ANA 873 Anesthesia Complications & MH

mortality

•Timeframe 24 hours to 30 days post anesthesia

•Coroner reports, surveys, malpractice

ASA risk mortality

mortality ASA 1 is 0.04 per 10,000 (0.0004%) anesthetics.

ASA physical status 2 risk is 0.5 per 10,000 (0.005%) anesthetics,

ASA physical status 3 risk is 2.7 per 10,000 (0.027%) anesthetics

ASA physical status 4 risk is 5.5 per 10,000 (0.055%) anesthetics

Morbidity

indicative of disase, incorporating any complication, excluding death, occurring during the perioperative period

most common events leading to injury in anesthesia claims included regional blocks (20% of claims), respiratory problems (17% of claims), CV(13% of claims), and equipment problems (10% of claims)’

morbidity classification

• Minor morbidity: Moderate distress without prolonging hospital stay. No permanent complications (PONV)

• Intermediate morbidity: Serious distress prolonging hospital stay or both. No permanent complications (e.g., dental injury).

• Major morbidity: Permanent disability or complication (SCI;anoxic brain injury).

The incidence of adverse outcomes with minor morbidity is 18%-22%).

hoarseness has been cited to occur in 14% to 50% of patients and may accompany a traumatic lesion in the larynx or hypopharynx in 6.3% of patients.

Drug errors (0.1%), equipment malfunction (0.23%), PONV (10%-79%), and accidental dural perforation (0.5%-0.6%)

complications of anesthesia identify by ASA

• Aspiration of gastric contents

● Failed intubation

● Esophageal intubation

● Other problems with the induction of general anesthesia

● Inadequate ventilation

● Airway obstruction

● Respiratory failure

● High spinal or massive epidural

● Neuraxial cardiac arrest

● Local anesthetic toxicity

● Drug reaction

● Anaphylaxis

● Overdose of sedatives

● Prolonged hypotension or hypertension

● intraoperative cardiac arrest during anesthesia of undetermined etiology

anesthesia related death by types of complications

emerging areas of anesthesia M&M

perip hyman erro

partiureint and neonatla resusciation

acute and chronic pain

elderly >70 yrs

pediatric brain growth and development

Adults with CHD
intraop cardiac arrest

supraglotic device and ETT intubation

domains of frailty measurements 5

1. Unintentional weight loss

2. Exhaustion measured by assessing effort and motivation

3. Decreased grip strength

4. Slowed walking speed

5. Low physical activity

Common post op complications

1. laryngospasm/ bronchospasm

2. airway obstruction

3. desaturation

4. PNA

5. PE

6. Atelectasis

7. Reintubation/mechanical ventilation for >48 hrs

8. severe coughing

9. Stridor

10. pleural effusion

11. pneumothorax

12. resp infection/ aspiration pneumonitis

13. worsening of OSA

14. Acute or worsening resp failure

during induction- instrumentation phase

dental injury with largynoscopy

cerical (cornea) injury

Soft tissue trauam (OA)
bloody airway (laryngospasm)

lip injury

During induction- intubation

Esophageal (Unrecognized)

Right Main stem

Aspiration

Bronchospasm

Laryngeal spasm

airway managmenet complications- mask ventialtion

Mucosal, skin irritation, conjunctivitis caused by cleansing agents

● Soft tissue damage from excessive pressure

● Corneal abrasion, retinal artery occlusion, blindness

● Damage to mandibular branch of facial nerve causing transient facial nerve paralysis

● Damage to mental nerves causing lower lip numbness

● Broken teeth, mucosal tears

● Worsening obstruction from malposition of tongue

● Subtuxation of the temporomandibular joint

● Gastric distention increasing risk for aspiration

● Gastric rupture

● Subcutaneous emphysema

Airway management complications LMA

Folding of epiglottis tip causing labored breathing, coughing, laryngospasm, and obstruction

● Excess lubricant that causes coughing or laryngospasm

● Lack of protection from aspiration of gastric contents

● Laryngospasm. coughing

● Sore throat

● Increased intracuff pressures with prolonged procedures with NO and CO2

● Dysarthria

● Edema of epiglottis, uvula, posterior pharyngeal wall

● Hypoglossal nerve paralysis

● Postobstruction pulmonary edema

● Tongue cyanosis

Airway management complications- ETT 13

1. Damage to teeth

2. Mucosal/ Lip injuries

3. Swelling tongue

4. Sore throat

5. Trauma to larynx/vocal cords

6. Arytenoid dislocation/subluxation

7. Tracheobronchial trauma/ Barotrauma

8. Nerve injury

9. Cervical spine injury

10. Vocal cord paralysis

11. Temporomandibular joint injury

12. Laryngospasm/ Bronchospasm

13. Hemodynamic perturbations

Airway management complications- extubation

1. Hemodynamic perturbations

2. Laryngospasm

3. Laryngeal edema

4. Bronchospasm

5. Negative-pressure pulmonary edema

6. Aspiration

7. Airway compromise

8. Difficult/accidental extubation

intraop awareness

High-risk cases (e.g., trauma, obstetric, CV

tachycardia and hypertension

hearing unwanted conversations and remembered bright lights during their procedure inconsistent with their expectations, making them distraught.

