CHAPTER 38 Complications in Anesthesia





Introduction


No domain in life is without risks, and compli­cations do occur during patient care and treatment. In this regard, anesthesia is no more an exception. The complications can range from mild anaphylactoid reaction to death in the worst scenario. This chapter is an overview of complications that may arise during anesthetic care, and one should be aware of them. These are listed below:




  • Mortality.



  • Respiratory complications:




    • Pulmonary aspiration.



    • Pulmonary embolism.



    • Hypoxia.



    • Hypocapnia.



    • Hypercapnia.



    • Oxygen toxicity.



  • Cardiovascular complications:




    • Hypotension.



    • Hypertension.



    • Myocardial ischemia.



    • Dysrhythmias.



    • Cardiac arrest.



  • Neurological complications:




    • Postoperative cognitive dysfunction (POCD).



    • Convulsion.



    • Delayed recovery.



    • Cranial nerve palsies.



    • Awareness.



    • Extrapyramidal side effects.



    • Agitation, delirium, and emergence excitation.



    • Peripheral neuropathies.



  • Gastrointestinal complications:




    • Postoperative nausea and vomiting (PONV).



  • Renal complications.



  • Hepatic complications:




    • Postoperative jaundice.



    • Postoperative hepatitis.



    • Postoperative cholestasis.



  • Positioning in anesthesia and their complication.



  • Ocular complications.



  • Temperature-related complications:




    • Hypothermia and shivering.



    • Hyperthermia.



    • Malignant hyperthermia (MH).



Mortality


Evidence suggests that perioperative mortality due to anesthesia is between 1 in 13,000 and 1 in 15,000 cases, but the incidence of mortality exclusive due to anesthesia is rare. Certain patient and procedure-related factors add to increased mortality:




  • Extremes of age (neonates, children less than 1 year, and elderly patients).



  • Males.



  • American Society of Anesthesiologists (ASA) III physical status or more.



  • Emergency surgeries during general anesthesia.



  • Cardiac surgery (followed by thoracic, vascular, abdominal, pediatric, and ortho­pedic surgeries).


The main causes of anesthesia-related mortality were airway management and cardiovascular events related to anesthesia and drug administration.



Respiratory Complications of Anesthesia



Pulmonary Aspiration


Aspiration is defined as the inhalation of oro­pharyngeal or gastric contents into the larynx and lower respiratory tract.


Mendelson’s syndrome is defined as a chemical injury of the lung due to the entry of acidic gastric content.


Aspiration pneumonia is defined as the infec­tious process caused by the entry of orophary­ngeal secretions or enteral content, colonized by pathogenic bacteria, into the lung.



Incidence



  • 1 to 5 per 10,000 cases under general anesthesia.



  • More frequent in emergency surgery than elective surgery.



  • Three times more common in pregnancy.



  • Extremes of age are at higher risk.



Protective Mechanism against Aspiration

The following structures help in preventing aspiration:




  • Upper esophageal sphincter (UES): It is formed by cricopharyngeous muscle, which is striated in nature. A conscious individual has a tone of around 25 to 38 cm of H2O. Anesthetic agents except ketamine reduce the tone of the sphincter.



  • Lower esophageal sphincter (LES): It lies at the junction of the stomach and esophagus. The resting end-expiratory LES is approximately 8 to 20 cm of H2O higher (barrier pressure) than resting end-expiratory intragastric pressure. Since succinylcholine increases both the pressures, as a result, the barrier pressure is maintained.



  • Gastroesophageal (GE) junction: Diaphrag­matic fibers act as pinchcock, thus prevent­ing the regurgitation of content.



  • Protective laryngeal reflexes: Protective reflexes like coughing, laryngospasm, etc., play important roles.



Risk Factors for Aspiration

The risk factors for pulmonary aspiration are summarized below:




  • Increased gastric volume:




    • Recent meal.



    • Gastric insufflation.



    • Increased intra-abdominal pressure due to pregnancy or pneumoperitoneum.



    • Increased secretion of gastric acid.



  • Delayed gastric emptying:




    • High protein or lipid diet.



    • Gastric outlet obstruction.



    • Intestinal obstruction.



    • Drugs like opioids and anticholinergics.



    • Obesity.



    • Diabetic gastropathy.



