Critical Care Arun Kumar Paul
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Respiratory DisordersChapter 1

Adult Respiratory Distress Syndrome (ARDS)
Adult respiratory distress syndrome (ARDS) is a nonspecific pulmonary condition characterized by abnormal perm-eability of pulmonary capillary endothelium leading to progressive accumulation of fluid within the lung parenchyma and alveoli. Mortality is mostly due to multisystem organ failure and systemic hemodynamic instability over and above acute severe lung dysfunction. It is also known as shock lung syndrome, or noncardiogenic pulmonary edema.
The exact cause is not always certain, but the possible disorders predisposing to ARDS are as follows:
  1. Shock
  2. Sepsis
  3. Multiple injuries, lung trauma, and head injury
  4. Aspiration of gastric contents
  5. Near-drowning
  6. Smoke inhalation and burns
  7. Acute radiation pneumonitis
  8. Snake poisoning
  9. Fat embolism
  10. Disseminated intravascular coagulation (DIC)2
  11. Acute pancreatitis
  12. High altitude, oxygen toxicity, and hypoxia
  13. Severe viral or bacterial pneumonia
  14. Overdose of heroin, methadone, etc.
  1. Progressive accumulation of extravascular fluid within the lung parenchyma due to derangement of alveolar capillary permeability.
  2. Excessive accumulation of fluid in the alveoli of lung leads to decreased pulmonary compliance, increased dead space ventilation, and increased intrapulmonary shunt fraction.
  3. Hypoxemia is mostly due to:
    1. Hypoventilation
    2. Diffusion defect
    3. Mismatched ventilation—Perfusion
    4. Intrapulmonary shunt.
  4. Hypercapnia is due to:
    1. Impaired CO2 elimination due to decreased alveolar ventilation.
    2. Mismatched ventilation—Perfusion.
Clinical Features
  1. Progressive hypoxemia, tachypnea, dyspnea, cough, sputum production, and air hunger.
  2. Restlessness, confusion, somnolence, and coma.
  3. Tachycardia, cyanosis, hypotension, hemodynamic instability, shock, and cold extremities.
  4. Hypoxia, hypercarbia, decreased lung compliance, pneumonia, decreased breath sounds, wheezing, and rhonchi or gurgles.
  5. Respiratory failure.
  6. Multisystem organ failure.3
  1. Chest X-ray:
    1. Pneumonia and atelectasis.
    2. Increased pulmonary vascularity, interstitial infiltration, opacities, white out of lung fields, and loss of lung volume.
  2. Arterial blood gas analysis:
    1. Increased PaCO2.
    2. Decreased PaO2.
    3. Decreased pH.
    4. Alveolar arterial oxygen gradient (A–aO2) becomes more than 20 mmHg.
    5. Ratio PaO2/FiO2 less than 200 mmHg.
  3. Pulmonary function tests:
    1. Decreased total lung capacity.
    2. Reduced vital capacity and forced expiratory volume.
    3. Increased closing volume.
    4. Pulmonary wedge pressure — Low.
  4. Total blood count.
  5. Sputum culture.
  6. Histological changes:
    1. Massive interstitial edema.
    2. Hyaline membrane.
    3. Loss of surfactant.
    4. Atelectasis.
  1. Ventilatory dynamics should be improved. Mechanical ventilation and controlled oxygen therapy are most vital. Endotracheal intubation and mechanical ventilation with positive-end expiratory pressure are most effective to minimize and open up the airway 4and alveolar collapse, to decrease the intrapulmonary shunt and to improve overall V/Q abnormalities and to increase the functional residual capacity of the lung. It will alleviate hypoxemia. But peak end-expiratory pressure (PEEP) level needs adjustment to get the optimum benefit. PEEP may reduce the cardiac output and adequate measures and inotropic drugs may have to be used to prevent hypotension.
  2. Monitoring of vital signs, blood gas analysis and central venous pressure (CVP) monitoring are essential. Pulmonary artery and wedge pressure needs attention.
