Scribd Logo
Upload

Welcome to Scribd!

    • 168 views

    Management of Intraoperative Bronchospasm: Dr. Imran

    Uploaded by

    hellodrvigneshwar
    This document discusses the management of intraoperative bronchospasm. It defines bronchospasm as constriction of the smooth muscles of the bronchi and bronchioles. It describes the anatomy, innervation, and causes of bronchospasm including allergic, non-allergic, and pharmacological factors. It discusses the differential diagnosis, pathophysiology, signs and symptoms, and diagnostic tests. Treatment options discussed include deepening anesthesia, suctioning the endotracheal tube, administering bronchodilators like salbutamol, and second line therapies like ipratropium bromide and magnesium sulfate. It also covers the pharmacology of agents used to treat bronchospasm and their mechanisms of action.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd

    Management of Intraoperative Bronchospasm: Dr. Imran

    Uploaded by

    hellodrvigneshwar
    168 views49 pages
    This document discusses the management of intraoperative bronchospasm. It defines bronchospasm as constriction of the smooth muscles of the bronchi and bronchioles. It describes the anatomy, innervation, and causes of bronchospasm including allergic, non-allergic, and pharmacological factors. It discusses the differential diagnosis, pathophysiology, signs and symptoms, and diagnostic tests. Treatment options discussed include deepening anesthesia, suctioning the endotracheal tube, administering bronchodilators like salbutamol, and second line therapies like ipratropium bromide and magnesium sulfate. It also covers the pharmacology of agents used to treat bronchospasm and their mechanisms of action.

    Original Description:

    uy

    Original Title

    Bronchospasmppt 160604121135 Converted

    Copyright

    © © All Rights Reserved

    Available Formats

    PPTX, PDF, TXT or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    This document discusses the management of intraoperative bronchospasm. It defines bronchospasm as constriction of the smooth muscles of the bronchi and bronchioles. It describes the anatomy, innervation, and causes of bronchospasm including allergic, non-allergic, and pharmacological factors. It discusses the differential diagnosis, pathophysiology, signs and symptoms, and diagnostic tests. Treatment options discussed include deepening anesthesia, suctioning the endotracheal tube, administering bronchodilators like salbutamol, and second line therapies like ipratropium bromide and magnesium sulfate. It also covers the pharmacology of agents used to treat bronchospasm and their mechanisms of action.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    168 views49 pages

    Management of Intraoperative Bronchospasm: Dr. Imran

    Uploaded by

    hellodrvigneshwar
    This document discusses the management of intraoperative bronchospasm. It defines bronchospasm as constriction of the smooth muscles of the bronchi and bronchioles. It describes the anatomy, innervation, and causes of bronchospasm including allergic, non-allergic, and pharmacological factors. It discusses the differential diagnosis, pathophysiology, signs and symptoms, and diagnostic tests. Treatment options discussed include deepening anesthesia, suctioning the endotracheal tube, administering bronchodilators like salbutamol, and second line therapies like ipratropium bromide and magnesium sulfate. It also covers the pharmacology of agents used to treat bronchospasm and their mechanisms of action.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 49

    MANAGEMENT OF

    INTRAOPERATIVE
    BRONCHOSPASM
    Dr. Imran
    BRONCHOSPASM

    Definition: constriction of smooth muscles of


    bronchi & bronchioles.
    ANATOMY
    Arterial supply:
     Right , one Bronchial Artery from 3rd posterior intercostal
    artery.
     Left , two Bronchial Arteries from descending thoracic
    aorta.
    Venous drainage:
    mostly from pulmonary veins, from bronchial veins.
    Lymphatic drainage : Interbronchial LN

    Tracheobronchial LN

    Bronchomediastinal LN
    INNERVATION OF BRONCHI
    PARASYMPATHETIC NERVOUS SYSTEM

    SYMPATHETIC ADRENERGIC SYSYTEM

    NON ADRENERGIC NON CHOLINERGIC


    SYSTEM
    PARASYMPATHETIC
    PREGANGLIONI
    C FIBRES FROM
    VAGUS

    POST M3
    GANGLIONIC
    FIBRES IN ACH
    AIRWAYS

    ANTI
    CHOLINERGI
    CS
    BRONCHO-
    CONSTRICTION
    SYMPATHETIC
    T2 –T4 ganglia of sympathetic trunk .

    ADERENERGIC
    Alpha receptors : clinically insignificant

    BETA 2 RECEPTORS
    Beta 2 receptors

    G proteins
    Adenylate cyclase

    ATP cAMP

    Ca efflux and into SR

    BRONCHIAL RELAXATION
    NON ADRENERGIC NON
    CHOLINERGIC SYSTEM
    EXCITATORY : SUBSTANCE P, NEUROKININ A.

    INHIBITORY: VIP & NO


    During the induction phase
    Airway irritation
    Anaphylaxis
    Misplacement of ETT
    Aspiration of gastric contents
    Pulmonary edema
    Unknown, possibly allergy.
    Intra operative bronchospasm
    Allergy
    Aspiration
    Acute exacerbation of asthma
    Airway irritation
    During Extubation
    Pulmonary edema
    Anaphylaxis/allergy
    Inadvertent extubation
    Extubation spasm
    Aspiration
    Unilateral bronchospasm and pulmonary edema
    (cause not determined)
    CAUSES OF BRONCHOSPASM
    Non allergic mechanism:
    Mechanical factors
    Pharmacological factors: via histamine
    releasing drugs.