    • Peptic ulcer disease.



    • Condition of sympathetic nervous system stimulation like active labor, acute pain, or stress.



  • Decreased LES tone:




    • Hiatus hernia.



    • Drugs like anticholinergics, opioids, and dopaminergic agonists.



    • Cricoid pressure.



    • Pregnancy.



  • Decreased UES tone:




    • Procedural sedation.



    • General anesthesia.



    • Muscle relaxant.



  • Loss of protective airway reflexes:




    • Advanced age.



    • Neurological diseases like multiple sclerosis, Guillain–Barre syndrome.



    • Neuromuscular disease like myasthenia gravis, myotonica dystrophica.



    • Altered consciousness due to sedative medication or coma.



Pathophysiological Manifestations

The aspiration of gastric content into the lungs can result in:




  • Blocking of upper airway.



  • Foreign body in the airway may lead to inflammation and granulomatous reaction.



  • Mucosal irritation.



  • Loss of surfactant may lead to alveolar collapse.



  • Noncardiogenic pulmonary edema.



  • Acute respiratory distress syndrome (ARDS).



Determinants of the Severity of Aspiration

The following factors affect the severity of aspiration:




  • pH less than 2.5.



  • The volume of aspirate: More than 0.4 mL/kg.



  • Physical nature: Particulate and feculent matter causes severe pneumonitis.



Prevention Measures for Aspiration

The preventive measures against pulmonary aspiration are summarized below:




  • Adherence to ASA preoperative fasting guidelines.




    • Adult:




      • 2 hours—water and clear fluids.



      • 6 hours—light meal.



      • 8 hours—heavy meal (fried/fatty food, meat).



    • Pediatric:




      • 2 hours—water and clear fluids.



      • 4 hours—breast milk.



      • 6 hour—infant formula, nonhuman milk, a light meal.



    • Diabetic:




      • 8 hours—semisolid food.



    • Pregnancy and labor:




      • Mothers are allowed to alleviate thirst during labor with sips of water or clear fluids.



      • Intravenous (IV) hydration is pre­ferred over oral intake in certain high-risk pregnancies with a difficult airway, difficult regional anesthesia, and high probability of cesarean section.



      • Solid or semisolid foods are avoided once the mother is in active labor or has received opioid analgesics.



  • Pharmacoprophylaxis:




    • Regulation of gastric acid secretion:




      • Neutralization of gastric acidity by nonparticulate antacids: 30 mL of 0.3 M Na citrate.



      • Decrease acidity and volume of secretions:




        • H2-receptor antagonist—cime­tidine, ranitidine, famotidine.



        • Proton pump inhibitors—panto­prazole, omeprazole, rabeprazole.



      • Increase gastric emptying: Meto­clopramide, erythromycin.



  • Preoperative gastric emptying:




    • Routine placement of the gastric tube is not recommended as it may impair the function of both LES and UES and does not guarantee an empty stomach.



  • Choosing the appropriate technique of anesthesia in full stomach patients:




    • Regional technique is preferred.



    • Rapid sequence induction (RSI) if regional techniques are not feasible.



    • Awake intubation is reserved for difficult airway patients.



Rapid Sequence Induction

It is done to protect the airway from aspiration of gastric content. It minimizes the interval between loss of consciousness and endotracheal intubation. The RSI includes:




  • Preoxygenation: Tidal volume breathing in 100% oxygen for 3 minutes or 4/8 vital capacity breaths in 30/60 seconds, respectively.



  • Predetermined dose of induction agents (thiopentone sodium).



  • Muscle relaxant: Scoline or rocuronium can be used.



  • Cricoid pressure.



  • Avoidance of positive pressure ventilation until the airway is secured with a cuffed endotracheal tube.



Modified Rapid Sequence Induction

Avoidance of positive pressure ventilation during conventional RSI precludes the ability of the clinician to check the airway and determine whether ventilation by the mask is possible. The failure to secure the airway during RSI may result in hypoxia, hypercarbia, and even death. Therefore, conventional RSI is modified. It consists of the following components:




  • Preoxygenation.



  • Induction of anesthesia.



  • Application of cricoid pressure.



  • Gentle positive pressure ventilation with pressure less than 20 cm of H2O.



  • Muscle relaxant.



