1. A 74-year-old female with a history of asthma and hypertension presented for an emergency CBD re-exploration surgery. 2. During induction, the patient aspirated, which precipitated a severe bronchospasm that led to irreversible hypoxia, hypotension, and cardiac arrest. 3. Despite maximal treatment and resuscitation efforts, the patient could not be revived and was declared dead. The case highlights the challenges of managing perioperative bronchospasm and aspiration in a high-risk asthmatic patient.

1. ANAESTHETIC MANAGEMENT OF A
PATIENT WITH PERIOPERATIVE ASTHMA [A
MORTALITY CASE REPORT]
PRESENTER- DR NANDINI DESHPANDE
GUIDE- DR V.K PARASHAR

2.  I am presenting an interesting case of intraoperative
bronchospasm that occurred during an emergency case of CBD
re-exploration .
 Aspiration during induction precipitated the bronchospasm in the
patient who was a known case of chronic asthma. The spasm lead
to severe irreversible hypoxia and haemodynamic instability
despite of all the protocol based treatment given and BCLS
protocol followed by the anaesthetists.
 The patient couldn’t be revived despite of all the efforts and this
case was discussed at the mortality meet last month at SDMH with
involvement of the consultants involved with case from the
department of Anaesthesia and Gastrointestinal surgery.

3. CASE DISCUSSION
Presenting a case of Mrs. Sarju devi , a 74 year old female, weight
57kg, height-158cm , admitted in SIDDS WARD 1,under GI surgery
was operated for laproscopic CBD exploration under general
anaesthesia in view of choledocholithiasis ,was post operative day
4 and had chief complaints of:
1. Pain in abdomen since 2 days
2. Vomiting -2 to 3 episodes since 1 day
3. Distension of abdomen since 1 day
Patient was posted for emergency CBD re-exploration in view of
suspected anastamotic bile leak[19th nov 2017].

4. HISTORY OF PRESENTING ILLNESS
1. Patient complained of pain in abdomen since 2 days, it
was generalized , dull aching in nature, non – radiating ,
continuously present throughout the day associated with
loss of appetite and nausea.
2. Patient also gave history of vomiting since 1 day, 2-3
episodes, vomitus was bilious coloured, non foul smelling,
non blood stained ,nonprojectile in nature.
3. Patient developed distension of abdomen on the day
when she was posted for emergency surgery which
aggravated the abdominal pain and nausea.

5. Past history
 Patient had history of Hypertension since 13 years, was on tab. Dilzem
120 mg o.d , tab cardace 2.5mg o.d, tab atorvas 30mg o.d.
 Patient gave history of bronchial asthma since 20 years. Patient was on
regular treatment with rothaler foracort 400mg which she took almost
every day twice. Patient had intermittent episodes of asthma with
asymptomatic periods of relief in between.
 Was a known case of IHD, patient had PTCA[drug–eluting] to one
coronary artery 1 year back was on tab ecosprin 75 mg, tab
clopidogrel 75mg o.d [ these were stopped four days prior to first
surgery ] and started back on first post-operative day and were
continued since then.

6. Past Surgical & Anaesthetic history
 Patient was operated for choledocholithiasis [14th nov 2017]
– laproscopic CBD exploration 4 days back before being
posted for emergency re-exploration . Surgery was done
under general anaesthesia with controlled endotracheal
intubation done . The anaesthesia course was uneventful
throughout the surgery and even post operatively . There
was no bronchospasm intraoperatively or postoperatively
,patient was extubated and shifted to SIDDS ICU for 2 days
for observation and later she was shifted to SIDDS ward .

7. Pre- anaesthetic examination during previous
laproscopic surgery
 Patient had chief complaints of dull aching abdominal pain
and yellowish discolouration of sclera for 10 days prior to
scheduled surgery[14 nov 2017].
 The past medical history was the same as in the current PAC
done. Patient had no previous surgical history.
• G/E & S/E- conscious, oriented, HR-65/min, RR-14/min,
temperature-98.6 F ,BP-150/80 mmhg, SPo2 on room air-
97%. CVS- WNL, R/S- air entry B/L equal, no wheezing , RR-
14/min, P/A-soft, non-tender.

