaesthesia
	Association of Anaesthetists of Great Britain and Ireland
	Interestingly contradicting case reports
	Severe Anaphylactic Shock with Methylene Blue Instillation
	A 30-yr-old woman was scheduled for surgical correction of tubal sterility. She did not suffer from any atopy.
	After 1 h of uneventful anesthesia (midazolam, sufentanil, propofol, atracurium) and surgery,an intrauterine 1% methylene blue instillation was administered to verify tubal permeability.
	Within 2 min after methylene blue instillation,there was a marked decrease in Spo2 to less than 80% and an end-tidal carbon dioxide concentration (18 mm Hg) together with a decrease in arterial blood pressure (60/26 mm Hg) associated with a tachycardia (140 bpm).
	At the same time, the patient developed a severe bronchospasm. All these symptoms were relieved by titrated epinephrine injections (total dose, 1.8 mg), intravascular fluid administration, salbutamol spray, and 40 mg methylprednisolone.
	When hemodynamic stability was restored, a generalized urticaria became apparent.
	The patient continued to require epinephrine for 18 h to maintain cardiovascular stability but was discharged home after a few days without sequelae.
	Plasma histamine level measured to confirm onset of histamine release was markedly increased to 700 nmol/L (normal 10 nmol/L).
	Six weeks later cutaneous tests to methylene blue was positive whereas cutaneous tests to latex and to all other drugs were negative.
	To confirm the responsibility of methylene blue, in vitro leukocyte histamine release assay (3) was performed with methylene blue and was positive.
	Interestingly, methylene blue inhibits guanylate cyclase, thus decreasing cyclic guanosine monophosphate and vessel relaxation in vascular smooth muscle, and it has therefore been proposed for use in hypotensive septic shock patients or as a lifesaving alternative drug for contrast-medium induced anaphylaxis to restore arterial blood pressure.
	Ref:
	Severe Anaphylactic Shock with Methylene Blue Instillation A & A July 2005 vol. 101 no. 1 149-150
	Methylene blue for clinical anaphylaxis treatment: a case report
	A 23-year-old female suddenly presented urticaria and pruritus, initially on her face and arms, then over her whole body.
	Oral antihistamine was administered initially, but without improvement in symptoms and signs until intravenous methylprednisolone 500 mg.
	Recurrence occurred after two hours, plus vomiting. Associated upper respiratory distress, pulmonary sibilance, laryngeal stridor and facial angioedema (including erythema and lip edema) marked the evolution.
	At sites with severe pruritus, petechial lesions were observed.
	The clinical situation worsened, with dyspnea, tachypnea, peroral cyanosis, laryngeal edema with severe expiratory dyspnea and deepening unconsciousness.
	Conventional treatment was ineffective. Intubation and ventilatory support were then considered, because of severe hypoventilation.
	But, before doing that, based on their previous experience, 1.5 mg/kg (120 mg) bolus of 4% MB was infused, followed by one hour of continuous infusion of another 120 mg diluted in dextrose 5% in water.
	Following the initial intravenous MB dose, the clinical situation reversed completely in less than 20 minutes, thereby avoiding tracheal intubation.
	Previously the same team has treated nine patients who developed anaphylactic shock and/or anaphylaxis with an intravenous bolus of methylene blue (1.5 to 2.0 mg/kg) treatment.
	These observations do not allow it to be assumed that methylene blue would be the first-choice drug for anaphylactic shock.
	Ref:
	Methylene blue for clinical anaphylaxis treatment: a case report Sao Paulo Med. J. vol.125 no.1 São Paulo Jan. 2007
	Methylene Blue revisited
	Methylene blue was identified by Paul Ehrlich about 1891 as a successful treatment for malaria.
	Methylene Blue was till now known mainly as a dye but is now entering into the field of cardiac surgery and critical care as a very important therapeutic agent with diverse applications. Methylene blue, an inhibitor of nitric oxide synthase and guanylate cyclase has many uses in medicine.
	It has been found to improve the hypotension associated with various clinical states like septic shock, Vasoplegic syndrome and hepatopulmonary syndrome.
	Physiology: The enzyme Guanylyl cyclase synthesizes cGMP. In smooth muscle, cGMP is the signal for relaxation, and is coupled to many homeostaic mechanisms including regulation of vascular and airway tone.
	Methylene Blue acts by inhibiting guanylate cyclase, thus decreasing C-GMP and vascular smooth muscle relaxation.
	It helps Methylene Blue to improve hypotension in anaphylaxis by decreasing vascular smooth muscle relaxation.
	Methylene blue does not interfere with Nitric Oxide release (not interfere with bronchospasm) but acts to block its action on vascular smooth muscles.
	The evidence for its use in methemoglobinemia is well established but that for its use in vasoplegia, septic shock, hepatopulmonary syndrome, malaria, ifosfamide neurotoxicity etc is limited but promising and commands more research.
	Source:
	Methylene Blue: Revisited: J Anaesthesiol Clin Pharmacol. 2010 Oct-Dec; 26(4): 517–520.
	Ref:
	1. Guanylate cyclase: From Wikipedia, the free encyclopedia
	2. Methylene blue in anaphylactic shock – google search