  3. Intravascular fluid volume should be maintained carefully. Crystalloid solutions may be used. Fluid overload should be avoided. Packed red cells or blood transfusion may be necessary.
  4. Diuretics: Frusemide.
  5. Dopamine to raise the blood pressure and to maintain adequate renal blood flow.
  6. Steroid therapy is controversial.
  7. Acid-base balance should be maintained according to blood gas analysis.
  8. Extracorporeal membrane oxygenation may have some value in such cases.
  9. Inhalation of nitric oxide 5–80 ppm may decrease pulmonary artery pressure and improve arterial oxygenation.
  10. Treatment of the underlying cause as in cases of sepsis where broad-spectrum antibiotics should be given according to culture and sensitivity test.
  11. Bronchodilators and mucolytic agents may often be helpful.
  12. Careful nursing care, care of the airway, tracheob-ronchial toilet, airway clearance, and adequate 5nutrition—Enteral or parenteral—All these are of vital importance for such critically ill patients.
  13. Prognosis largely depends on:
    1. Underlying precipitating factors.
    2. Degree of ventilatory dysfunction.
    3. Degree and severity of hypoxemia.
    4. Degree of capillary leakage.
    5. Response on drug therapy and mechanical ventilation.
    6. Early detection and intensive therapy and care are essential to reduce the incidences of mortality.
    7. Mortality is mostly due to the effect of hypoxia, infection, systemic hemodynamic instability, and multisystem organ failure.
Severe Asthma: Status Asthmaticus
Status asthmaticus is a serious medical emergency and may be life-threatening, refers to a severe asthmatic attack, often refractory to usual bronchodilator therapy. Bronchial asthma is a respiratory disease characterized by increased responsiveness of the airways to various stimuli, reversible expiratory airflow obstruction and chronic inflammatory changes in the submucosa of airways.
Essential Pathophysiology
  1. Release of some chemical mediators like histamine, immunoglobulin E, prostaglandins, etc.
  2. Some abnormalities of autonomic nervous system regulation of airway tone causing imbalance between excitatory and inhibitory airway tone.
  3. Widespread bronchoconstriction causing hypoxemia, airway narrowing, increased airway resistance, increased work of breathing, decreased vital capacity, 6increased functional residual capacity, hypove-ntilation, hypercarbia, and so on.
  4. Chronic airway inflammatory response resulting to emphysematous lung changes.
Predisposing Factors for Acute Attacks of Asthma
  1. Inhalation of irritant gases, vapours, dusts, smokes, foreign substances, and antigens.
  2. Ingested antigens.
  3. Upper respiratory tract infections—Viral and bacterial.
  4. Reflux of acid gastric fluid into the lower esophagus.
Clinical Features
  1. History of asthma.
  2. Difficulty in respiration, dyspnea, coughing, and wheezing.
  3. Tachypnea.
  4. Exhaustion, fear, and dizziness.
  5. In acute attack, nasal flaring, respiratory distress, flushed, moist, diaphoretic skin, cyanosis, restlessness, agitation, progressive fatigue, wheezing, expiratory stridor, and so on.
  1. Total blood count.
  2. Arterial blood gas analysis, hypoxemia, hypercarbia, and acidosis.
  3. Chest X-ray.
  4. Pulmonary function tests.
  5. Electrocardiogram.
Warning Signs
  1. Cyanosis.
  2. Tachycardia and pulsus paradoxus.7
  3. Level of consciousness—Confusion and drowsy.
  4. Breathlessness.
  5. Inability to expectorate.
  6. Sleeplessness.
  7. Arterial blood gas analysis, hypoxemia, and hypercarbia.
  8. Pulmonary function tests—Decreased. Forced expiratory volume in one second (FEV1) less than 35 percent predicted.
  1. Adequate ventilation and oxygenation:
    1. Humidified oxygen.
    2. Mechanical ventilation.
  2. Bronchodilator drugs:
    1. β2-agonists, albuterol by metered dose inhaler. Salbutamol by intravenous (IV) infusion.
