COMPLICATIONS OF GENERAL ANESTHESIA

By

Dr. Salah A. Ismail

Assistant Professor of Anesthesia
Faculty of Medicine, King Faisal University
2007/2008
 OBJECTIVES

At the end of this lecture, the student should be able to:

• Enumerate the complications of general anesthesia.

• Describe the management of respiratory
complications of general anesthesia.
• Describe the management of cardiovascular
complications of general anesthesia.
• Describe the management of neurological
complications of general anesthesia.
• Describe the management of postoperative nausea
and vomiting.
• Describe the management of temperature changes.
• Describe the management of adverse drug
reactions and hypersensitivity.
• Describe the management of complications of
position.
 Complications of general anesthesia

 Respiratory complications
I- Complications of laryngoscopy and intubation
II- Respiratory obstruction
III- Hypoxemia
IV- Hypercapnia and hypocapnia
V- Hypoventilation
VI- Aspiration pneumonia
 Cardiovascular complications
I- Hypotension
II- Hypertension
III- Arrhythmias
 Neurological complications
I- Awareness
II- Delayed recovery
III- Perioperative neuropathy
 PONV
 Temperature changes: Hypothermia and
hyperthermia
 Adverse drug effect and hypersensitivity
 Complications of positioning
 Miscellaneous
 A) Respiratory complications

I- Complications of laryngoscopy and intubation

1. Errors of ETT positioning:

a. Esophageal intubation
b. Endobronchial intubation
c. Position of the cuff in the larynx

2. Airway trauma:

a. Tooth damage.
b. Dislocated mandible.
c. Sore throat.
d. Pressure injury on trachea.
e. Edema of glottis or trachea.
f. Post intubation granuloma of vocal cords.

3. Physiologic responses to airway instrumentation:

a. Sympathetic stimulation
b. Laryngospasm
c. Bronchospasm

4. ETT malfunction:

a. Risk of ignition
b. ETT obstruction
c. Cuff perforation
II- Respiratory obstruction:

Signs:
1. Inadequate tidal volume.
2. Retraction of the chest wall and of the
supraclavicular, infraclavicular and suprasternal
spaces.
3. Excessive abdominal movement.
4. Use of accessory muscles of respiration.
5. Noisy breathing (unless obstruction is absolute and
complete).
6. Cyanosis.
7. The natural heave of the chest and abdomen becomes
replaced by an indrawing of the upper chest and an
outpushing of the abdomen because of strong
diaphragmatic action.

Sites of obstruction:
a. At the lips.
b. By the tongue
c. Above the glottis
d. At the glottis: laryngeal spasm, relaxed vocal
cords and FB.
e. Bronchospasm
f. Faults of apparatus: Kink or obstruction of
ETT
 Upper airway obstruction in PACU

A. Causes: include incomplete anesthetic recovery, laryngospasm,

airway edema, wound hematoma, and vocal cord paralysis. Airway
obstruction in unconscious patients is most commonly due to the
tongue falling back against the posterior pharynx.

B. Treatment: supplemental oxygen while corrective measures are

undertaken. Jaw thrust, head-tilt, oral or nasal airways.

Laryngospasm and laryngeal edema

A. Definition: Laryngospasm is a forceful involuntary spasm of the

laryngeal musculature caused by sensory stimulation of the superior
laryngeal nerve. Triggering stimuli include pharyngeal secretions
extubating in stage 2. The large negative intrathoracic pressures
generated by the struggling patient in laryngospasm can cause
pulmonary edema.

B.Treatment of laryngospasm: initial treatment includes 100%

oxygen, anterior mandibular displacement, and gentle CPAP (may
be applied by face mask). If laryngospasm persists and hypoxia
develops, succinylcholine (0.25-1.0 mg/kg; 10-20 mg).

C.Treatment of glottic edema and subglottic edema: administer

humidified oxygen by mask, inhalation of racemic epinephrine,
repeated every 20 minutes, hydrocortisone IV may be considered.
Reintubation with a smaller tube may be helpful.

III- Hypoxemia:
PaO2 less 60 mmHg or SaO2 less 90%

Causes:
1. Decreased FiO2
2. Hypoventilation
3. V/Q mismatch
4. Increased O2 utilization by tissues
5. Tissue hypoxia

Clinical signs of hypoxia (sweating, tachycardia, cardiac arrhythmias,

hypertension, and hypotension) are nonspecific; bradycardia,
hypotension, and cardiac arrest are late signs.
  Increased intrapulmonary shunting relative to closing capacity
is the most common cause of hypoxemia following general
anesthesia.