	Perioperative beta-blockade for noncardiac surgery—proven safe or not?
	Don Poldermans, MD, PhD and P. J. Devereaux, MD, PhD -
	Perioperative myocardial infarction (MI) can occur by one of two mechanisms
	Perioperative beta-blockade improves outcomes
	Don Poldermans, MD, PhD
	Perioperative beta-blockade improves mortality and cardiac outcomes in select high and intermediate-risk patients undergoing noncardiac surgery.
	Patients on chronic beta-blocker therapy should have it continued perioperatively.
	For patients not already on beta-blockade who are at cardiac risk, initiation of low-dose beta-blocker therapy should be considered prior to surgery; such therapy should be started approximately 1 month before surgery, with dose titration to achieve hemodynamic stability.
	The improved outcomes of patient with proven coronary artery disease with perioperative beta-blocker usage are emerged from the following two popular clinical trials.

Perioperative Ischemic Evaluation    (POISE)	Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography (DECREASE I &IV)
8,351 Noncardiac surgery patients with or at risk of atherosclerotic disease	112 underwent randomization: 59 were assigned to receive bisoprolol   plus standard care and 53 to receive standard care alone
Extended-release metoprolol succinate started 2 to 4 hours preoperatively (100-200 mg )   and continued (200 mg/day) for 30 days.	5-mg dose of bisoprolol was initiated 30 days prior to surgery and was titrated, if necessary, according to heart rate
Reduction in Cardiovascular death, nonfatal MI, or nonfatal cardiac arrest (5.8% vs 6.9% with placebo)	Death from cardiac causes or nonfatal MI was reduced from 34% in the standard-care group to 3.4% in the bisoprolol group
Increases in total mortality and stroke incidence(Mortality was 3.1% with metoprolol versus 2.3% with placebo)	No increase in stroke observed
Starting dose of metoprolol was two to eight times the commonly prescribed dose	The maintenance dose of bisoprolol was half of the maintenance dose used in POISE
Narrow time window for titration may be important, since the beneficial effects of beta-blockade on coronary plaque stability are likely to take weeks to develop.	Ample time for beta-blocker titration is key to stroke avoidance
Starting a beta-blocker at a high dose(400mg on the first day) may lead to hypotension which is a postoperative predictor of stroke

 

CONCLUSIONS

  Don Poldermans advices: Start early and titrate dose; continue chronic beta-blockade  

