Anaphylactic Shock in General Anesthesia

Presented by R1 顏郁軒 2003/3/

18

General Data (1)

80 y/o , Female , about 70 kgwHx of HTN Hx of right knee & wrist fracture s/p op ,gall stone s/p op , uterus prolapse s/p op No any complication was noted after general anesthesia No drug allergy history

General Data (2)

Fell down on 92/3/2 ; right distal radial fracture was impressed and operation was arranged

General anesthesia was done . Induction with Fentanyl 100 ug , Pentothal 275 mg ,SCC 100 mg , Cis-atracurium 4 mg , Xylocaine 100 mg

General Data (3)

About 15 mins later , tachycardia about 130 ~ 140 , low end tidal CO2 (30+ 10+) and high airway pressure were noted .Pulse : weak and then impalpable Breathing sound : bil decreased EKG : ST depression over lead II CPR was done Bosmine infusion Set A-line , but failed

General Data (4)

About 3 mins later , pulse was returned and A-line was set successfully then .

Erythematous change over trunk & four limbs were noted

BP=110/65 , PR =148

Transferred to SICU for further treatment and evaluation

What Happened ?

D/D : AMI , Anaphylaxis , Pneumothorax , Pulmonary embolism

Time sequence of drug administration

Hints over physical examination

How to explain the EKG change

Lab Data

Series EKG was F/U

Cardiac enzyme F/U 3/2 3/2 3/3 CK/CKMB 61/32.1 64/13.3 73/4.4 Troponin-I 0.1 3.3 7.3

Con’s returned at that night , and endo was removed on the next day smoothly .

Operation was done on 3/12 Anesthesia with IVG was performed Agent : Fentanyl 100 ug , Propofol infusion No any complication was noted during anesthesia The post operative condition was good , and then discharged smoothly .

Anaphylaxis during anesthesia (1)

Allergy,anaphylaxis ,and general anesthesia Immunology and Allergy Clinics of North AmericaVolume 21 • Number 4 • November 2001

Anaphylaxis . What is Monitored to Make a Diagnosis? How is Therapy Monitored? Anesthesiology Clinics of North AmericaVolume 19 • Number 4 • December 2001

Anaphylaxis during anesthesia(2)

Definition Anaphylaxis : rapid, generalized immunologically mediated events involving an antigen-specific IgE-mediated mechanism that occur after exposure to foreign substances in previously sensitized p

ersons Anaphylactoid reaction : not mediated by way of the IgE antibody and prior exposure is not n

ecessary

Anaphylaxis during anesthesia(3)

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

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.

RECOGNITION OF ANAPHYLAXIS DURING ANESTHESIA

System Vital Sign Changes Other Signs Symptoms

Pulmonary Increased respiratory rate Stridor (laryngeal edema), wheezing (bronchospasm), coughing, sneezing, decreased pulmonary compliance, pulmonary edema, respirator

y failure

Dyspnea, chest discomfort

Cardiovascular Increased blood pressure Decreased systemic vascular resistance, dysrhythmias, pulmonary hypertension, car

diac arrest

Retrosternal pain

  Increased heart rate    

Cutaneous Increased skin temperature (redistribution of blood)

Urticaria (hives), flushing, periorbital edema, perioral ed

ema diaphoresis

Itching, burning

Neurologic Nonspecific Disorientation, loss of consciousness

Dizziness, light-headedness, malaise

Gastrointestinal Nonspecific Vomiting, diarrhea Nausea, abdominal pain

Treatment (1)

Airway maintenance, 100% oxygen administration, intravascular volume expansion, and epinephrine

Treatment (2)

Initial therapy 1. Stop administration of antigen 2. Maintain airway with 100% oxygen 3. Discontinue all anesthetic agents 4. Start intravascular volume expansion (2–4 L of

crystalloid with hypotension) 5. Administer epinephrine (5–10 μg intravenous i

nitial bolus with hypotension, titrated as needed; 0.1–0.5 mg intravenously with cardiovascular collapse)

Treatment (3)

Secondary treatment1. Antihistamines (0.5–1 mg/kg diphenhydramine) 2. Catecholamine infusions (starting doses: epinephri

ne, 5–10 μg/min; norepinephrine, 5–10 μg/min, as an infusion, titrated as needed)

3. Bronchodilators (inhaled albuterol or terbutaline with bronchospasm)

4. Corticosteroids (0.25–1 g hydrocortisone; alternating 1–2 g methylprednisolone)

5. Sodium bicarbonate rarely needed (0.5–1 mEq/kg with persistent hypotension and acidosis refractory to volume repletion and epinephrine)

6. Airway evaluation (before extubation)

An anaphylactic reaction possibly associated with an intraoperative coronary artery spasm during general anesthesia

Journal of Clinical AnesthesiaVolume 13 • Number 3 • May 2001

A 72 y/o male with choledocholithiasis

HTN & smoking , no allergy history

Epidural and GA with Fentanyl , vecuronium and propofol were done

Hypotension ( 60/42 mmHg ) and tachycardia ( 122 beats /mins ) after antibiotics given (Cefa)

ST elevation over lead II , III , AVF and V6PE : flush over neck and chest Anaphylaxis with coronary spasm was considered Tx with Epinephrine and solu-medrol(500 mg) ; 5 mins later BP elevation and ST returned normal

histamine causes dilation in both epicardial and resistance coronary arteries that are free of atherosclerosis

histamine induces profound vasoconstriction in segments of coronary arteries with a defective endothelial vasodilation mechanism

coronary artery spasm in their case may be explained by an increased histamine level and an impaired endothelial coronary vasodilation mechanism

the adventitial mast cells of the coronary artery may play an important role in the pathogenesis of coronary artery spasm

degranulated mast cells are increased in the adventitia of the coronary artery segments with ruptured plaque that are responsible for MI, suggesting histamine and other vasoactive substances released from the adventitial mast cells may locally provoke coronary artery spasm

Thanks for your Attention !!