Explore Ebooks
Categories
Explore Audiobooks
Categories
Explore Magazines
Categories
Explore Documents
Categories
By
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
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.
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
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
IV) Hypercapnia
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.
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:
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.
B) Hemodynamic Complications
I. Hypotension
II. Hypertension
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.
Causes:
(1) Metabolic and electrolyte causes:
Hypoglycemia, hyperglycemia, hypokalemia, hyponatremia,
hypoxia, hypercapnia, hypocapnia, renal and hepatic failure.
Nerve palsies
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.
2. Anaphylactoid reactions
1A. Anaphylactoid reactions resemble anaphylaxis but are not
mediated by IgE and do not require prior sensitization to an antigen.
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.
3. Clinical findings
A. Signs of onset: tachycardia, tachypnea, hypercarbia (increased
end-tidal CO2 is the most sensitive clinical sign).
G) MISCELLANEOUS