NON-OPERATING ROOM

ADVERSE EVENT
(Significant Bradycardia and Tachydysrhythmia)

Ruby Anne D. Batobalonos, MD

Anesthesia Resident
 PATIENT S.A.
15 YEARS OLD
37 KG ◦ CHIEF
COMPLAINT:
12/22/21
◦ FOR CHANGE OF
PATIENT DATA CHILD TRACHEOSTOMY
ROMAN CATHOLIC TUBE ANND
GASTROSTOMY
TUBE

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 HISTORY OF PRESENT ILLNESS
patient noted bilateral lower
2 years prior to consult
extremity weakness,
abdominal pain and
vomiting. Admitted for
progressive ascending
weakness. Imaging, blood
chem and studies were taken.
Managed as a case of GBS.
Patient had difficulty
PICU admission
breathing and was
subsequently intubated and
tracheostomy and
gastrostomy tube inserted
after prolonged intubation
and hospital stay.
while admitted, patient had
episodes of tonic-clonic
seizure thus maintained on
Valproic Acid 11mkd 2x a
day.
patient discharged and scheduled for change of
discharged
on day of procedure
instructions given for home tracheostomy and
care and follow up visits. gastrostomy tube.
Advised tracheostomy
change to be done 3-6moths,
however, due to the current
pandemic, change of
tracheostomy done yearly.
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 PAST MEDICAL HISTORY
DELIVERED TERM VIA NSD AT A LOCAL INSTITUTION

COMPLETE IMMUNIZATION

MOTHER WITH COMPLETE PRENATAL CHECK UP AND NO PRENATAL ILLNESS

S/P TRACHEOSTOMY 2019

S/P GASTROSTOMY TUBE INSERTION 2019

NO KNOWN FOOD AND DRUG ALLERGIES

DIAGNOSED WITH GBS

DIAGNOSED WITH SEIZURE DISORDER

 ◦ Awake, Alert, pupils equally reactive
◦ No facial asymmetry
◦ Anicteric Sclera, Pink palpebral conjunctiva
◦ Tracheostomy in place
◦ Equal chest expansion, clear breath sounds
PHYSICAL ◦ Adynamic precordium, Normal rate and regular rhythm
EXAMINATION ◦ Globular, soft, NBS, no tenderness
◦ Full pulses
◦ Motor function
◦ 0/5 both upper and lower extremities
◦ With muscle wasting and disuse atroph

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 DIAGNOSIS
GUILLAINE BARRÉ SYNDROME

SEIZURE DISORDER

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 Mallampati – not
assessed
Limited mouth
opening and neck
mobility
Pre anesthetic NPO for 8 hours
evaluation Risk discussed to
parents
Patient examined and
history were reviewed
Anesthetic consent
secured.
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 ASA: 3
WEIGHT: 37KG
NO ALLERGIES
Intraoperative GCS:12 (E4 V3 M5)

anesthetic AWAKE, ALERT, NOT IN DISTRESS

record BASELINR VS:

BP 95/40
HR 92
SPO2 100%

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 • Midazolam 1mg IV given
• Vital
10:32AM

• transferred to endoscopy unit room 1

• Standard monitors attached
• O2 at 4 LPM via tracheostomy
• Baseline vital signs:
9AM • BP 110/60, 95 bpm, O2 sat 100%

• Midazolam 1.2 mg and fentanyl 25 mcg IV given

• vital signs monitored every 2 minutes
• Vital signs: BP 100/55, HR 96bpm O2 sat 99%
9:30AM

• change of gastrostomy started

9:32AM

• gastrostomy tube procedure ended.

