2. General Data
16 y/o , Indian Female , 40 kgw
No underlying comorbid
Hx of allergy to ? Antibiotics –
generalized rashes
No history of previous surgery
3. General Data
Diagnosed to have: frontoethmoidal
mucocele
Planned for: FESS
Before op: requested by surgeon for
controlled hypotension, propofol
infusion for maintenance and
tranexemic acid prophylaxis
General anesthesia was done .
Induction with Fentanyl 80 ug , propofol
100mg, atracurium 30mg , morphine
3mg
4. General Data
Maintenance:
isoflurane 1.0
propofol infusion –running at 30-50mg/H
atracurium 10mg (stat dose at 30 and 1 H
after induction)
- in 1st hour of op:
Bp: 90-100/50-60, MAP: 60-70
no episode of hypotension
HR: 90-110
ET CO2 : 32-40
SpO2 : 99-100
5. General Data
At 1H of op: 1g tranexemic acid given
(was put in 300cc NS infusion)
After 10min: noted ETCO2 wave
showed bronchospasm, no desaturation
-increase isoflurane flow
BP: 60/40, reduce isoflurane,
bronchospasm resolved
but BP further decrease despite
ephedrine 6mg x2 given
6. General Data
Pulse : weak
ECG: sinus tachycardia HR 120-130
BP drop to 43/24 (MAP 30)
SpO2 : 99%
wave form: pulsus paradoxus
EtCO2: waveform normal
32-34
Given IV adrenaline 1:10,000 x1ml
twice
7. General Data
Subsequently after few minutes
Sp O2: waveform normal
99%
BP: pick up
60/40- 80/60
HR : 100-110
Operation finished after 1H 15min, patient
extubated well, discharged to general
ward
9. Anaphylaxis during anesthesia
Definition
Anaphylaxis : rapid, generalized
immunologically mediated events involving an
antigen-specific IgE-mediated mechanism that
occur after exposure to foreign substances in
previously sensitized persons
10. Anaphylaxis during anesthesia
The incidence of anaphylaxis in GA is
about 1:5000 to 1: 20000 and with a
mortality rate of up to 6%
Mechanism :
1.Specific IgE cross-linked by allergen (drug)
2. Complement activation by specific IgG or IgM
binding to antigen (drug)
3. Direct complement activation by way of the
alternate pathway
4. Direct activation of mast cells or basophils
11. CAUSES OF ANAPHYLAXIS AND ANAPHYLACTOID REACTIONS DURING ANESTHESIA
Causes
Rate of Reaction (%)
Muscle relaxants
61.6
Latex
16.6
Antibiotics
8.3
Hypnotics
5.1
Colloids
3.1
Opioids
2.7
Other (aprotinin, ethylene oxide, local
anesthetics)
2.6
Data from French survey by Perioperative Anaphylactoid Reactions Study Group; 1648 patients, July 1994 to December 1996.
15. Colloids
Prior drug allergy and male
Gelatins(0.34%) and dextrans(0.27%)
more likely than albumin(0.1%) and
hetastarch(0.06%)
16. Pathophysiology
Multiple organ systems are affected
Initial exposure to antigen → IgE
production and bind to mast cells and
basophils
Reexposure → release of mediators
from mast cells and basophils
20. From FDA reports: Tranexamic acid and Shock anaphylactic
This is a study of Shock - anaphylactic (Anaphylaxis)
among people who take Tranexamic acid. The study
analyzes: the time on Tranexamic acid when people
have Shock - anaphylactic, age of these people, the
severity of Shock - anaphylactic, how they recovered,
and common conditions and drugs used besides
Tranexamic acid. In total 1,505 Tranexamic acid
users are studied. The study is created by eHealthMe
based on reports from FDA and is updated regularly.
21. From FDA reports: Tranexamic acid and Shock anaphylactic
Tranexamic acid has active ingredients of tranexamic
acid. Commonly reported side effects of Tranexamic
acid include haemoglobin decreased, fever, rectal
haemorrhage, melaena, vaginal haemorrhage.
Shock - anaphylactic has been reported by people
with multiple sclerosis, asthma, blood pressure
management, high blood pressure, premedication.
22. From FDA reports: Tranexamic acid and Shock anaphylactic
1,505 people reported to have side effects when taking
Tranexamic acid. Among them, 19 people (1.26%) have Shock Anaphylactic.
26. Pulsus paradoxus
During inspiration, the right ventricle distends due to increased venous return,
the interventricular septum bulges into the left ventricle reducing its size
(reversed Bernheim effect), and increased pooling on blood in the expanded
lungs decreases return to the left ventricle, decreasing the stroke volume of the
left ventricle.
Additionally, negative intrathoracic pressure during inspiration is transmitted to
the aorta. The relatively higher negative pressure in the pulmonary circulation
compared to the left atrium in patients with pericardial pathology causes back
flow of blood from the left atrium into the pulmonary veins during inspiration.[2]
Therefore, during inspiration the fall in the left ventricular stroke volume is
reflected as a fall in the systolic blood pressure. The converse is true for
expiration. During quiet respiration, the changes in the intrathoracic pressures
and blood pressure are minor. The accepted upper limit for fall in systolic blood
pressure with inspiration is 10 mmHg.