could lead to complications of awareness, PTSD, future surgery apprehension, and enhanced medicolegal risks associated with anesthesia.

Postoperative sequelae reported related to PTSD include sleep disturbances (19%), nightmares (21%), fear of future anesthetics (20%), and daytime anxiety (17%).

assessing incidence of awareness

Modified Brice Interview

● What was the last thing you remember before going to sleep?

● What is the first thing you remember after waking up?

● Do you remember anything between going to sleep and waking up?

● Did you dream during your procedure?

● What was the worst thing about your operation?

Risk Factors for Awareness 9

1. Female sex

2. Age (younger adults, but not children)

3. Obesity

4. Clinician experience

5. Previous awareness

6. After normal hours of operation

7. Emergency procedures

8. Type of surgery (obstetric, cardiac, thoracic)

9. Use of nondepolarizing relaxants

What is bronchospasm and what are 3 causes

Spasmodic contraction of smooth muscle

Causes:

1. Histamine Release

2. Reflex bradycardia (PNS stimulation w airway manipulation)

3. medications:

• Muscle relaxants (Sch, Rocuronium)

• Non-selective BB- (block beta2) (Propranolol)

• Anticholinesterases (neostigmine) counteract muscarinic choline receptor effects

• Prostaglandin inhibitors

bronchospasm risk factors 4

Reactive Airway Disease (Asthma, COPD)

Pediatric 

 Recent URI

 Atopy (eczema, hay fever)

 Cigarette smoke

Bronchospasm clinical signs 7

1. Wheezing

2. Prolonged expiration

3. Reduced (or absent) lung sounds

4. Increased airway pressure during PPV

5. decreased pulmonary compliance

6. Decreased SPO2

7. Decreased ETCO2 or upsloping wave (obstructing pattern)

8. Hypotension

bronchospasm prevention

1. Delay 2 weeks after URI

2. Continue & consider: Preop inhaled beta agonist & inhaled corticosteroid

3. Adequate depth of anesthesia

• IV induction preferred (Propofol & Ketamine bronchodilators)

• IV Lidocaine MAY help

4. Avoid endotracheal intubation, if possible

• LMA, mask ventilation, regional

bronchospasm treatment

Remova cause

#1 -Manual ventilate 100% FiO2

Auscultate, Confirm ETT placement / patency

 r/o mucous plug, kink, tensions pneumo, PE

#2 -Deepen anesthesia

 Volatile Agent

 Bolus: Prop, Ketamine, Lidocaine

#3 -Albuterol (Beta 2-agonist) 8-10 puffs

#4 -Epinephrine IV

Magnesium or steroids

what is laryngospasm

Sustained & involuntary contraction of laryngeal muscles causing closure of vocal cords

Inadequate ventilation d/t airway obstruction

May involve false vocal cords / supraglottic soft tissue

match intrinsic larynx muscle with fxn

thyroarytenoid= (shortens) “They Relax”

cricothyroid= tenses/ elongates “cords tense”

posterior cricoarytenoid= ABducts

lateral cricoarytenoid= ADDucts

laryngospasm reflex includes

Afferent limb:

• Internal branch of the superior laryngeal nerve

• Sensory only

Efferent branch consists of:

• Recurrent laryngeal nerve

• Innervates vocal cord adductors -

  • Lateral cricoarytenoid

  • Thyroarytenoid

  • Transverse (interarytenoid)

External branch of the superior laryngeal nerve

•innervates the cricothyroid muscle

•Adjusts cord tension (pitch) only

•Does not adduct cords

“Triggered by the internal SLN, executed by the RLN"

(RLN= Real reflex, Locks, No Air)

•Blocking the internal SLN decreases afferent stimulation so decreased laryngospasm risk

•Succinylcholine works because it relaxes RLN‑innervated intrinsic adductors

•Cricothyroid tension is not what closes the cords in laryngospasm

Larynospasm risk factors

1. Light anesthesia (induction / emergence)

2. Airway irritation [Manipulation (suction), Secretions, blood, bile, Volatile agents (des > sevo)]

3. Reactive airway (Asthma, URI, smoker)

4. Obesity / OSA

laryngospasm clinical signs

Inspiratory stridor (squeak)

No ETCO2 waveform

Paradoxical breathing movements

Supraclavicular retractions / rocking boat

Rapidly decreasing SPO2

NPPE

laryngospasm complications

1. airway obstruction

2. Negative Pressure Pulmonary Edema (NPPE) risk

   • Negative pulmonary pressure develops after spontaneous ventilation against a closed glottis, presenting with pink, frothy sputum and decreased oxygen saturation leading to acute respiratory failure.