Treatment: oxygen therapy with or without positive airway pressure.

Additionally, treatment of the cause.

IV) Hypercapnia

PaCO2 or ETCO2 > 40 mmHg.

Causes:
1- Increased FiCO2
2- Hypoventilation
3- Increased dead space
4- Increased CO2 production by tissues
Treatment: of the cause.

V) Hypoventilation

A. Causes:

1- Respiratory obstruction
2- Factors affecting the ventilatory drive
a. Respiratory depressant drugs
b. Hypothermia
c. CV stroke
3- Peripheral factors
a. Muscle weakness
b. Pain
c. Decreased diaphragmatic movement.
d. Pneumo or hemothorax.
e. Decreased chest wall compliance e.g. kyphoscoliosis.

B. Hypoventilation in the PACU is most commonly caused by residual

depressant effects of anesthetic agents on respiratory drive or
persistent neuromuscular blockade.

C. Treatment: should be directed at the underlying cause. Marked

hypoventilation may require controlled ventilation until contributory
factors are identified and corrected.
VI- Pulmonary aspiration

Aspiration is defined as the inhalation of material into the airway

below the level of the true vocal cords. The material may include
foreign bodies, saliva, nasopharyngeal secretions or gastric contents.
Pulmonary aspiration occurs as the protective airway reflexes are
lost, such decreased consciousness and impaired cough or gag
reflexes. In the surgical patient it is most likely to occur at induction or
during emergence from anaesthesia. Incidence and severity increase
in emergency cases, especially patients with delayed gastric
emptying such as CS, intestinal obstruction.

Pathophysiology
 The clinical consequences of pulmonary aspiration are variable.
 The primary determinants are the nature of the material
aspirated and the host’s response to it.
- Aspiration of material with a pH less than 2.5 causes extensive lung
damage. An inflammatory cascade is triggered in the lungs, mediated
in particular by the activation of neutrophils. Alveolar epithelial and
endothelial damage, and surfactant dysfunction, result in pulmonary
atelectasis. Fluid and protein leak into the alveoli and bronchi, leading
to pulmonary edema. The result is ventilation–perfusion mismatch
and consequent hypoxia.
- Aspiration of solid particles may result in upper airway obstruction or
localized atelectasis.
 In severe cases of aspiration the resulting acute lung injury is
global. However, damage may be localized. In supine patients,
aspirated material settles in the posterior segment of upper
lobes and superior segment of lower lobes particularly in the
right lung.

Manifestations:

They vary depending on the degree of aspiration. The patient may

become hypoxic, tachycardic and tachypnoeic. Bronchospasm often
occurs and auscultation of the chest may reveal wheeze and
crepitations. Aspiration at induction or emergence from anesthesia
may be obvious with gastric contents at the oropharynx and in the
trachea at laryngoscopy. However, it may occur silently, particularly if
an airway device other than a cuffed orotracheal tube is used during
anesthesia.
Airway pressures increase in patients receiving volume-controlled
ventilation and tidal volumes decrease in those who are ventilated
using pressure-controlled ventilation.

Management
The risks of aspiration in patients undergoing general anaesthesia
should be reduced. Patients at high risk must be identified.

Initial management:
- Administer 100% oxygen and reduce the risk of further aspirate
contaminating the airway.
- If the patient is conscious and breathing, the oropharynx must be
suctioned and the patient placed in the recovery position.
- If the patient is unconscious and breathing, then cricoid pressure
should be applied, the oropharynx suctioned and the patient placed in
a left lateral head-down position. Cricoid pressure should not be
applied if the patient is vomiting because the high intra-oesophageal
pressures generated may result in rupture.
- If the patient is apneic, intubation should proceed immediately. The
airway should be suctioned via the tracheal tube before positive-
pressure ventilation begins, to avoid contaminating the distal airways
further. However, if the patient is severely hypoxic, ventilation should
not be delayed. Once the airway is secure, suction any remaining
gastric contents via a large bore nasogastric tube. Surgery should be
abandoned or postponed if possible. Most patients will be extubated
and managed with supplementary oxygen. However, in general, if the
patient remains hypoxic with oxygen saturations below 90% on 100%
oxygen then they should remain intubated and be transferred to the
ICU.