10:25 • vital signs: 125/55, HR 105, 02 sat 100%

AM
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 • O2 increased to 6LPM
• midazolam 1mg IV given
• Vital signs: 100/60, HR 100, O2 sat 99%
10:32AM

• Skin prep done

• procedure started
• Baseline vital signs:
• BP 110/60, 95 bpm, O2 sat 100%
10:35 AM

• procedure ended
• oral and tracheal secretions suctioned
• vital signs: BP- weak pulses, HR 70s-48bpm, O2 Sat 99%
• Atropine 0.5 mg IV given
10:50 AM • noted loss of consciousness

• O2 supported and assisted with 100% (10LPM)

• additional 0.5mg atropine given
• patient still remained unconscious
• Vital signs:
10:51 AM • BP 80/40, HR 170s, o2 sat 100%

• SVT noted, HR of 170s

• vital signs: weak pulses ands unappreciable BP, 02 sat 100%
• Synchronous cardioversion with 150J
• SVT converted to sinus tachycardia
10:55- • Vital signs: 90/60, HR 150s, O2 sat 100%
• Amiodarone 150mg very slow IV given
11:10AM • Vital signs: BP 110/60, HR 110, (sinus tachycardia), O2 sat 100%

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 • paracetamol 600mg IV given
• patient started regaining consciousness
11:15AM • Pupils equally reactive to light

• patient awake, conscious and started crying

• vital signs: 100/60, HR 105, o2 sat 100%
11:30 AM

• patient transferred to endoscopy recovery unit.

• parents apprised and was advised admission for
11:35 monitoring.

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 ◦ Procedure
◦ Change of gastrostomy tube abd tracheostomy
 Anesthetic technique
 MAC-sedation
Total operative time

Intraoperative 1 hour and 45 minutes

summary Medications given

Midazolam – 2.2 mg
Fentanyl 25 mcg
atropine 1mg
Paracetamol 600mg
Critical event:
Dysrhythmia requiring treatment
Significant bradycardia 12
POST ◦ Patient awake, no episode of seizure nor syncope.

PROCEDURE ◦ No cough, colds, fever

AND EVENTS ◦ Clear breath sounds
DAY 2 ◦ Normal heart rate and regular rhythm
◦ Stable vital signs
unremarkable ◦ For discharge

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 ◦ Patient admitted

◦ On gastrostomy feeding

◦ Labs

◦ 12 Leads ECG
◦ CBC
◦ Na, K, Ca
◦ Hgb 134/ Hgb 0.42/WBC
POST Therapeutics:
12.4/Plt 282
PROCEDURE 5ml Q12H
Valproic Acid 250mg/5ml,

AND EVENTS Rifampicin 200mg/5ml, 5ml ◦ Sodium 141

DAY OD
◦ Potassium 4.5
zinc sulfate 55mg/5ml, 1ml
OD ◦ Calcium 2.23
unremarkable ascorbic Acid 5ml OD

Folic Acid 5ml OD

◦ ECG- Sinus rhythm 102 bpm
Diazepam 5mg IV PRN for
seizure

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 Signs and
Procedure Drug administered
symptoms
What is the • Atropine 1mg IV • Significant
most likely • Change of • Amiodarone bradycardia
• tachydysrhythmia
gastrostomy tube 150mg slow IV
diagnosis and
tracheostomy
What could have happened

• Autonomic • Significant
dysfunction bradycardia
• Vasovagal • Hypotension
syncope • Tachydysrhthmia

STATEMENT
Adverse
OF THE
outcome
PROBLEM

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DISCUSSION

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 o an acute inflammatory polyneuritis that is triggered by humoral and cell-
mediated autoimmune response to a sensitizing event.
o etiology is unknown
Guillain-Barré o (in many cases a timely association with a viral (influenza-

Syndrome like) or bacterial infection or even lymphomatous disease can

be demonstrated)
o an ascending paralysis characterized by symmetric weakness
Acute inflammatory o Fulminant cases can present with severe ascending weakness
demyelinating
o leading to complete tetraplegia, and paralysis of cranial
polyradiculopathy
nerves and phrenic and intercostal nerves with facial and
respiratory muscle weakness neces- sitating tracheostomy
and ventilatory support

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Epidemiology
GBS worldwide is 1.1–1.8 cases per
100,000 per year, with higher rates in
males than females.