3. aspiration of gastric contents

4. dysrhythmias

5. cardiac arrest

6. death

laryngospasm prevention 4

1. Propofol induction

2. Lidocaine before extubation (1-2mg/kg IV, 4mg/kg vocal cords)

3. Magnesium bolus (15mg/kg before extubation)

4. Removal of blood & secretions

laryngospasm treatment 3

#1 -FiO2- 1.0

remove noxious stsimuli

deepen anesthesia

#2 -Continuous PPV 5-10cmH2O, chin lift & Larson's maneuver

• bilateral inward anterior pressure

#3 - Succinylcholine

• adult and child IV= 1mg/kg

• adult and child IM= 4 mg/kg

• neonate/ infant IV= 2 mg/kg

• neonate/infant IM= 5 mg/kg

• if <5 yrs= give atropine 0.02 mg/kg

(0.2mg/kg IV or 4-5mg/kg IM) (Propofol 0.5mg/kg IV)

valsalva maneuver

exhalation against closed glottis or obstruction

pressure applired 3-5 seconds, released 5-10 sec

Ex. coughing, bucking, bearing down

risk= increased pressure in throax, abdomen, and brain

Muller’s maneuver

inhalaiton against closed glottis or obstru tion

Ex. patient bites down on ETT and takes deep breath

RIsk= substmospheric pressure in throax→ negative pressure pulmonary edema

CV complications during maintenance phase

1. MI

2. Oxygen carrying capacity

3. Blood pressure control

4. Factors that can cause hypotension: 4

• Decreased contractility

• Decreased SVR

• Decreased preload

• Dysrhythmias

Multisystem complications

• Thermoregulation (Hyper & hypothermia)

• Kidney perfusion

• Position diligence

Intraop MI risk factors 5

70% mortality rate

1. Age: 51-70 years old

2. ASA 3 & 4

3. Males > Females

4. General > Regional

5. Excessive surgical bleeding in 70% procedure related deaths

Intraop anesthesia CV complications

1. Co-morbidities

• MI, Angina, CHF pre-op predictors

2. Inadequate risk assessment

3. Inappropriate anesthetic management

4. Human error / misjudgment

What is the strongest predictors for increases risk for periop MI & increased risk of postop death

Ischemic heart disease (previous MI or angina) and CHF

Thermoregulation- hypothermia

Redistribution of heat from core to vasodilation

defined as temp <36 C

age extremes greatest risk of periop hypothermia

*1-1.5 C degree decrease in first hour

Radiation - Loss to environment through radiation - most significant

Convection – Loss to air currents 2nd most significant

Conduction – Loss from physical contact

Evaporation – Loss from transfer of liquid to gas

3 stages of intraop heat transfer

phase 1 heat redistribtuion from core to periphery

phase 2: heaat transfer? heat production

phase 3: heat tx- heat production

phase 1

with general, spinal, or epidural, there is redistribtion of heat fro central comparement (thorax, abdomen) to heripheral comparement (extremeities and skin)

anesthethic agensts impair thermoregulatory response in hypothalmauc, revnet shivering, and cause vasodilation

only nominal amount of heat loss to enviornemnt during phase 1. agai heat redistrubtion is way more importnat durign this phase

simple interventions, warm blanket on patient before OR, minimizes centrla to pheriapher temperature gradient and goes a long way towards preserving core temp

