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Anesthetic management for strabismus surgery. Associated neurological abnormalities include: cerebral palsy, myelomeningocele, hydrocephalus, craniofacial.

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Presentation on theme: "Anesthetic management for strabismus surgery. Associated neurological abnormalities include: cerebral palsy, myelomeningocele, hydrocephalus, craniofacial."— Presentation transcript:

1 Anesthetic management for strabismus surgery

2 Associated neurological abnormalities include: cerebral palsy, myelomeningocele, hydrocephalus, craniofacial syndromes, neurofibromatosis, seizure disorders structural abnormalities of the eye

3 In the preanesthetic evaluation, it is important to consider diseases or syndromes associated with strabismus, such as congenital heart disease or cardiomyopathy, as each has its specific anesthetic considerations that are important to review

4 Malignant hyperthermia, masseter muscle spasm

5 Patients with MH were noted as having a higher incidence of musculoskeletal abnormalities, such as strabismus or ptosis A review of more than 2,500 patients tested for MH susceptibility was unable to show an association with strabismus surgery patients Children with strabismus are now routinely anesthetized with inhalational anesthetics without any apparent increase in the incidence of MH

6 fourfold incidence of MMS in pediatric strabismus patients compared with nonstrabismus patients after a halothane induction followed by a single dose of succinylcholine The jaws of steel represents a clinical state during which the mandible cannot be displaced from the maxilla to facilitate insertion of any airway Some suspect that certain cases of MMS may be a normal response to succinylcholine

7 Summary: Association between strabismus and MH is no longer an issue; however, if MMS is suspected in a patient, it is important to recognize that this patient may be susceptible to MH The importance of a detailed anesthetic family history is emphasized

8 Oculocardiac reflex Definition: 20% decrease in heart rate(HR) from baseline, dysrhythmias, or sinoatrial arrest associated with ocular muscle traction 10-30% decrease in HR from baseline

9 It is a trigeminal-vagal reflex that can lead to a variety of arrhythmias, including sinus bradycardia, junctional rhythm, atrial ectopic, atrioventricular block, ventricular bigeminy, wandering pacemaker, multifocal premature ventricular contractions, idioventricular rhythm, ventricular tachycardia, or asystole

10 Incidence : 14-90% depending on: administration of an anticholinergic, the choice of anesthetic agents, the definition of OCR used

11 Triggers 1:traction on the extraocular muscles 2: pressure on orbital structures or on the tissue remaining in the orbital apex after enucleation, 3: ocular trauma 4: increase in intraorbital pressure from an injection or hematoma

12 The response generally disappears as the stimulation is discontinued This phenomenon is called vagal escape or OCR fatigue It is a physiologic defense mechanism where the HR response diminishes after sustained or repeated extraocular muscle manipulation

13 Oculorespiratory reflex: Reduction in tidal volume and respiratory rate The afferent pathways are the same as in OCR, but they are directed to the respiratory control area of the brainstem instead, and the efferent fibers travel along the phrenic nerve and other nerves involved in respiration The oculorespiratory reflex may produce hypercapnia and hypoxemia that can increase the incidence of OCR

14 Prevention of OCR: surgical manipulation must be gentle, depth of anesthesia must be adequate, hypoxia and hypercarbia must be avoided Administering atropine or glycopyrrolate decreases the incidence of OCR

15 systematic prophylactic anticholinergic administration remained controversial in the past because it was associated with ventricular arrhythmias the incidence of OCR is affected significantly by the type of anesthetic administered

16 Treatment: The initial response to OCR is to ask the surgeon to stop surgical manipulation immediately, Assess the patients ventilatory status to rule out hypercarbia or hypoxia Evaluate the depth of anesthesia Atropine should be administered if hemodynamic instability or arrhythmias occur as a result of bradycardia

17 Postoperative nausea and vomiting: Incidence of PONV without prophylaxis varies from 37-90% Complications: dehydration, electrolyte imbalance, subconjunctival hemorrhage, loosening of surgical attachments, delayed discharge, unplanned admissions, decrease satisfaction, increase the use of resources

18 Major risk factors: General:The type of surgery (e.g., strabismus surgery, tonsillectomy), age>three years, duration of anesthesia>30 min, and a personal or family history of POV, PONV, or motion sickness Specific: oculoemetic reflex, alteration in visual perception postoperatively, positive OCR, the surgical technique, and the number of repaired eye muscles The surgical technique, myopexy, where posterior fixation of the muscle via a suture results in a more sustained stimulation, is associated with an increased incidence of PONV

19 Treatment: Droperidol 75mic.kg.IV Dexamethasone : 50 mic.kg.IV Ondansetron: mg.kg.IV Combination anti-emetic therapy

20 Factors affecting the incidence of the oculocardiac reflex: Increase: Propofol, Light anesthesia, Hypercarbia, Hypoxia, Traction on extraocular muscles, Stimulation of orbital structures, Halothane>sevoflurane, Remifentanil>sevoflurane, Desflurane

21 Deacrease: Anticholinergics, Ketamine, Midazolam, Rocuronium No effect: Sevoflurane = desflurane, Spontaneous ventilation, Controlled ventilation

22 Analgesia: 1: Opioids: fentanyl, meperidine, Remifentanil 2: Topical analgesics: topical tetracaine, topical diclofenac; low incidence of PONV 3: Blocks: Regional blocks

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24 Malignant Hyperthermia

25 Genetic counseling: Malignant hyperthermia susceptibility (MHS) is inherited in an autosomal dominant manner

26 pharmacogenetic disorder of skeletal muscle calcium regulation associated with uncontrolled skeletal muscle hypermetabolism

27 Manifestations of malignant hyperthermia (MH) are precipitated by certain volatile anesthetics :halothane, isoflurane, sevoflurane, desflurane, enflurane, either alone or in conjunction with depolarizing muscle relaxants (succinylcholine)

28 The triggering substances release calcium stores from the sarcoplasmic reticulum, causing contracture of skeletal muscles, glycogenolysis, and increased cellular metabolism, resulting in production of heat and excess lactate

29 Affected individuals experience: acidosis, hypercapnia, tachycardia, hypoxemia, rhabdomyolysis with subsequent increase in serum creatine kinase (CK) concentration, hyperkalemia with a risk of cardiac arrhythmia or even arrest, and myoglobinuria with a risk of renal failure

30 the first manifestations of MH, tachycardia and tachypnea, occur in the operating room; however, MH may also occur in the early postoperative period

31 Diagnosis/testing: In vitro measurement of contracture response of biopsied muscle to graded concentrations of caffeine and the anesthetic halothane

32 Management: Treatment of manifestations: Early diagnosis of MHS Discontinuation of potent inhalation agents and succinylcholine Treatment of metabolic abnormalities Administration of dantrolene sodium intravenously

33 Prevention of primary manifestations: avoidance of potent volatile anesthetic agents and succinylcholine

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