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

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 (maybe applied by face
mask). If laryngospasm persists and hypoxiadevelops, 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 residualdepressant
effects of anesthetic agents on respiratory drive orpersistent neuromuscular
blockade.
C.Treatment: should be directed at the underlying cause. Markedhypoventilation may
require controlled ventilation until contributoryfactors are identified and corrected.

VI- Pulmonary aspiration

Aspiration is defined as the inhalation of material into the airwaybelow the level of the
true vocal cords. The material may includeforeign bodies, saliva, nasopharyngeal
secretions or gastric contents.Pulmonary aspiration occurs as the protective airway
reflexes arelost, such decreased consciousness and impaired cough or gagreflexes.
In the surgical patient it is most likely to occur at induction orduring emergence from
anaesthesia. Incidence and severity increasein emergency cases, especially patients
with delayed gastricemptying 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 lungdamage. An
inflammatory cascade is triggered in the lungs, mediatedin particular by the activation
of neutrophils. Alveolar epithelial andendothelial damage, and surfactant dysfunction,
result in pulmonaryatelectasis. Fluid and protein leak into the alveoli and bronchi,
leadingto pulmonary edema. The result is ventilation–perfusion mismatchand
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 upperlobes and superior segment of lower lobes
particularly in theright lung.
Manifestations:
They vary depending on the degree of aspiration. The patient maybecome hypoxic,
tachycardic and tachypnoeic. Bronchospasm oftenoccurs and auscultation of the
chest may reveal wheeze andcrepitations. Aspiration at induction or emergence from
anesthesiamay be obvious with gastric contents at the oropharynx and in thetrachea
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-controlledventilation and tidal
volumes decrease in those who are ventilatedusing 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 pressureshould be applied,
the oropharynx suctioned and the patient placed ina left lateral head-down position.
Cricoid pressure should not beapplied if the patient is vomiting because the high
intra-oesophagealpressures generated may result in rupture.
- If the patient is apneic, intubation should proceed immediately. Theairway should be
suctioned via the tracheal tube before positive-pressure ventilation begins, to avoid
contaminating the distal airwaysfurther. However, if the patient is severely hypoxic,
ventilation shouldnot be delayed. Once the airway is secure, suction any
remaininggastric contents via a large bore nasogastric tube. Surgery should
beabandoned or postponed if possible. Most patients will be extubatedand managed
with supplementary oxygen. However, in general, if thepatient 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 chestradiographs, blood
gas monitoring and sputum culture. Lungprotective strategies should be used to limit
further lung injury causedby mechanical ventilation. Using low tidal volumes of 4-6
ml/kg withincreased ventilation frequency to maintain minute volume
reducespulmonary injury. In severe cases, oxygenation may be improved byusing
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 toidentify and remove
particulate matter. The use of steroids has notbeen shown to improve survival.
Bronchial culture must be used toguide the use of antibiotic therapy. Acid aspiration
is usually sterileand causes a pneumonitis rather than an infective pneumonia,
suchthat antibiotic therapy is not required. Long-term sequelae ofpulmonary
aspiration include the development of lung abscesses andempyema, which are best
identified using chest CT.
B) Hemodynamic Complications
I. Hypotension
A.Causes: hypoxemia, hypovolemia, decreased myocardial
contractility (myocardial ischemia, pulmonary edema), decreasedsystemic vascular
resistance, cardiac dysrhythmias, pulmonaryembolus, pneumothorax, cardiac
tamponade.
B.Treatment: fluid challenge; pharmacologic treatment includes
inotropic agents (dopamine, dobutamine, epinephrine) and alphareceptor agonists
(phenylephrine). CVP and PA catheter monitoringmay 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-Awa reness:
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

.Preexisting chronic nerve dysfunction .4

.Some anatomic variations .5
.Vascular disease .6
.Hypotension .7
.DM .8
.Prolonged postoperative bed rest .9
Picturie

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, GranisetronPropofol 10-20
mg IV, Dexamethasone, Promethazine. Combinationtherapy 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).

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 temperatureincrease, 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 andarterial carbon
dioxide tensions confirms the diagnosis of malignanthyperthermia.
F. Laboratory: respiratory and metabolic acidosis, hypoxemia,increased serum levels
of potassium, calcium, myoglobin, CPK, andmyoglobinuria.
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

Faaaaade

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.