Further management: intensive care management of patients with

aspiration pneumonia is supportive. Investigations include chest
radiographs, blood gas monitoring and sputum culture. Lung
protective strategies should be used to limit further lung injury caused
by mechanical ventilation. Using low tidal volumes of 4-6 ml/kg with
increased ventilation frequency to maintain minute volume reduces
pulmonary injury. In severe cases, oxygenation may be improved by
using positive end-expiratory pressures of up to 10 cmH2O.
Bronchodilators such as salbutamol and ipratropium bromide can be
given to relieve bronchospasm.
Specific therapy includes the use of fibreoptic bronchoscopy to
identify and remove particulate matter. The use of steroids has not
been shown to improve survival. Bronchial culture must be used to
guide the use of antibiotic therapy. Acid aspiration is usually sterile
and causes a pneumonitis rather than an infective pneumonia, such
that antibiotic therapy is not required. Long-term sequelae of
pulmonary aspiration include the development of lung abscesses and
empyema, which are best identified using chest CT.

B) Hemodynamic Complications

I. Hypotension

A.Causes: hypoxemia, hypovolemia, decreased myocardial

contractility (myocardial ischemia, pulmonary edema), decreased
systemic vascular resistance, cardiac dysrhythmias, pulmonary
embolus, pneumothorax, cardiac tamponade.

B.Treatment: fluid challenge; pharmacologic treatment includes

inotropic agents (dopamine, dobutamine, epinephrine) and alpha
receptor agonists (phenylephrine). CVP and PA catheter monitoring
may be needed to guide therapy.

II. Hypertension

A. Causes: enhanced SNS activity (pain, bladder distension),

preoperative hypertension, hypervolemia, hypoxemia, increased
intracranial pressure, and vasopressors.

B.Treatment: correction of the initiating cause; various medications

can be used to treat hypertension including beta blockers, calcium
channel blockers, nitroprusside or nitroglycerin.

III. Cardiac dysrhythmias

A. Causes: hypoxemia, hypercarbia, hypovolemia, pain, electrolyte
and acid-base imbalance, myocardial ischemia, increased ICP,
digitalis toxicity, hypothermia, anticholinesterases and malignant
hyperthermia.

B.Treatment: of the cause.

C) Neurologic Complications
I- Awareness:

Incidence: 0.2%
Increased in obstetric, cardiac anesthesia and hypovolemic patients.
Types of patient awareness during anesthesia:

1. Implicit memory:
- The information is retained in the memory, but not accompanied by
conscious recall of events.
- C/P: Postoperative psychic trauma e.g. insomnia, depression, sleep
disturbances, dreams, anxiety and fear of death.
- persist for months or years.

2. Explicit memory:
- The information is retained in the memory, but accompanied by
conscious recall of events (unpleasant sensations e.g. auditory and
visual perception, sensation of paralysis and pain).
- C/P: Intraoperative stress that causes sympathetic stimulation.
- Postoperative psychic trauma e.g. insomnia, depression, sleep
disturbances, dreams, anxiety and fear of death.
Causes:
a-Limited doses of anesthetic agents.
b- Machine malfunction
c- Increased dependence on muscle relaxants
Measures for prevention:
A. Preoperative:
- Preoperative visit
- Preoperative check of equipments and anesthetic machine
- Informed consent
B. Intraoperative:
- continuous monitoring of depth of anesthesia
 - Anesthetic techniques:
Amnestic agents, avoid muscle relaxants unless indicated,
minimum MAC 0.8, supplement opioid-based anesthesia with
potent inhalational or IV agents.
C. Postoperative:
- visit the patient.
- Apology
- Psychotherapy.

II- Delayed recovery:

Causes:
(1) Metabolic and electrolyte causes:
Hypoglycemia, hyperglycemia, hypokalemia, hyponatremia,
hypoxia, hypercapnia, hypocapnia, renal and hepatic failure.

(2) Cerebral hypoperfusion:

Risk factors are old age, atherosclerosis, ch. hypertension,
previous CNS lesions and cardiovascular and cranial surgery
caused by severe hypotension or hypertension, cerebral embolism
and Hge.

(3) Cerebral depression by drugs:

Risk factors: Hypothermia, old age, renal and liver diseases,
hypothyroidism, hypoalbuminemia, cimetidine and B-blockers.

Management: detect and treat the cause.

III- Perioperative Neuropathy:

Causes
1. Stretch (traction)
2. Compression
4. Metabolic causes
5. Direct surgical trauma
Risk Factors:
1. Old age.
2. High body mass index ≥38.
3. Prolonged surgery.
4. Preexisting chronic nerve dysfunction.
5. Some anatomic variations.
6. Vascular disease.
7. Hypotension.
8. DM.
9. Prolonged postoperative bed rest.
Complications of positioning

Complication Position Prevention

Air embolism Sitting, prone, reverse Maintain venous pressure above
Trendelenburg 0 at the wound.