    Non allergic mechanism: by nonspecific stimuli


    (by ETT or Suction catheter)
    Hyper reactive airway: Asthma, chronic smoker,
    COPD, URTI.
    Immediate hypersensitivity: ALLERGY
    Ig E mediated Anaphylaxis
    Anaphylactoid: Non immune mechanism.

    Drugs causing bronchospasm: Adenosine, Non


    selective beta blockers ( propanolol, timolol,
    nadolol, pindolol, alprenolol,oxprenolol)
    DIFFERENTIAL DIAGNOSIS
    •Mechanical obstruction due to kinking, secretions,
    overinflation of tracheal tube cuff
    •Laryngospasm
    •Esophageal intubation
    •Inadequate depth of Anesthesia
    •Endobronchial intubation
    •Obstruction of tube by foreign body
    •Pulmonary aspiration
    •Pulmonary edema
    •Pulonary embolus
    •Pneumothorax
    •Extreme Head down position & bowel packing.
    BRONCHOSPASM LARYNGOSPASM
    Expiratory and accompained Inspiratory usually
    by a wheeze or croup accompained by a stridor
    Accessory muscles of Indrawing of the intercostals
    respiration suprasternal notch present
    Expiration is prolonged Not prolonged
    Cyanosis is slow to develop Develops rapidly
    PATHOPHYSIOLOGY
    Exaggerated bronchoconstrictor response to
    trigger - airway edema , increased secretions,
    smooth muscle contraction.

    Airway inflammation increases bronchial hyper


    responsiveness.

    Anaphylaxis: release HISTAMINE, ECF,


    LEUKOTRIENES C4 D4 E4, PGD2 and KININS
    ANESTHETIC AGENTS

    INDUCTION AGENTS: BARBITUARATES,


    ETOMIDATE, PROPOFOL

    LOCAL ANESTHETICS: ESTER GROUP

    MUSCLE RELAXANTS: Sch, GALLAMINE, d-


    TUBOCURARUNE, METOCURINE, PANCURONIUM,
    VECURONIUM, ATRACURIUM, MIVA , DOXACURIUM

    OPIODS: MEPERIDINE,MORPHINE, FENTANYL.

    OTHER AGENTS

    ANTIBIOTICS, BLOOD PRODUCTS, DRUG


    PRESERVATIVES,

    FRUSEMIDE, INSULIN, MANNITOL, NSAID’S,


    PROTAMINE, RADIOCONTRAST DYES, LATEX,
    GRAFTS, VIT K, COLLOIDS
    Signs and symptoms
    Rash

    Increased peak airway pressure during IPPV

    Wheeze(Expiratory)/ silent chest

    Hypotension due to development of auto PEEP.

    Falling oxygen saturation

    Increased ET CO2

    Capnography change: ‘sharkfin’ appearance


    Auto PEEP/ Intrinsic PEEP?
    Accumulation of air in alveoli if breath is delivered
    before complete exhalation of previous breath
     Positive airway pressure at the end of
    Expiration.

    Over expansion of lungs leading to dynamic


    hyperinflation of lungs.

    HYPOTENSION
    Treated by increasing expiratory time.
    Other causes of auto PEEP
    Mucus plugging of airways
    Large Minute Ventilation
    Block in expiratory limb of breathing circuit
    Smaller ETT with inadequate expiratory time.

    DIAGNOSIS by APNEA TEST for 30sec.


    Anesthetic management
    Preoperative assessment
    For COPD: stop smoking, infection control, chest
    physiotherapy, use of bronchodilators and
    steroids.

    All patients should be counselled and encouraged


    to stop smoking preoperatively. Six to eight weeks
    of abstinence before surgery significantly reduces
    the risk of respiratory complications including
    bronchospasm.
    • Evaluate the patients asthma over the past half
    year.

    • Improve lung function to predicted values before


    surgery, possibly with short course of oral
    steroids.

    • Give patients who have received steroids for


    longer than 2 weeks 100 mg hydrocortisone TID
    iv. Taper within 24hrs.
    URTI in children increases the risk of
    bronchospasm and so it may be necessary to
    postpone surgery. The complete resolution of
    symptoms (approximately 2 weeks) correlates
    well with a decreased incidence of airway hyper
    reactivity.
    Pretreatment with an inhaled/nebulised beta
    agonist, 30 minutes prior to surgery, induction of
    anaesthesia with propofol and adequate depth of
    anaesthesia before airway instrumentation
    reduces the risk of bronchospasm.
    Regional v/s General??
    • Instrumentation of airway is the main trigger for
    wheezing during anesthesia.

    • LMA cause less airway resistance increase than


    ETT.

    • RA is ideal for reactive airway disease.