8.  Airway- mouth opening – 3 fingers, Mallampati grade -1,
edentulous, loss of buccal pad of fat, neck movements – normal
 All basic routine investigations with routine haemogram , LFT, RFT,
electrolytes, ECG, CXR, PT, INR , glucose were done and
documented.
 Cardiologist consultation along with 2D-echo for known case of
HTN and CAD was done – fitness was given with mild to
moderate cardiac risk.
 Pulmonology reference was done for chronic bronchial asthma-
nebulization was advised pre-op and post-op and fitness was
given for laproscopic surgery.

9. General and systemic examination[19th nov2017]
• Patient was conscious, oriented, anxious, complaining of pain
• No icterus, no pallor, no cyanosis and oedema
• Was well hydrated , tongue –moist, Iv fluids were being continued
via 20G IV cannula, skin turgor- normal, eyes-not sunken.
• HR-100/min, RR-29/min, temperature-98.6 F ,BP-140/80 mmhg,
SPo2 or room air- 92%.
• Airway- same as in the previous PAC
• No NG tube in situ.
• Systemic- CVS- WNL, R/S- air entry was decreased in the bases
bilaterally, occasional wheeze was present, no intercostal
retraction, RR- 29/min, P/A-distended

10. Pre-operative laboratory investigations:
• CBC- Hb-10.2 gm%, TLC- 12,740/ul, platelete count- 3.15 lakh/ul
• Serum electrolytes- Na/k/Cl-137/4/109
• LFT- serum bilirubin D/T-0.3/0.7, SGOT/SGPT-58/72, ALP-100
• RFT- BUN-9mg%, creatinine- 0.8mg%
• PT/INR-18.9/1.53, viral markers- non –reactive
• Ecg- showed t wave inversion in lead 2, 3 and avf
• CXR- increased bronchovascular markings and blunting of b/L CP
angles
• 2D ECHO- EF- 55%, LVDD I , NO RWMA[ reported on 13th nov 2017
prior to first surgery]
• Cardiac and pulmonary reference was done for the prior surgery-
fitness was given with mild to moderate risk, hence, no additional
investigations and references were required.

11. Pre-operative instructions, consent and
optimization
 NBM status was confirmed. Patient was NBM since 1 day.
 High risk anaesthesia consent for cardiorespiratory problems, age
related and emergency surgery in setting of continued anticoagulants
was taken.
 Ryles tube insertion was advised for gastric decompression to GIS
resident.
 Nebulization with duolin and budecort was advised, patient s rotahaler
to be brought to OT. IV hydrocort 100mg was given stat.
 Maintain IV hydration and discontinue the next dose of aspirin and
clopidogrel.
 Patient had taken atorvas and cardace tablet with sips of water. Dilzem
was discontinued.

12. Intraoperative management
Baseline
vitals
• After attaching standard ASA monitors, ECG- T inversion, HR- 104/min, patient
restless and irritable.
• BP- 100/70 mmhg , SPo2- 92 % or room air, chest auscultation – wheeze +
Premedicati
on
• IV hydrocort 100mg given stat, IV glycopyrollate 0.2 mg, RT wasn’t inserted .
• Patient was not co-operative , hence, RT insertion was planned after mild sedation.
• Mild sedation given with IV fentanyl 50 ug
Induction
• Preoxygenated with 100 % O2 on mask for 4-5 minutes, SPo2- 100% on monitor
after preoxygenation
• Rapid sequence induction with cricoid pressure given with IV propofol 50 mg

13. What happened during induction??
Patient started regurgitating as
soon as patient lost consciousness
after induction
Immediate head- down position
with head turned to right side was
done.
Excessive bilious vomiting started .
Thorough oropharyngeal
suctioning was done