		If a patient is on chronic beta-blocker therapy, do not stop it perioperatively
		In a patient not on a beta-blocker, consider adding one if the patient is at intermediate or high risk of a cardiac event, but start at a low dosage (ie, 2.5 mg/day for bisoprolol and 25 mg/day for metoprolol). Treatment ideally should be started 30 days preoperatively
		If a beta-blocker is not started because of insufficient time for titration, do not add one to treat tachycardia that develops during surgery, since tachycardia may represent a response to normal defense mechanisms

  Safety of perioperative beta-blocker use has not been adequately demonstrated   P. J. Devereaux, MD, PhD  

Even though little doubt that perioperative beta-blockade prevents MI, looking in to the negative outcomes from POISE hypotension as the predictor of death potentially accounted for 37.3% of deaths and hypotension as the predictor of stroke accounted for 14.7% of strokes in the study.  

So, in the POISE study hypotension was associated with a nearly fivefold increase in the risk of death and a doubling in the risk of stroke.  

The link between hypotension and death in POISE is consistent with findings from other largest beta-blocker trials undertaken.  

CONCLUSIONS

 

		If you want to use betablockers, use them sensibly, use them carefully, and act during surgery. If many of your patients are developing hypotension, then you are doing something wrong.
		The central take-away message is that patients are unlikely to want a perioperative beta-blocker if they are unwilling to accept a probable increase in mortality or if they place three times more value on avoiding a perioperative stroke than on avoiding an MI.
		It is time for perioperative medicine to enter the age of evidence-based practice and have re look in to the ACC/AHA guidelines on Perioperative Beta Blockade.

  Evidence does not support the use of β-blocker therapy

  American College of Cardiology and American Heart Association (ACC/AHA) guidelines on perioperative assessment recommend perioperative β blockers for non-cardiac surgery, although results of some clinical trials seem not to support this recommendation.

  33 trials included 12,306 patients. β blockers were not associated with any significant reduction in the risk of all-cause mortality, cardiovascular mortality, or heart failure, but were associated with a decrease in non-fatal myocardial infarction and decrease in myocardial ischemia at the expense of an increase in non-fatal strokes.

Evidence does not support the use of β-blocker therapy for the prevention of perioperative clinical outcomes in patients having non-cardiac surgery. The ACC/AHA guidelines committee should soften their advocacy for this intervention until conclusive evidence is available.                                     THE LANCET

  Resource:

  The experts debate: Perioperative beta-blockade for noncardiac surgery—proven safe or not? Don Poldermans, MD, PhD and P. J. Devereaux, MD, PhD: Cleveland Clinic Journal Of Medicine Volume 76 • Supplement 4 November 2009

  Ref:

  1. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery: Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group.N Engl J Med 1999; 341:1789– 1794.

  2. POISE Study Group. Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial.Lancet 2008; 371:1839–1847.

  3. Perioperative β blockers in patients having non-cardiac surgery: a meta-analysis.The Lancet, Volume 372, Issue 9654, Pages 1962 – 1976.

  4. β-Blockade in the perioperative management of the patient with cardiac disease undergoing non-cardiac surgery. Br. J. Anaesth. (2011) 107 (suppl 1): i3-i15.

  5. Similar articles in PubMed

  Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery (ACC/AHA 2007& 2009)

 
  Preoperative Evaluation

		Assessment of LV Function – For patients with dyspnoea of unknown origin Routine perioperative evaluation of LV function is not recommended.
		The 12-Lead ECG
		Treadmill Exercise Stress ECG test
		Dobutamine Stress Echocardiography

  Perioperative Therapy

  Coronary revascularization before noncardiac surgery (PCI or CABG)
  It is not recommended that routine prophylactic coronary revascularization be performed in patients with stable CAD before noncardiac surgery.
  It is advised in patients with:

		Stable angina who have significant left main coronary artery stenosis
		Stable angina who have 3-vessel disease
		stable angina who have 2-vessel disease with significant proximal LAD stenosis and either EF less than 0.50 or demonstrable ischemia on noninvasive testing
		High-risk unstable angina or non–ST-segment elevation MI
		Acute ST-elevation MI