phase 2

heat loss ot evnrioenemnt exessed heat production

phase 3

an equilibrium develops between heat loss to environment and heat production

periop events contributing to heat loss

recalibration of hypothalamic set point

drug-induced vasodilation

impaired shivering

core to pheripahrl temp redistribution

cool ambient temp

cold OR table

amdin room temp fluids and cold blood products

Hypothermia adverse events

1. Coagulopathy

• Impaired PLT aggregation

• Reduced coagulation cascade enzyme activity

2. Prolonged drug effects (esp NDMR

Hypothermia complications

1. Delayed emergence

2. Myocardial ischemia

• Sympathetic stimulation

3. Post operative Shivering

• Increased oxygen demand —> Increases myocardial workload

hyperthermia causes

1. Environmental (warming device)

2. Drug reactions

• Neuroleptic malignant syndrome- dopamine depletion

• Serotonin syndrome- excess 5HT activity

• Anticholinergic toxicity- an excess Ach blockade

3. Thyroid Storm

4. Transfusion reaction/infection

5. Malignant Hyperthermia

Hyperthermic syndromes tx

• Neuroleptic malignant syndrome- bromocriptine, drantrolene

• Serotonin syndrome- cyproheptadine

• Anticholinergic toxicity- physostigmine

hyperthermia complications

Increased metabolic rate

Increased myocardial oxygen consumption

Ocular injuries & postoperative blindness risk factors

1. •Intraoperative hypotension

2. •Male sex

3. •Obesity

4. •Anemia from blood loss greater than 1 liters

5. •Surgery greater than 5 hours in duration

6. •Use of a Wilson frame

7. •Decreased percent colloid administration.

ocular injuries are more common in

older adults. Most common in  nose, neck, sinus, spine surgeries

corneal abrasions

•Eye pain

•Tearing / photophobia

•Foreign body sensation

•Pain increased with blinking and ocular movement

•Present immediately after emergence

Anterior ischemic optic neuropathy- know

•Sudden, painless vision loss, usually unilateral

•Typically post-op day #1

•Temporary reduction in blood flow to the vessels supplying anterior portion of optic nerve

•Shows optic disc swelling= EXAM

Posterior ischmeia optic neuropathy- know

•Reduction of oxygen supply to retrolaminar aspect of optic nerve

•Delayed, painfree vision loss (24-48 hrs, even weeks)

•Bilateral blindness common

•Less common than AION

bone cement implantation syndrome

There are several proposed mechanisms of bone cement implantation syndrome, including: Bone marrow debrisembolization during pressurization of the femoral canal Toxic effects of incompletely mixed methyl methacrylate, resulting in the release of the monomer Activation of inflammatory cytokines with femoral reaming, resulting in the release of microemboli.

The emboli move into the pulmonary circulation with the subsequent release of vasoactive mediators, causing an abrupt increase in pulmonary vascular resistance. This can lead to right heart failure and circulatory collapse

Bone cement implantation syndrome

After methyl methacrylate is injected into the femur:

•Acute hypotension

•Decreased oxygen levels

•Bronchospasm

•Decline in end-tidal carbon dioxide 

•Cardiac dysrhythmias

•Increased pulmonary vascular resistance --> right failure and cardiac arrest

Initial indicators of bone cement implantation syndrome

• Awake (under spinal anesthesia), dyspnea and altered mental status are the initial indicators

General anesthesia, the first sign is a decrease in end-tidal carbon dioxide.

high risk for BCIS

hip arthroplasty is highest risk

other high risk: knee arthroplasty, vertebroplasty, and kyphoplasty

bone cement implantation syndrome tx

first line: 100% O2

Supportive

1. IV fluids

2. vasopressors- phenylephrine

3. adequate ventilation and oxygenation

bone cement implantation syndrome risk factors

1. presence of metastatic disease,

2. a previous femoral prosthesis

3. preexisting pulmonary hypertension or right heart failure,

4. and the use of large volumes of methyl methacrylate cement

Pneumoperitoneum Insufflation- resp implicatins

•Decreased Functional Residual Capacity (FRC)

•Decreased Respiratory Compliance

•Increased Peak Airway Pressure

•Increased V/Q mismatch

Pneumoperitoneum Insufflation- cardiac implications

•Increased SVR

•Increased Mean Arterial Pressure

•Vagal response = bradycardia

•Decreased Cardiac Output

Pneumoperitoneum Insufflation- tx

•Preop Volume loading

•Slow / lower insufflation pressures

Peritoneal insufflation

an increase in SVR and MAP due to compression of the abdominal aorta and increased afterload.

Hypotension response more profound with positive pressure ventilation or positioning such as reverse trendelenburg.

Tourniquet standards

1.Width minimum half the diameter of limb

2.Insufflate 50-100 mmHg above SBP

3.Increase risk of limb loss after 2 hours

4.Hypotension with deflation typical

tourniquet duration and safety

Insufflation safely for 2 hours

• 0-2 hrs increasing pain

• 2-3.5 hrs Nerve and Muscle injury

• 3.5 - 5 hrs Widespread muscle & Nerve damage

• 5+ hrs. Severe effects with systemic involvement

  • Cardiac – hypotension/arrhythmias

  • Renal – AKI from myoglobin proteins

when deflating tourniquet cuff

several physiological events occur,

1. transient metabolic acidosis

2. Increased carbon dioxide levels

3. drop in systemic blood pressure.