14. What was done???
Cricoid pressure continued with
immediate intubation with ETT no 7.5 .
Thorough ETT suctioning done . Ryle s
tube of 16 fr inserted. ETT connected to
ventilator and maintained on inhalational
sevoflurane with 100%O2.
Ventilatory settings: PCV mode- FiO2-
100%, TV-350ml,PEEP-10cmH20, peak
pressure-39cmH20, Pinsp-33cmH20,RR-
20/min

15. Clinical and monitor findings for
bronchospasm?? Due to aspiration?
“Tight bag”, low
tidal volume,
increased peak
airway
pressures.
Chest- b/l
wheeze+,
crepts+,BP-
75/42mmHg,
pulse -150/min,
low volume,
SPo2-79% on
100%FiO2
Further
desaturation-
SP02- from
68%to54%,
ETCO2- 50%
with “shark- fin”
pattern[
prolonged
expiratory
slope”

16. Further deteriorating course
6-8 puffs of patient’s rotahaler were
given via ETT. IV hydrocort 100mg
stat+ IV deriphylline 2cc stat, ETT
changed and thorough suctioning-
SPo2-54%
Ionotropic support- IV Norad[4/50]
started @5ml/hr then increased to
15ml/hr- BP- still 60/40 mmhg
Intraop ABG- pH-7,PC02-
76.3,PO2-59.8,HCO3-22.5,
anion gap-6

17. Icu shifting & management
 No improvement in the vitals on maximum ionotropic support with IV
noradrenaline[8/50]@15ml/hr and IV adrenaline[2/50]@12ml/hr.
 Immediate left femoral line of 16 g vygon was taken .Inhalational was
discontinued due to unstable haemodynamics .
 The surgery lasted for 2 hours and during that period patient had
waxing and waning episodes of desaturation. SP02 – 58% to 85%.
 Surgeon asked to complete the surgery as soon as possible and close
the abdomen and decision taken to shift the patient to SIDDS ICU.
 ICU- patient went into ventricular fibrillation – on ECG, carotid – not
palpable, BP- not recordable, peripheries-cold , pupils- mid-dilated. DC
shock of 200joules was given. CPCR started. Multiple doses of IV
ATROPINE and IV ADRENALINE were given.
 Resuscitation continued for 45 minutes. Patient could not be revived
was declared dead .

18. Challenges faced during this case
Aspiration during induction
due to inadequate gastric
decompression
Severe irreversible
bronchospasm in a
known asthmatic
Respiratory
acidosis
Hypoxemia and
severe hypoxia
Haemodynamic
instability,
advanced age
cardiac arrest due to
severe irreversible hypoxia

19. Intraoperative bronchospasm
D/D of intraoperative bronchospasm:
• Kinked ETT
• Solidified secretions ,blood
• Pulmonary edema
• Tension pneumothorax
• Aspiration pneumonitis[Mendelson’s
syndrome] [probable cause of
bronchospasm in this case]
• Endobronchial intubation
• Pulmonary embolism
• Persistent coughing and straining

20. What is BRONCHOSPASM??
 Bronchospasm is the reflex contraction of the
bronchial musculature which causes constriction of the
smaller air passages and may be associated with
laryngospasm in some cases.
 It may be centrally mediated as in asthma or may be
local response to airway irritation.
 Bronchospasm may appear as an entity in its own or
be a component of another problem such as
anaphylaxis, or in patients with pre-existing airway
disease such as asthma.

21.  It is characterised by prolonged expiration, wheeze,
increased peak airway pressures during IPPV or in
severe cases complete silence on auscultation.
 Wheeze may be audible either with or without
auscultation, but can only be present if there is gas flow
in the patient’s airways. Thus, in cases of severe
bronchospasm, the chest may be silent on auscultation..
 If untreated it can cause hypoxia, hypotension and
increased morbidity and mortality.
 Suspected bronchospasm during anaesthesia should be
assessed and treated promptly.