Backache Any Lumbar support, padding, and

slight hip flexion.

Compartment Especially lithotomy Maintain perfusion pressure and

syndrome avoid external compression.

Corneal abrasion Especially prone Taping and/or lubricating eye.

Nerve palsies

Brachial plexus Any Avoid stretching or direct

compression at neck or axilla.

Common Lithotomy, lateral Pad lateral aspect of upper

peroneal decubitus fibula.

Radial Any Avoid compression of lateral

humerus.

Ulnar Any Padding at elbow, forearm

supination.

Retinal ischemia Prone, sitting Avoid pressure on globe.

Skin necrosis Any Padding over bony

prominences.

D) Postoperative Nausea and Vomiting

Risk factors

A. Patient risk factors: short fasting status, anxiety, young age,

female, obesity, gastroparesis, pain, history of postoperative
nausea/vomiting or motion sickness.

B. Surgery-related factors: gynecological, abdominal, ENT,

ophthalmic, and plastic surgery; endocrine effects of surgery;
duration of surgery.

C. Anesthesia-related factors: premedicants (morphine and other

opioids), anesthetics agents (nitrous oxide, inhalational agents,
etomidate, methohexital, ketamine), anticholinesterase reversal
agents, gastric distention, longer duration of anesthesia, mask
ventilation, intraoperative pain medications, regional anesthesia.

D. Postoperative factors: pain, dizziness, movement after surgery,

premature oral intake, opioid administration.

Treatment of Postoperative Nausea and Vomiting (PONV)

Droperidol, Metoclopramide, Ondansetron, Dolasetron, Granisetron
Propofol 10-20 mg IV, Dexamethasone, Promethazine. Combination
therapy is the most effective.

E) Allergic Drug Reactions

1. Anaphylaxis
A. Anaphylaxis is an allergic reaction which is mediated by an
antigen-antibody reaction (type I hypersensitivity reaction). This
reaction is initiated by antigen binding to immunoglobulin E (IgE)
antibodies on the surface of mast cells and basophils, causing the
release of chemical mediators, including, leukotrienes, histamine,
prostaglandins, kinins, and platelet-activating factor.

B. Clinical manifestations of anaphylaxis

11. Cardiovascular: hypotension, tachycardia, dysrhythmias.
22. Pulmonary: bronchospasm, cough, dyspnea, pulmonary edema,
laryngeal edema, hypoxemia.
33. Dermatologic: urticaria, facial edema, pruritus.

2. Anaphylactoid reactions
1A. Anaphylactoid reactions resemble anaphylaxis but are not
mediated by IgE and do not require prior sensitization to an antigen.

B. Although the mechanisms differ, anaphylactic and anaphylactoid

reactions can be clinically indistinguishable and equally life-
threatening.
3. Treatment of anaphylactic and anaphylactoid reactions
1A. Initial therapy
21. Discontinue drug administration and all anesthetic agents.
32. Administer 100% oxygen.
43. Intravenous fluids (1-5 liters of LR).
54. Epinephrine (10-100 mcg IV bolus for hypotension; 0.1-0.5 mg IV
for cardiovascular collapse).

B. Secondary treatment
11. Antihistaminic medications IV.
22. Epinephrine 2-4 mcg/min, norepinephrine 2-4 mcg/min.
33. Aminophylline 5-6 mg/kg IV over 20 minutes.
44. 1-2 grams methylprednisolone or 0.25-1 gm hydrocortisone.
55. Sodium bicarbonate 0.5-1 mEq/kg.
66. Airway evaluation (prior to extubation).

7
Temperature changes

I) Hypothermia:
It is unintentional decrease of core body temperature to < 35 C during
anesthesia
Causes:
1- Drop in core temperature.
2- Central inhibition of thermoregulation.
By interfering with the hypothalamic function (decreased VC and
shivering threshold and increased sweating threshold) so, the body
cannot compensate for hypothermia.
Contributing factors:
- Extremes of age, prolonged surgery, cold infusion or irrigation
fluids, muscle relaxants.
- Heat loss by radiation, evaporation, convection and conduction.
Prevention:
1- increase ambient temp and humidity
2- warm solutions
3- enclose exposed viscera
4- humidify the inspired gases
5- warm mattress and blanket
6- use low flow anesthesia.

Shivering
- More common after hypothermia, inhalational anesthetics,
anticholinergic premedication, female in the luteal phase.
Mechanism:
May be due to alteration in the descending control of spinal
reflexes after GA.
Effects:
- increased O2 consumption
- increased CO2 production
- increased CO and minute ventilation
- increased myocardial ischemia.
Treatment:
- normothermia
- O2
- Pethidine 25 mg.