    On suspecting bronchospasm
    • Switch to 100% oxygen

    • Ventilate by hand

    • Stop stimulation / surgery

    • Consider allergy / anaphylaxis; stop administration of


    suspected drugs / colloid / blood products

    Thorough ETT suction after deepening of anesthesia.


    hypoxia & reverse
    bronchoconstriction
    Deepen anaesthesia

    If ventilation through ETT difficult/impossible, check


    tube position and exclude blocked/misplaced tube.

    If necessary eliminate breathing circuit occlusion by


    using self-inflating bag
    In non-intubated patients exclude laryngospasm and
    consider aspiration
    DRUG THERAPY
    PHARMOCOLOGY
    Beta 2 Ach
    agonists Vagus
    histamine
    Cholinergi
    G proteins c
    Adenylate antagonist
    cyclase Phospholi s
    pase C & cGMP
    cAMP IP3

    Calcium sensitivity and ca infux

    Myosin light chain kinase

    BRONCHOCONSTRICTION
    DRUGS ACTING ON ANS
    SYSTEMIC ADRENERGIC AGONIST INHALED ADRENERGIC AGONISTS

    TERBUTALINE SHORT ACTING

    EPINEPHRINE ALBUTEROL, LEVALBUTEROL

    ALBUTEROL METAPROTERENOL, PIRBUTEROL

    LONG ACTING

    SALMETEROL, FORMOTEROL,

    ARFORMOTEROL
    INHALED CHOLINERGIC SYSTEMIC CHOLINERGIC
    ANTAGONISTS ANTAGONISTS

    SHORT ACTING: IPRATRROPIUM ATROPINE

    LONG ACTING: TIOTROPIUM SCOPOLAMINE

    GLYCOPYRROLATE
    PHARMACOLOGIC INFLUENCE ON
    INFLAMMATION
    INHALED LEUKOTRIENE MAST CELL METHYLXANTHIN
    CORTICOSTEROI MODIFIERS STABILIZERS ES
    DS
    MONOTHERAPY ANTAGONISTS:
    BECLOMETHASO MONTELUKAST, CROMOLYNSODI THEOPHYLLINE,
    NE, ZAFIRLUKAST, UMNEDOCROMIL AMINOPHYLLINE
    BUDESONIDE, PRANLUKAST
    CICLESONIDE, INHIBITORS:
    FLUNISOLIDE, ZILEUTON
    FLUTICASONE
    ,MOMETASONE,
    TRIAMCINALONE

    COMBINATIO
    N THERAPY
    BUDESONIDE/
    FORMOTEROL
    FLUTICASONE/
    SALMETEROL
    Glucocorticoid receptor alpha of airway epithelial
    cells is target of ICS.

    Interact with transcription factors responsible for


    pro inflammatory mediators.
    Arachidonic acid is converted into Leukotrienes
    via the 5- lipoxygenase pathway.

    Leukotrienes C4, D4, E4 causes


    bronchoconstriction, tissue edema, eosinophil
    migration and increased airway secretion.
    METHYLXANTHINES
    AMINOPHYLLINE:
     inhibitor of phosphodiesterase :increases cAMP
    and cGMP
     Adenosine receptorA1 A2 antagonism causing
    inhibition of release of histamine and
    leukotrienes.
     Activates histone deacetylase reducing
    expression of inflammatory genes..
    DOSE: 6mg/kg bolus fb infusion 1mg/kg/hr.

    LOW THERAPEUTIC INDEX : 20mg/L


    • Side effects: arrythmias and seizures.
    ANESTHETICS WITH
    BRONCHODILATION
    VOLATILE ANESTHETICS INTRAVENOUS ANESTHETICS

    ISOFLURANE PROPOFOL

    SEVOFLURANE KETAMINE

    HALOTHANE MIDAZOLAM
    Blockade of T-type voltage dependent calcium
    channels on distal airway smooth muscles.

    Decreases intracellular calcium by decreasing


    sensitivity of calcium mediated by Protein kinase
    C and also increase in cAMP.
    Other agents
    Antihistamines : allergen induced broncho-
    constriction

    Magnesium sulfate.
    1st line Drug therapy

    Salbutamol
     MDI: 6-8 puffs, 100micrograms per puff, repeat
    as necessary.
     Nebulisation : 5mg repeat as necessary.
     Intravenous: 250 mcg slow iv followed by
    5mcg/min upto 20 mcg/min.
    2nd line of therapy
    Ipratropium bromide : 0.5 mg nebulization 6th
    hourly.
    Magnesium sulfate : 50mg/kg iv over 2min upto
    2grams.
    Hydrocortisone: 200mg iv 6th hourly.
    Ketamine: bolus of 10-20 mg fb infusion 1-
    3mg/kg/hr.
    Aminophylline: 6mg/kg bolus fb infusion
    1mg/kg/hr.
    Chlorphenaramine : 10mg slow iv.
     Epinephrine : neb 5ml of 1:1000
    REFERENCES
     STOELTING’S PHARMACOLOGYAND
    PHYSIOLOGY- 5TH EDITION.
     BARASH CLINICAL ANESTHESIA : 7TH
    EDITION.
     MILLERS ANESTHESIA : 7TH EDITION.
    THANK YOU

    You might also like