22. Pathophysiology:
Decrease in
release of the
bronchodilators
Increase in the release of
bronchoconstrictors [histamine,
bradykinin, leukotrienes, substance
P , acetylcholine]

23. Bronchocons
triction,
airway
inflammation
, oedema
and
increased
secretions
Narrowing of
airways and
increase in
resistance to
airflow
Expiration
time is
increased
RV, FRC is
increased
Hyperinflated
lungs

25. PREDISPOSING FACTORS:
• Patients with hyperreactive airway like in chronic bronchitis ,
asthma , URI , smokers.
• Irritant stimulus to airways in light planes of anaesthesia like
laryngoscopy , blood , vomitus secretions etc.
• During intubation or extubation.
• Oral endoscopy , bronchoscopy.
• Histamine releasing drugs like morphine , atracurium etc.
• Use of irritant inhalational agent like isoflurane in
spontaneously breathing patient specially in pediatric age
group.

26. Inhalational: isoflurane,
desflurane [ due to pungent
odour]
IV Induction drugs:
thiopentone, etomidate
Opioids: morphine,
pethidine
Muscle relaxants:
atracurium,
mivacurium[>histamine
release],
succinylcholine[<histamine]
Anaesthetic
drugs
causing
bronchospas
m

27. Inhalational:
sevoflurane[sweet-
smelling],halothane [best
bronchodilator]
IV Induction drugs:
propofol[ haemodynamically
stable patients] , ketamine[
haemodynamically unstable
patients]
Opioids: fentanyl
Muscle relaxants:
cisatracurium , vecuronium
, rocuronium
Anaesthetic
drugs
preferred in
asthmatics

28. • Bronchospasm occurs most commonly and approximately
equally during the induction and maintenance stages of
anaesthesia and is less often encountered in the emergence
and recovery stages.
• Bronchospasm during the induction stage is most
commonly caused by airway irritation, often related to
intubation.
• During the maintenance stage of anaesthesia,
bronchospasm may result from an anaphylactic or serious
allergic reaction.

29. Intraoperative recognition of bronchospasm
• Bronchospasm during anaesthesia usually manifests as prolonged
expiration. An associated expiratory wheeze may be auscultated
in the chest or heard in the breathing circuit.
• Breath sounds may be reduced or absent.
• An anaesthetized pt. is difficult to ventilate due to diminished
compliance.
Marked increase in airway pressure required to ventilate
↓
Air trapping and hypoxemia
↓
Impaired venous return and decreased cardiac output

31. PREVE
NTION
Stop
smokin
g
Control of
URTI
[postpone
elective
surgery for
2-3 weeks
Use
antisialagouges
and non triggering
induction agents
Use LMA over
ETT where
needed.
Use humidified
gases
Use of
RA
over
GA
Inhaled
bronch
odilator
s and
steroids

32. Treatment

35. Drug therapy:
First Line Drug Therapy —
Salbutamol
• Metered Dose Inhaler: 6-8 puffs repeated as
necessary(using in-line adaptor/barrel of 60ml syringe with
tubing or down ETT directly)
• Nebulised:5mg(1ml 0.5%)repeated as necessary
•Intravenous:250mcg slow IV then 5mcg./min up to
20mcg./min

36. Second Line Drug Therapy —
• Ipratropium bromide: 0.5mg nebulised 6 hourly
• Magnesium sulphate: 50mg/kg IV over 20min(max 2g)
• Hydrocortisone : 200mg IV 6 hourly
• IN EXTREMES: Epinephrine (Adrenaline) Nebulised: 5ml
1:1000 Intravenous: 10mcg (0.1ml 1:10,000) to 100mcg (1ml
1:10,000) titrated to response

37. • Intravenous agents:
1. Sympathomimetics:
-Adrenaline :0.25-1 ug/kg/min
-Terbutaline : 0.25mg SC. in adults
0.01mg/kg SC in children
2. Methylxanthines:
- IV Aminophylline :
Loading dose of 6mg/kg slowly followed by 0.5 – 1mg/kg/hr infusion.
- IV Deriphylline : 2cc IM or slow IV in adults.
3. Steroids
-Decrease inflammation & inhibit histamine release.
- IV Hydrocortisone 1- 4 mg /kg
- IV Dexamethasone 0.1-0.2mg/kg
- IV Methylprednisolone 2mg/kg

38. OTHER METHODS—
• Deepening of plane of anaesthesia-
 Can be done with inhalational agent.
 Intravenous agents when ventilation is impaired.
 Ketamine causes bronchodilation by catecholamine
release.
 Propofol can also be used.
• If oxygenation is impaired, increase inspired concentration
of oxygen.
• Position of ETT should be checked and removed slightly as
carinal stimulation is potential cause.