 
Duration of antiplatelet therapy and recommended delays for non-cardiac surgery after PCI

Duration of antiplatelet therapy	Recommended delays for non-cardiac surgery after PCI
Dilatation without stenting: 2–4 weeks	Surgery postponed for 2–4 weeks (vital surgery only)
PCI and BMS: 4–6 weeks	Vital surgery postponed for ≥6 weeks Elective surgery postponed for ≥3 months
PCI and DES: 12 months	Elective surgery postponed for ≥12 months
Aspirin: lifelong therapy, whichever is the revascularization technique

  PCI - percutaneous coronary intervention, BMS - bare metal stent, DES- drug-eluting stent
 
Perioperative Management of Patients with Prior PCI Undergoing Noncardiac Surgery
 
  Perioperative antiplatelet therapy: the case for continuing therapy in patients at risk of myocardial infarction
  Proposed scheme for management of patients taking antiplatelet therapy and requiring surgery. MI, myocardial infarction; CABG, coronary artery bypass graft; PCI, percutaneous coronary intervention; BMS, bare metal stent; DES, drug-eluting stent; EF, ejection fraction
 

Surgical haemorrhagic risk	Cerebro- and cardiovascular risk
	Low	Intermediate	High
	>6 months after MI, PCI, BMS, CABG, stroke >12 months if complications	6–24 weeks after MI, PCI + BMS, CABG, or stroke (Ø complication); >12 months after DES; high-risk stents (long, proximal, multiple, overlapping, small vessels, bifurcation); low EF, diabetes	<6 weeks after MI, PCI, BMS, CABG; <6 months after same if complications; <12 months after high-risk DES; <2 weeks after stroke
Low risk
Transfusion normally not required; peripheral, plastic, and general surgery, biopsies; minor orthopaedic, ENT, and general surgery; endoscopy; eye anterior chamber; dental extraction and surgery	Elective surgery: OK; maintain aspirin	Elective surgery: OK; maintain aspirin, clopidogrel (if prescribed)	Elective surgery: postpone; vital or emergency surgery: OK; maintain aspirin and clopidogrel
Intermediate risk
Transfusions frequently required; visceral surgery; cardiovascular surgery; major orthopaedic, ENT, reconstructive surgery; endoscopic urology	Elective surgery: OK; maintain aspirin	Elective surgery: postpone; surgery absolutely required: OK; maintain aspirin, clopidogrel (if prescribed)	Elective surgery: postpone; vital or emergency surgery: OK; maintain aspirin and clopidogrel
High risk
Possible bleeding in a closed space; intracranial neurosurgery; spinal canal surgery; eye posterior chamber surgery	Elective surgery: OK; maintain statin; withdraw aspirin (maximum 7 days)	Elective surgery: postpone; surgery absolutely required: OK; maintain aspirin, or replace aspirin by ibuprofen; stop clopidogrel	OK only for vital or emergency surgery; maintain aspirin Bridge with tirofiban/eptifibatide and heparin

Copyright ©  2013 the British Journal of Anaesthesia

 
Algorithm for preoperative management of patients under antiplatelet therapy  

Copyright ©  2013 the British Journal of Anaesthesia

  Monotherapy with aspirin need not be routinely discontinued for elective noncardiac surgery. Possible exceptions were intracranial surgery and prostatectomy.

  Aspirin should only be discontinued if the known bleeding risks are similar or more severe than the observed cardiovascular risks of aspirin withdrawal.

  ACC/AHA recommendation that clopidogrel should be withheld for at least 5 to 7 days in patients scheduled for elective CABG surgery.

  Clopidogrel with aspirin during the week preceding an operation is an accepted contra-indication to any form of regional anaesthesia (RA)

  The half-life of clopidogrel is 4 h and its plasma level is close to zero after 12 h (three half-lives). In emergency situations or in the case of major bleeding, therefore, haemostasis can be restored by administration of fresh platelets within a few hours of the last clopidogrel intake.