    2. Theophylline 5 mg/kg IV followed by 0.5–1 mg/kg/hr.
  3. Anti-inflammatory drugs: Corticosteroids in high doses.
  4. Correction of abnormal gas exchange:
    1. Acidosis should be corrected with hyperventilation or medications.
    2. Bronchospasm should be relieved.
    3. Monitoring of arterial blood gas analysis.
  5. Care of the airway.
  6. IV fluid infusion to correct dehydration.
  7. Antibiotics to control bacterial infection.
  8. Anticholinergics: Ipratropium may have some value.
  9. Mucolytics: Acetylcysteine to liquefy and promote expectoration of mucus.
  10. Emergency treatment of status asthmaticus should include:
    1. Repetitive administration of a β2-agonist by inhalation or injection.
    2. Corticosteroids in high doses.8
    3. Intubation and intermittent positive-pressure ventilation (IPPV) in desperate cases.
    4. General anesthesia with volatile anesthetic may be tried to produce bronchodilation on rare occasions when even aggresive drug therapy fails.
Acute Exacerbations of Chronic Obstructive Pulmonary Disease
In chronic obstructive pulmonary disease there is limitation of airflow secondary to either airway disease (chronic bronchitis) or destruction of lung parenchyma (emphysema) or both. There may be sudden progressive hypoxemia and hypercapnia in such patients resulting in acute respiratory failure.
  1. Infection is the most common cause. In chronic bronchitis expiratory airflow is obstructed by mucous gland hypertrophy, mucous plugging and narrowing of the bronchial tree. In emphysema, dilatation of airspaces distal to terminal bronchioles and destruction of alveolar walls cause a loss of the elastic recoil of the lungs and reduce the expiratory airflow.
  2. Progressive hypoxemia and hypercapnia.
  3. Often related to smoking and urban pollution.
Clinical Features
  1. History of productive cough and sputum for years.
  2. Shortness of breath and fatigue.
  3. Headache, restlessness, confusion, somnolence, and coma.
  4. Dsypnea, tachypnea, and cough.
  5. Cyanosis, tachycardia, diaphoresis, and arrhythmia.
  6. Rhonchi, decreased breath sounds, and decreased lung expansion.9
  1. Chest X-ray: Flattened diaphragm, increased antero-posterior chest diameter, bullae, hyperlucency, and hyperinflation of lungs.
  2. Lung function tests:
    1. Vital capacity—Reduced.
    2. Total lung capacity—Increased.
    3. Ratio FEV1 and forced vital capacity (FVC)—diminished less than 75 percent.
    4. Maximum breathing capacity—Reduced.
    5. Maximal mid-expiratory flow rate—Reduced.
    6. Residual volume—Increased.
    7. Functional residual capacity—Increased.
  3. Arterial blood gas:
    1. Decreased PaCO2
    2. Increased PaCO2
    3. Decreased pH
  4. Total blood count
  5. Sputum culture.
Clinical Features Suggesting Respiratory Failure
  1. Exhaustion and fatigue
  2. Irritability, restlessness, drowsiness, and somnolence
  3. Coma
  4. Rapid shallow breathing
  5. Diaphoresis
  6. Cyanosis
  7. Inability to expectorate.
  1. Reversible factors of the disease such as infection, bronchospasm, and heart failure need adequate attention and management.10
    1. Infection: Antibiotics.
    2. Bronchospasm: Bronchodilator therapy and steroids.
    3. Heart failure: Diuretics.
  2. Sedatives, narcotics, and tranquilizers should be avoided as they suppress respiratory drive and cough.
  3. Chest physiotherapy and exercise training are the most important to clear tracheobronchial secretion and to preserve airway patency.
  4. Adequate oxygenation: The dangers of oxygen therapy in chronic respiratory failure should be borne in mind. The risk of respiratory depression is always there and sensible precautions should be taken. Humidification of inspired gases may help expectoration.
  5. Management of such respiratory cripple patients should aim to maximize the pulmonary function, to reduce the frequency of acute attacks and to treat complications of hypoxemia.
