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:

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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 positivepressure 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 Air embolism Backache Compartment syndrome Position Sitting, prone, reverse Trendelenburg Any Especially lithotomy Prevention Maintain venous pressure above 0 at the wound. Lumbar support, padding, and slight hip flexion. Maintain perfusion pressure and avoid external compression. Taping and/or lubricating eye.

Corneal abrasion Especially prone Nerve palsies Brachial plexus Any Common peroneal Radial Ulnar Retinal ischemia Skin necrosis Lithotomy, lateral decubitus Any Any Prone, sitting Any

Avoid stretching or direct compression at neck or axilla. Pad lateral aspect of upper fibula. Avoid compression of lateral humerus. Padding at elbow, forearm supination. Avoid pressure on globe. 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 lifethreatening. 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.

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