  Non-steroidal anti-inflammatory drugs (NSAIDs) ibuprofen or indobufen inhibit COX-1 like aspirin, but their blocking action on platelet activity is reversible within 24 h. As platelet function is completely recovered after NSAID withdrawal, these drugs can be used to maintain an efficient antiplatelet activity during the week between aspirin cessation and surgery.

  When and how to use bridge anticoagulation therapy for warfarin?

  Before surgery
  Discontinue warfarin 5 days before surgery (ie, hold four doses) if the preoperative international normalized ratio (INR) is 2 to 3, and 6 days before surgery (hold five doses)if the INR is 3 to 4.5.

  For bridge therapy, start LMWH (enoxaparin 1mg/kg or dalteparin 100 IU/kg subcutaneously every 12 hours) beginning 36 hours after the last dose of warfarin.

  Give the last dose of LMWH approximately 24 hours prior to surgery.

  After surgery
  For minor surgery, reinitiate LMWH at full dose approximately 24 hours after surgery. For major surgery and for patients at high risk of bleeding, consider using prophylactic doses on the first two postoperative days.

  Restart warfarin at preoperative dose 1 day after surgery

  Discontinue LMWH when the INR is between 2 and 3 for 2 consecutive days.

The risk/benefit ratio of preoperative withdrawal of antiplatelet drugs in order to perform a regional or neuraxial blockade is not justified

  Perioperative Beta-Blocker Therapy (UPDATED)

  Class I (Recommended) indication for perioperative beta-blocker use exists, for continuation of a beta blocker in patients already taking the drug.

  Class IIa (It is reasonable) recommendations exist for patients with inducible ischemia, coronary artery disease, or multiple clinical risk factors who are undergoing vascular (i.e., high-risk) surgery and for patients with coronary artery disease or multiple clinical risk factors who are undergoing intermediate-risk surgery.

  Initiation of therapy, particularly in lower-risk groups, requires careful consideration of the risk: benefit ratio for an individual patient.

  Initiation well before a planned procedure with careful titration perioperatively to achieve adequate heart rate control while avoiding frank bradycardia or hypotension is also suggested.

  Perioperative Statin Therapy

  For patients currently taking statins and scheduled for noncardiac surgery, statins should be continued.

  Prophylactic Valvular Intervention Before Noncardiac Surgery

  If the stenosis is severe, percutaneous catheter balloon valvotomy should be considered as definitive therapy or as a bridge to care for the patient through pregnancy, labor, and surgical delivery. Excessive changes in intravascular volume should be avoided

  Anesthetic Considerations and Intraoperative Management
  PAC, ST-segment monitor

  Tranesophageal echocardiography (TEE) (the routine use of TEE in noncardiac surgery does not appear warranted)

  Intravenous nitroglycerin (take into account the anesthetic plan and patient hemodynamics)

  Volatile anesthetic agents

  Neuraxial anesthetic techniques include spinal and epidural approaches (Infra inguinal procedures can be performed under spinal or epidural anesthesia with minimal hemodynamic changes. Abdominal procedures can also be performed with neuraxial techniques; however, may be associated with significant hemodynamic effects)

  General or regional anesthesia preferred over “Monitored anesthesia care”

  Pain management may be a crucial aspect of perioperative care.( Epidural or spinal opiates or patient-controlled analgesia techniques )

  Postoperative troponin measurement is recommended in patients with ECG changes or chest pain typical of acute coronary syndrome

  Resources:

  1. 2009 ACCF/AHA Focused Update on Perioperative Beta Blockade Incorporated Into the ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery. Practice Guidelines: Full Text

  2. Perioperative antiplatelet therapy: the case for continuing therapy in patients at risk of myocardial infarction Br. J. Anaesth. (2007) 99 (3): 316-328