  • Securing of the airway with a cuffed endotracheal tube.



Sellick’s Maneuver

Its main objective is to prevent aspiration by compressing the esophagus between the cricoid cartilage and body of C6 vertebra. The current recommendations regarding the amount of pressure are as follows:




  • Adults: 1 to 20 N at the beginning of induction, which is gradually increased to 30 N as the patient loses consciousness.



  • Pediatrics:




    • <1 year: 8 N



    • 1 to 4 years: 9 N



    • 4 to 8 years: 10 N



    • >10 years: 15 N



Adequacy of Pressure

The adequacy of Sellick’s maneuver can be checked by the following:




  • There will be blanching of more than half of the nail bed.



  • Equivalent pressure will induce pain when applied to the bridge of the nose.



Limitations of Cricoid Pressure

The cricoid pressure is not without limitations, and the ones mentioned below are noteworthy:




  • In an awake patient, it may induce vomiting due to reflex relaxation of LES.



  • Coughing or retching may lead to rupture of the esophagus.



  • It may worsen laryngoscopy view.



  • Pressure > 40 N may distort airway anat­omy, obstruct the airway, impair intubation, or mask ventilation.



  • It may not occlude esophagus completely.



  • It hinders successful placement of laryngeal mask airway (LMA).



  • It may impede tracheal intubation through intubating LMA.



  • Cricoid fracture has also been reported.



Precaution at Extubation and Postoperative Period

The following measures at the time of extubation can reduce the chances of aspiration to a great extent:




  • Avoid extubation in the deeper plane of anesthesia in patients at risk of aspiration.



  • Patients should be extubated only when conscious and obeying commands.



  • Sim’s position for recovery when the patient is drowsy and regurgitating or has upper airway bleeding.



Pulmonary Embolism


Pulmonary embolism (PE) is defined as a blockage of the pulmonary artery or one of its branches by a thrombus that had originated in the venous system or right side of the heart.



Clinical Manifestations



  • Dyspnea is the most frequent symptom.



  • Tachypnea is the most frequent sign.



  • Chest pain is common and is usually sudden and pleuritic in origin and may mimic angina pectoris or myocardial infarction.



  • Anxiety.



  • Fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis, and syncope.



Management



  • Emergency medical management:




    • The immediate objective is to stabilize the cardiopulmonary system.



    • Oxygen is administered immediately to relieve hypoxemia, respiratory distress, and central cyanosis.



    • Vasopressors, inotropic agents, and anti­dysrhythmic agents may be indicated to support circulation.



    • Perfusion scan, hemodynamic monit­oring, and serial arterial blood gas (ABG) analysis is needed to monitor the response to treatment.



    • The patient may need intubation and mechanical ventilation, depending upon the clinical picture and ABG result.



    • Small doses of IV morphine or sedative may be administered to relieve patient anxiety.



    • Elastic compression stocking or inter­mittent pneumatic leg compression devices may be used to reduce venous stasis.



  • Pharmacologic and surgical therapy:




    • Anticoagulation therapy: Heparin and warfarin have traditionally been the primary method for managing acute deep venous thrombosis (DVT) and PE.



    • Thrombolytic therapy (urokinase, stre­ptokinase, alteplase, and reteplase): Thrombolytic therapy resolves the thrombi or emboli and restores the pulmonary circulation’s normal hemo­dynamic functioning, thereby reducing pulmonary hypertension and improving perfusion, oxygenation, and cardiac output.



    • Surgical management: A surgical “embolectomy” is rarely performed but may be indicated if the patient has a massive PE or hemodynamic instability or if there are contraindications to thrombolytic therapy.



Prevention

For patients at risk of PE, the most effective approach for prevention is to prevent DVT by way of the following:




  • Active leg exercises to avoid venous stasis.



  • Early ambulation.



  • Promoting the use of elastic compression stocking and sequential compression devices.



Hypoxia


Hypoxia is defined as the failure of oxygenation at the tissue level, while hypoxemia is defined as a condition where the arterial oxygen tension is below normal (normal PaO2 = 80–100 mm Hg). The hypoxemia can be of the following types:




  • Hypoxemic hypoxia: Insufficient oxygen is reaching the blood.



  • Stagnant or circulatory hypoxia: Decreased blood flow to the tissues, leading to reduced oxygen delivery to the tissue.