39. Aspiration pneumonitis [mendelson’s syndrome]
 First recognized as a cause of an anesthetic-related
death in 1848
 In 1946, Mendelson described the relationship
between aspiration of solid and liquid matter
 Rare but potentially devastating complication of
general anaesthesia
 1 in 3200 in adults
 In patients having emergency surgery, it is 1 in 900.
 The actual mortality of a documented aspiration
episode is extremely low[about 1 in 71,000].

40. Definition:
Inhalation of material into the airway below
the level of the true vocal cords.
Linked with a range of clinical outcomes
Asymptomatic in some instances and resulting
in severe pneumonitis and ARDS.

41. Pathophysiology:
 LOS acts as a valve preventing the reflux of gastric contents.
 Barrier pressure is the difference between LOS pressure
(normally 20-30mmhg) and intra-gastric pressure (normally
5-10mmhg)
 Both are influenced by different factors.
 LOS pressure is reduced by :
 Peristalsis, vomiting, during pregnancy (a progesterone
effect)
 Pathological conditions such as achalasia, and various
drugs (anticholinergics, propofol, thiopentone, opioids).

42. Intragastric pressure is increased if the
gastric volume exceeds 1000ml, and with
raised intra-abdominal pressure such as
that occurring with pneumoperitoneum
during laparoscopy.

43. Vomiting vs regurgitation
 Regurgitation is a passive process that may occur at any
time & often silent.
 The common cause of regurgitation is a decreasing in
closing pressure of the sphincter.
 In contrast, vomiting is an active process which involves
contraction of abdominal muscles that occur in lighter
stages of anesthesia.

44. Gastric volume is influenced by:
 Rate of gastric secretions (0.6ml/kg/hr)
 Swallowing of saliva (1ml/kg/hr)
 Ingestion of solids/liquids, and
 The rate of gastric emptying - The rate of gastric emptying
for non-caloric clear fluids is rapid –the halftime being
about 12 minutes. Solids however, require six hours or
more to be cleared from the stomach, displaying zero-
order kinetics.

45. Severity and effects of aspiration:
 Effects of aspiration
1. Airway obstruction
2. Chemical pneumonia
3. Bacterial contaminations can result in death
 Factors w/c increase severity
1. Volume of aspirate, >25ml=severe
2. PH of aspirated matter < 2.5 =fatal
3. Extent of lung involved, one or both
4. Type of aspiration-solid/blood/fluid

46. Who are at risk?
1. Patient factors :
 Intestinal obstruction
 Full stomach
 Drugs
 Delayed gastric emptying
 LOS incompetence ,Hiatus hernia , Gastro-oesophageal
reflux
 Pregnancy ,Morbid obesity , Neuromuscular disorders

47. Decreased laryngeal reflexes
 Head injury
 Bulbar palsy
Gender -Male
Age –Elderly
 2. Operation factors : Anaesthetic factors:
• Procedure Difficult airway
• Emergency Gastric insufflation
• Laparoscopic Inadequate depth
• Position-Lithotomy

48. Aspiration pneumonitis:
 AKA mendelson’s syndrome
 Involves lung tissue damage as a result of aspiration of
non-infective but very acidic gastric fluid.
 Two phases :
1. Desquamation of the bronchial epithelium causing
increased alveolar permeability. Results in:
 Interstitial oedema
 Reduced compliance

49. 2. Due to acute inflammatory response
Occur within 2 to 3 hrs
Mediated by proinflammatory cytokines, i.e.
• Tumour necrosis factor alpha
• Interleukin 8
• Reactive oxygen products
Clinically may be
• Asymptomatic or
• Present as tachypnoea, bronchospasm, wheeze, cyanosis
and respiratory insufficiency.