There is an association with precedent

infections in 70% of cases that are
predominantly respiratory and gastrointestinal
in origin

It has been suggested there has been an

association between GBS and vaccinations,
although the evidence for this is weak

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 Signs and
symptoms
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 GBS SUBTYPES
ACUTE INFLAMMATORY ACUTE MOTOR AND SENSORY
DEMYELINATING AXONAL NEUROPATHY
POLYRADICULOPATHY
• both motor and sensory fibres are
• most common form involved

• involves inflammation and destruction of • more severe and associated with

the myelin sheaths. prolonged or even partial recovery.

ACUTE MOTOR AXONAL NEUROPATHY

• association with precedent infection • presents with ataxia, areflexia and

with Campylobacter jejuni
ophthalmoplegia.
• primarily sensory conduction failure.
• selective motor nerve and axonal
involvement MILLER FISHER SYNDROME

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 Creatine kinase may be raised
Serum biochemistry
ESR is usually raised and CRP is sometimes
elevated.
Anti-GM1 associated with worse outcome. Anti
Inflammatory markers GD1 associated with AMAN, Anti GQ1b with
MFS.

Infection screen evidence of gastrointestinal infections

INVESTIGATIONS particularly Campylobacter jejuni.
CT brain to exclude other causes
Radiological MRI — selective anterior spinal
nerves root enhancement

Cell count and glucose are usually

Lumbar puncture normal with a raised protein

Nerve
majority show demyelinating
conduction pattern
study

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 Differential diagnoses

Neurological Metabolic Infective Drugs / toxins Other

• Myasthenia gravis • Hypokalaemic periodic • Post diphtheria • Heavy metal poisoning • Acute polymyositis
• Eaton-Lambert paralysis neuropathy (e.g. lead) • Critical illness
(myasthenic) syndrome • Hypermagnesaemia • Polio • Biological toxins myopathy
• Multiple sclerosis • Hypophosphataemia • Botulism (including snake and
• Transverse myelitis • Acute intermittent • Tick paralysis scorpion toxins)
porphyria • Drugs (including
stavudine,
nitrofurantoin and
aminoglycosides)

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MANAGEMENT AND
ANESTHETIC
CONSIDERATION
Succinylcholine- contraindicated
non-depolarizing drugs- avoided
 ◦ Around 30% of patients with GBS require ventilatory
support.
◦
◦ Close monitoring of respiratory function tests is
SUPPORTIVE imperative.

◦ Arterial blood gases may be measured to provide

objective evidence of the development of respiratory
failure.
 ◦ Blood pressure may fluctuate
◦ Autonomic dysfunction between severe hypertension
and hypotension.
may be life-threatening.
Monitoring of the ECG, ◦ Care should be taken when
treating extremes of blood
blood pressure and fluid
Cardiovascular balance is advisable.
pressure
◦ Intubated patients with
◦ The most common autonomic dysfunction may
arrhythmia seen is sinus develop instability after
tachycardia tracheal suction
 ◦ Good nutrition
◦ Poor oral intake may
necessitate instigation of
enteral or parenteral feeding.
Gastro- ◦ ensure adequate calorific,
◦ susceptible to the
development of a paralytic
ileus.
◦ metoclopramide or

intestinal micronutrient, fluid and

electrolyte intake.
erythromycin.

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 ◦ Neuropathic pain
◦ Venous thromboembolism
◦ Non-opioid analgesics
prophylaxis
(paracetamol, NSAIDs) in
combination with opioid ◦ Low molecular weight
analgesia Adjunctive heparin in combination with
neurologic treatments such as either pneumatic
anticonvulsants (e.g. compression devices or
gabapentin or anti-embolism stockings.
carbemazepine), and
tricyclic antidepressants
may be effective.

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 ◦ There is a high incidence of
depression among patients
with GBS. –
◦ Careful attention should be
◦ it is important for the paid to limb positioning and
patient and their family to posture.
Psychological and have access to support
◦ Patients may also suffer from
rehabilitation groups.
persistent fatigue, which may
◦ counselling and respond to an exercise
psychiatric help be program.
available if needed.