II) Malignant Hyperthermia

1. Definition: It is a fulminant skeletal muscle hypermetabolic

syndrome occurring in genetically susceptible patients after exposure
to an anesthetic triggering agent. Triggering anesthetics include
halothane, enflurane, isoflurane, desflurane, sevoflurane, and
succinylcholine.
2. Etiology: the gene for malignant hyperthermia is the genetic coding
site for the calcium release channel of skeletal muscle sarcoplasmic
reticulum. The syndrome is caused by a reduction in the reuptake of
calcium by the sarcoplasmic reticulum necessary for termination of
muscle contraction, resulting in a sustained muscle contraction.

3. Clinical findings
A. Signs of onset: tachycardia, tachypnea, hypercarbia (increased
end-tidal CO2 is the most sensitive clinical sign).

B. Early signs: tachycardia, tachypnea, unstable blood pressure,

arrhythmias, cyanosis, mottling, sweating, rapid temperature
increase, and cola-colored urine.

C. Late (6-24 hours) signs: pyrexia, skeletal muscle swelling, left

heart failure, renal failure, DIC, hepatic failure.

D. Muscle rigidity and masseter spasm in the presence of

neuromuscular blockade.

E. The presence of a large difference between mixed venous and

arterial carbon dioxide tensions confirms the diagnosis of malignant
hyperthermia.

F. Laboratory: respiratory and metabolic acidosis, hypoxemia,

increased serum levels of potassium, calcium, myoglobin, CPK, and
myoglobinuria.

4. Incidence and mortality

A. Children: approx 1:15,000 general anesthetics.
B. Adults: approx 1:40,000 general anesthetics when succinylcholine
is used; approx 1:220,000 general anesthetics when agents other
than succinylcholine are used.
C. Familial autosomal dominant transmission.
D. Mortality: 10% overall; up to 70% without dantrolene therapy. Early
therapy reduces mortality for less than 5%.

5. Anesthesia for malignant hyperthermia susceptible patients

A. Malignant hyperthermia may be triggered in susceptible patients
who have had previous uneventful responses to triggering agents.
B. Pretreatment with dantrolene is not recommended. If deemed
necessary, may give 2.5 mg/kg IV over 10-30 minutes prior to
induction.
C. The anesthesia machine should be prepared by flushing the circuit
with ten liters per minute of oxygen for 20 minutes. Changing the
fresh gas hose will hasten the reduction of the concentration of
inhalation agents. Fresh carbon dioxide absorbent and fresh delivery
tubing are also recommended.

6. Malignant hyperthermia treatment protocol

A. Stop triggering anesthetic agent immediately, conclude surgery as
soon as possible. Continue with safe agents if surgery cannot be
stopped.
B. Hyperventilate: 100% oxygen, high flows, use new circuit and soda
lime.
C. Administer dantrolene 2.5 mg/kg IV; repeat every 5-10 minutes
until symptoms are controlled or a total dose of up to 10 mg/kg is
given.

D. Correct metabolic acidosis: administer sodium bicarbonate,

1-2 mEq/kg IV guided by arterial pH and paCO2. Follow with ABG.

E. Hyperkalemia: correct with bicarbonate or with glucose, 25-50 gm

IV, and regular insulin, 10-20 u.

F. Actively cool patient

1. Iced IV NS (not LR) 15 mL/kg every 10 minutes times three if
needed.
2. Lavage stomach, bladder, rectum, peritoneal and thoracic
cavities.
3. Surface cooling with ice and hypothermia blanket.

G. Maintain urine output >1-2 mL/kg/hr. If needed, mannitol 0.25 g/kg

IV or furosemide 1 mg/kg IV (up to 4 times) and/or hydration.
H. Labs: PT, PTT, platelets, urine myoglobin, ABG, K, Ca, lactate,
CPK.

I. Consider invasive monitoring: arterial blood pressure and CVP.

J. Postoperatively: continue dantrolene 1 mg/kg IV q6 hours x 72 hrs
to prevent recurrence. Observe in ICU until stable for 24-48 hrs.

 Calcium channel blockers should not be given when dantrolene

is administered because hyperkalemia and myocardial
depression may occur.

G) MISCELLANEOUS

Renal dysfunction: Oliguria (urine output less then 0.5 mL/kg/hour)

most likely reflects decreased renal blood flow due to hypovolemia or
decreased cardiac output.