  • Anemic hypoxia: Due to the decreased oxygen-carrying capacity of the blood.



  • Histologic hypoxia: Due to impaired util­ization of oxygen by the tissues.


The hypoxemia can occur due to the causes listed in Table 38.1.




Table 38.1 Causes of hypoxemia




























Table 38.1 Causes of hypoxemia

Hypoventilation

A spontaneously breathing anesthetized patient may hypoventilate due to drug-induced respiratory depression, while in patient who is paralyzed and ventilated, hypoventilation may occur due to inadequate mechanical ventilation


Reduced functional residual capacity

Induction of general anesthesia causes a reduction in functional residual capacity by 15–20%, which is more pronounced in patients with preexisting lung disease and obesity


Atelectasis

It is a condition of alveolar collapse which may manifest as micro atelectasis, macro atelectasis, or lobar collapse. It leads to V/Q mismatch, right to left shunting of blood, and arterial hypoxemia


Diffusion defect

Even though the adequate oxygen is supplied to the alveoli, the defect at alveolar level may prevent its absorption into blood. This is due to:




  • Thickened alveolar membrane



  • Thickening of air–blood interface



  • Inflammation



  • Edema



  • Fibrosis or loss of alveolar surface area (sarcoidosis, emphysema)


Inhibition of HPV

It is a protective phenomenon to prevent hypoxemia. When PaO2 decreases in a region of the lung, pulmonary vasoconstriction occurs in that particular region. It diverts the blood flow from the lung’s hypoxic regions to better-ventilated regions, thus decreasing V/Q mismatch and preventing hypoxemia. Inhibition of HPV leads to the development of arterial hypoxemia


Poor oxygen delivery to tissues

It can occur due to:




  • Systemic hypoperfusion



  • Embolus



  • Sepsis



  • Local problems like a cold limb, Raynaud phenomenon, sickle cell disease, etc


Increased oxygen demand

It can occur in case of:




  • Fever



  • Malignant hyperpyrexia



  • Shivering



  • Sepsis


Abbreviation: HPV, hypoxic pulmonary vasoconstriction.



Treatment



  • Treatment of the underlying cause.



  • Ventilation with 100% oxygen.



Hypocapnia


Hypocapnia occurs when the level of carbon dioxide (CO2) in the blood is less than 35 mm of Hg. Causes of hypocapnia are as follows:




  • Increased elimination of CO2:




    • Increased minute ventilation in patients on controlled ventilation.



    • Increased minute ventilation in spon­taneously ventilating patients in response to the following:




      • Pregnancy.



      • Pain.



      • Metabolic acidosis.



      • Central nervous system (CNS) pathology like infection and tumor.



  • Decreased dead space ventilation.



  • Reduced pulmonary perfusion:




    • Hypovolemia.



    • Hypotension.



    • Cardiac arrest.



    • PE.



  • Reduced CO2 production:




    • Hypothermia.



    • Hypothyroidism.



    • Low metabolism.



Management



  • Evaluate the oxygen status.



  • Confirm hypocapnia by ABG.



  • Decrease minute ventilation if hypocapnia is due to iatrogenic hyperventilation.



  • Assess and maintain circulation.



Hypercapnia


Hypercapnia occurs when the level of CO2 in the blood is more than 45 mm Hg. Causes of hypercapnia are as follows:




  • Hypoventilation:




    • Reduced minute ventilation in patients on controlled ventilation.



    • Decreased minute ventilation in spont­aneously ventilating patients due to drug-induced depression of the venti­latory response to CO2. Common agents are opioids, benzodiazepines, sedative-hypnotics (propofol), and halogenated inhalational agents.



  • Increased dead space ventilation.



  • Rebreathing:




    • Faulty breathing circuits.



    • Inadequate fresh gas flow.



    • Exhausted absorbent agents.



    • Faulty expiratory check valves.



  • Increased CO2 production:




    • Fever.



    • Sepsis.



    • Systemic absorption during laparoscopic procedures.



    • Thyroid storm.



    • MH.



Management



  • Confirm hypercapnia by ABG.



  • Treat the cause.

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Dec 11, 2022 | Posted by in ANESTHESIA | Comments Off on CHAPTER 38 Complications in Anesthesia

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