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 ◦ Plasma exchange
◦ IV immunoglobulin

medications ◦ cortocosteroid

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 ◦ Most patients with GBS recover fully
◦ 15% of patients suffer persistent disability.
◦ 10% are unable to walk unaided at one year.
◦ The mortality from GBS ranges from 2–12%.
prognosis ◦ venous thromboembolism,
◦ pneumonias, arrhythmias and
◦ complications related to dysautonomia.

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 “
◦ Pediatric Advanced
Life Support

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 Age Awake rate (/min) Sleeping rate
(/min)
Neonate 100-205 90-160
Heart rate and
Infant 100-180 90-160
rhythm Pre-school 80-120 80-120

School age child 75-118 58-90

Adolescent 60-100 50-90

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 quickly determine if the arrhythmia is causing hemodynamic
instability or other signs of deterioration.

The signs of instability in a patient with arrhythmia include the

following:
Principles of • Respiratory distress or failure
managing •
•
Shock with poor end-organ perfusion
Irritability or a decreased level of consciousness
pediatric • Chest pain or a vague feeling of discomfort in older
children
arrythmias • Sudden collapse

Priorities in initially managing arrhythmias are the same as they are for all critically ill children:
• support the ABCs- airway,
• breathing, and
• circulation- and
• treat the underlying cause.

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38

Epinephrine
◦ for symptomatic bradycardia that
persists despite effective
oxygenation and ventilation.
increases heart rate and cardiac
contractility, and alpha adrenergic
activity causes vasoconstriction.
Medications ◦ For IV/IO route, give 0.01 mg/kg
(0.1 mL/kg of 0.1 mg/mL
concentration)
◦ For endotracheal route, give 0.1
mg/kg (0.1 mL/kg of 1 mg/mL
concentration)
◦ Repeat every 3 to 5 minutes
Atropine
◦ a parasympatholytic (or anticholinergic) drug
that accelerates sinus or atrial pacemakers and
enhances atrioventricular (AV) conduction.
◦ for bradycardia caused by increased vagal
tone.
◦ For IV/IO route, give 0.02 mg/kg; minimum
◦
0.1 mg, maximum 0.5 mg
May repeat dose once, in 5 minutes.
◦ For endotracheal route, give 0.04 to 0.06
mg/kg.
◦ Tachycardia may follow atropine
administration, but it is generally well
tolerated in the pediatric patient.
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 ◦ assess and look for signs of hypotension, altered mental status, shock
(ie, poor perfusion), or life-threatening hemodynamic instability.
◦ Maintain a patent airway; assist breathing as necessary.
◦ Use a cardiac monitor to identify the rhythm, and monitor pulse, blood
pressure, and oximetry.
Managing ◦ Establish IV/IO access.
Tachyarrythmias ◦ Obtain a 12-lead ECG if available (but do not delay urgent
intervention).
◦ Obtain laboratory studies
◦ Assess neurologic status.
◦ Anticipate the need for medications Simultaneously try to identify and
treat
◦ reversible causes.

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 ADENOSINE
• Drug of choice for treating
SVT
• With continuous ECG
monitoring, administer 0.1
mg/kg (maximum initial
dose 6 mg) as a rapid IV
bolus.
AMIODARONE
• May be considered when
treating hemodynamically
unstable SVT refractory to
vagal maneuvers,
adenosine, and
cardioversion
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 • Synchronized shocks • Use synchronized • Start with an energy
are used for cardioversion for dose of 0.5 to 1 J/kg
cardioversion from Hemodynamically for cardioversion of
SVT and VT with a unstable patients (poor SVT or VT with a
SYNCHRONOUSED pulse. perfusion, hypotension, pulse.
or heart failure) with • If the initial dose is
CARDIOVERSION tachyarrhythmias (SVT, neffective, increase the
atrial flutter, VT), but dose to 2 J/kg.
with palpable pulses

INDICATION ENERGY DOSE

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THANK YOU

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