  Ref:
  1. Perioperative Antiplatelet Therapy Am Fam Physician. 2010 Dec 15;82(12):1484-1489

  2.Antiplatelet Agents in the Perioperative PeriodArch Surg. 2009;144(1):69-76

  3.Perioperative management of antiplatelet drugs Update in Anaesthesia

  4.Perioperative Anticoagulation Management in Patients who are Receiving Oral Anticoagulant Therapy : A Practical Guide for Clinicians

  5. Perioperative management of warfarin and antiplatelet therapyCleveland Clinic Journal of Medicine November 2009 vol. 76 Suppl 4 S37-S44

 

	Informed consent for Anaesthesia
	The legal and ethical requirements related to an anaesthetist’s communication with patients in preparing them for anaesthesia, assisting them in making appropriate decisions and obtaining consent in a formal sense are complex. Doing these things well takes time, skill and sensitivity. The primary focus should be to adequately prepare patients for surgery and to ensure that they are sufficiently well informed to make the choices that best meet their own needs.
	Anesthesiologists, should consider the need to achieve informed consent in two symbiotic senses: the legal sense and the ethical sense.
	The best way to fulfill both senses is to be vigilant in pursuing the spirit of informed consent. Establishing the patient‐physician relationship, tailoring the disclosure of risks, and making the patient a full partner in decision making will improve the quality of the informed consent process and, as a result, decrease the likelihood of litigation.
	Standard Disclosure Requirements for Informed Consent
	Threshold elements (pre-conditions) 1. Competence (to understand and decide) 2. Voluntariness (in deciding) Information elements 3. Disclosure of material information 4. Explanation of alternative treatments 5. Recommendation of a plan 6. Understanding of 3-5 Consent elements 7. Decision in favour of a plan 8. Authorisation of a plan Refusal elements 9. Decision against a plan
	Factors which anaesthetists should consider when disclosing risks to patients
	The nature of the matter to be disclosed More likely and more serious risks require disclosure. The nature of the proposed procedure Complex interventions typically require more information, as do procedures where the patient has no illness. The patient’s desire for information Patients who ask questions make known their desire for information and should be told. The temperament and health of the patient Anxious patients and patients with health problems or other relevant circumstances that make a risk more important for them (such as their medical condition or occupation) may need more information. The general surrounding circumstances The information appropriate for elective procedures, where several consultations are possible, may be different from that required in emergency settings.
	Skene L, Smallwood R. Informed consent: lessons from Australia. BMJ 2002; 324:39-41
	Claims in negligence
	Liability in tort would only be imposed if:
		The anaesthetist did not disclose a material risk (breach of the duty of care – failure to inform); and
		The risk in fact eventuated so that the patient suffered harm (injury or loss); and
		The patient was able to persuade the court that he or she would not have agreed to the procedure if informed of the risk in question (causation).
	You can download Anaesthesia Informed Consent as pdf or MS word format and modify according to your hospital need.
	Downloads:
	1. ANESTHESIA INFORMED CONSENT 2.ANESTHESIA INFORMED CONSENT
	Source: A Risk Management News Letter (Anaesthesia and the Law) Preferred Physicians Medical Risk Retention Group, INC
	2. New Texas Informed Consent Rules & Anesthesia Consent Form
	Applications and Forms - Health Facility Program
	Ref:
	1. Informed Consent Anesthesiology: October 1997 - Volume 87 - Issue 4 - p 968–978
	2. Consent for Anaesthesia Revised Edition 2006 The Association of Anaesthetists of Great Britain and Ireland
	3. Reviews; Informed consent for anaesthesia in Australia and New Zealand The Anaesth Intensive Care 2010; 38: 809-822
	4. Informed Consent for Surgical Anesthesia Care: Has the Time Come for Separate Consent? A & A February 2010 vol. 110 no. 2 280-282