50. Prevention:
A. Preoperative fasting
Current guidelines are:
 2 hours for clear fluids,
 4 hours for breast milk and
 6 hours for a light meal, sweets, milk (including formula) .
B. Reducing gastric acidity
 Histamine (H-2) antagonists and proton pump inhibitors (PPIs)
commonly used to increase gastric Ph.

51.  They do not affect the Ph of fluid already in the stomach
 Oral sodium citrate solution reliably elevates gastric Ph above
2.5, but it increases gastric volume, and is associated with
nausea and vomiting.(30ml 1hr before operation)
 An oral H2 antagonist (ranitidine 150-300mg PO) must be
given night before and 1-2 hours before anaesthesia and a PPI,
(omeprazole 40mg before the night and 2hr preoperatively)
 Ranitidine superior to PPIs in both reducing gastric fluid volume
and acidity. (Clark et al )

52.  Metoclopramide has a prokinetic effect promoting gastric
emptying and it also increases the tone of lower
oesophageal sphincter[LOS].
 Usual pre-medication for caesarean section under general
anaesthesia.
 Dose- 0.15mg/kg 15min before surgery, slowly to avoid
abdominal cramp.

53.  C. Rapid Sequence Induction (RSI)
 High risk of aspiration? Do a RSI, unless difficult airway to
warrant an awake fibreoptic intubation.
 Adequate depth of anaesthesia is important to avoid
coughing, laryngospasm and vomiting.

54. Cricoid pressure:
 Described by Sellick in 1961
 Remains an essential maneuver performed as part of
RSI
 Aim is to compress the oesophagus between the cricoid
ring cartilage and the sixth cervical vertebral body thus
preventing reflux of gastric contents.
 Force recommended is 15-20N when the patient is
conscious and 30-40N when the patient has lost
consciousness.

55. Current theories related to cricoid pressure
 There have been 2 imaging studies that showed that the oesophagus
often does not lie between the cricoid cartilage and the vertebral
column when the cricoid force[CF] is applied.
 In fact, when CF was applied , the oesophagus was displaced laterally
relative to the cricoid cartilage in over 90% of patients and an
unopposed oesophagus was observed in 71% of patients.
 Sellick’s maneuver went for “bench to bedside” in a very little time . It
was never tested in human beings before being accepted clinically.
 Hence, it’s role in preventing aspiration during anaesthesia is
controversial.

56. D. Nasogastric tube placement
E. Airway device
 A cuffed ETT is considered the gold standard device used
for airway protection.
 Alternative supraglottic devices include the classic
laryngeal airway (LMA) .
 The proseal LMA, providing a higher seal pressure (up to
30 cm H2O and a drainage channel for gastric contents .
 LMAs during difficult airways

57. Management: key points:
1. Head-down tilt
2. Oropharyngeal suction
3. 100% oxygen
4. Apply cricoid pressure and ventilate
5. Deepen anaesthesia/perform RSI
6. Intubate trachea
7. Release cricoid pressure once airway is secured
8. Tracheal suction
9. Consider bronchoscopy
10. Bronchodilators if necessary

58.  Clinical decision b/n surgeon and anesthetist to proceed or not!!
 Depends on
 Underlying health of the patient,
 The extent of the aspiration, and
 Urgency of the surgical procedure.
 A chest x-ray (CXR) can be useful in the case of suspected
pulmonary aspiration, although in about 25% of cases there are
no radiographic changes initially.
 If stable extubate and send to RR
 If patient develop a new cough/wheeze, tachycardia or
tachypnea, drop their spo2 on room air (by >10% of pre-
operative value), or
 Have new pathological changes on CXR should be further
managed in an ICU

59. Take home message:
Treat
broncho
spasm
intraop
Use sellick’s
method if
not NPO
Optim
ize
bronc
hospa
sm
pre-
opUse
BCLS
suppo
rt in
severe
cases
Early
recogn
ition &
treatm
Use
H2
blocke
rs and
PPI
Keep
NPO