MH DX

unexpalined increased ETCO2

fever

tachycardia

cyanosis

rigity

failure of massesster musle to relax (trismus)

What elecrtrolytes effected in MH

increases

• H

• K

• Ca2+

• CO2

Decreased

• O2

MH physiology

• Ryanodine (RYR1) mutation

  • Autosomal dominant inherited trait= EXAM

  • Sometimes random mutation (Mayo Clinic,2022)

• Skeletal Muscle Hypermetabolism

• Excessive Calcium release from the Sarcoplasmic Reticulum—> Increased intracellular calcium leads to sustained contractions with increased metabolsim

MH triggers

1. Halogenated Anesthetics (Iso, des, halothane, enflurane, sevo)

2. Depolarizing muscle relaxants (Succs)

3. Physiological stressors

4. Extreme heat

5. Strenuous exercise

WHAT IS NOT A TRIGGER FOR MH

N2O

MH S/S 11

1. None until exposed to trigger

2. Trismus( masseter spasm) 50%

3. Whole body muscle rigidity 75%

4. High body temperature

5. Tachycardia & tachypnea

   1. from SNS stimulation secondary to hypermetabolism & hypercarbia

   2. tachycardia is 2nd sign

6. Increased ETCO2/ Decreased pH

7. Combined metabolic and respiratory acidosis

8. Cardiac arrhythmia

9. Renal Failure

10. HyperK

11. Cyanosis

what is earliest, most senstiive and specific sign of MH

elevated ETCO2

how fast can temp increase in MH

1-2 C q 5 min

know

MH risk factors

• Family History of Malignant Hyperthermia (MHAUS, 2024)

  • autosomal dominant inheritance pattern

  • children and siblings of a patient with MH susceptibility usually have a 50% chance of inheriting a gene defect

• Exposure to Succinylcholine or Inhaled Anesthetics

• Associated susceptibility disorders (Watt & McAllister, 2023)

  • Central Core Disease (rare, non-progressive myopathy)

  • King-Denborough Syndrome (rare myotonia)

current safe anesthetic practice

• First Case of the day

• Fresh anesthetic circuit and 20 min 100% oxygen flush

• Benzodiazepines and Nitrous Oxide are safe

• TIVA Propofol anesthetic w BIS monitor

• No Succinylcholine

• No Halogenated Inhaled agents

current helath practice for dx

• Contracture Caffeine – Halothane test

  • Gold Standard, controlled setting

  • Sensitivity: close to 100%

  • Specificity: 80%

• Genetic testing only 50-86% of MH affected individuals

  • Very low sensitivity

  • Gene sequencing mutations from DNA (Yang et al., 2020)

    • RYR1 (48)

    • CACNA1s (2)

  • Triggering event

MH tx

• Notify MH Hotline for help (1-800-MH-HYPER)

• Dantrolene (Dantrium, Revonto, Ryanodex)

  • Suppresses the calcium release from SR

  • Only disease-specific drug available (Yang et al., 2020)

    • Mortality rate from 70% down to 9.5% after Dantrolene

• Body Cooling interventions (Ice Packs, Cold IVF, Gastric Lavage)

• Hyperventilate with 100% oxygen

• Bicarbonate 1-2mg /kg as needed

• Treat arrhythmias (no Calcium Channel blockers)

• Mortality Rate 3-5%  (Watt & McAllister, 2023)

8 initial management for MH

1. DC inahled anesthetic and succs

2. hyperventilate with 100%

3. admin dantrolene (dosing based on HR and temp)

4. tx acidosis with Na bicarb (1-2 mM/kg)

5. Lower body temp to 38 C with external ice packs, gastric lavage

6. replace anesthethic cirut and cannister

7. monsitor with capnography and ABG

8. tx hyperk and dysrythmias

If a pt experiences massteter msucle rigidity from sucs. what lab value may confirm dx of MH

elevation in creatine phosphokinase (CPK> 20,000)

how does dantrolene work

acts on ryanodine recpetor ot decrease Ca level in skeletal muscle by decreasing release of ca from SR. skeletal muscle relaxes when supply of calcium to contractile proteins is impaired

dantrolene dose

2.5 mg/kg q5 min until episode is terminated.

max 20 mg/kg

ppx dantrolene dose is 2.5 mcg/ml

each vial of dantrolene contains 20mg withh 3g mannitol- mix with 60ml warmed sterile water

½ life of dantrolee

10 hrs

so readmin q 10-15 hrs for at least one, but possible several doses