Management of Acute Exacerbations
  1. Adequate oxygenation, and IPPV
  2. Bronchodilator therapy
  3. Antibiotics
  4. Chest percussion and postural drainage
  5. Corticosteroids
  6. Mucolytic agents
  7. Tracheobronchial toilet and care
  8. Other supportive measures
  9. Adequate nutrition.
Pulmonary Embolism
Pulmonary embolism may be defined as the partial or complete obstruction of the pulmonary arterial circulation by some substances such as thrombus, fat, air, amniotic 11fluid, etc. migrated to the lung from elsewhere in the body. Massive pulmonary embolism often results in sudden cardiovascular collapse and death. It is mostly due to acute reduction of cardiac output, acute right ventricular failure and disturbance of pulmonary perfusion and ventilation.
Predisposing Factors
  1. Deep vein thrombosis
  2. Recent fracture and/or leg injury
  3. Prolonged immobilization
  4. Major abdominal or orthopedic surgery
  5. Varicose veins
  6. Pregnancy and patients with oral contraceptives
  7. Cardiac failure and atrial fibrillation
  8. Smoking, obesity, and polycythemia vera.
Main Types of Emboli
  1. Thromboembolus: It is mostly due to venous stasis of blood, hypercoagulability of blood and abnormalities or damage of vessel wall. Prolonged immobilization or bed rest may be a factor. Spontaneous dislodgement can occur.
  2. Fat embolus: It is mostly due to fracture of long bones, sternal slitting operation, trauma or injury to subcutaneous fat, etc. It may occur 12–24 hours after injury.
  3. Air embolus: Air usually enters the circulation through the venous system. A 100 ml of air may be fatal. Infusion of air or other gas under pressure into the vein in IV lines may cause air embolism. Other causes include pulmonary artery balloon rupture, tubal insufflation, hemodialysis, chest trauma, neck surgery, rapid decompression, and so on.12
  4. Miscellaneous: Amniotic fluid, sheared catheter tip, infected tissue or tissue fragment, etc. may cause embolism.
  5. Predisposing factors regarding venous thrombosis and pulmonary embolism: Prolonged bed rest, trauma, surgery, obesity, pregnancy, congestive cardiac failure, oral contraceptives, and general immobility.
  1. These emboli may travel through both the venous and arterial system. It is said that right lung is involved more than left and lower lobes more than the upper lobes. Small emboli less than 4 mm in diameter rarely become problematic, but larger emboli may cause serious problems.
  2. Pulmonary embolism increases pulmonary dead space and there is mismatched ventilation—Perfusion.
  3. Loss of surfactant also occurs and it causes alveolar collapse, atelectasis, shunting of blood, and hypoxemia.
  4. Pulmonary artery hypertension occurs mostly due to mechanical obstruction in pulmonary vascular bed. Right ventricular failure is common.
  5. Bronchoconstriction and bronchospasm can also occur.
  6. The dual blood supply of lungs (pulmonary and bronchial arterial systems) and good collateral circulation may be beneficial in such patients.
Clinical Manifestations
  1. Sudden onset of acute dyspnea, confusion, agitation, and loss of consciousness.
  2. Pleuritic chest pain.
  3. Hemoptysis.13
  4. Tachypnea, nonproductive cough, and hypoxemia.
  5. Tachycardia, profuse perspiration, cyanosis, hypotension, and atrial arrhythmias.
  6. Wheezing and moist sound over lung fields.
  7. Acute right ventricular failure. There may be elevation of jugular venous pressure and gallop rhythm at left sternal angle.
  8. Acute drop in cardiac output.
  9. Cardiopulmonary arrest.
  10. In amniotic fluid embolism squames may be found on microscopic examination of sputum.
  11. In air embolism in the right ventricle there may be churning sound on auscultation.
  12. In fat embolism, petechial rash may be seen on chest, shoulders, and axillae. DIC, thrombocytopenia, bleeding, fat globules in urine, sputum and retinal vessels, hypoxemia, confusion, coma, convulsion, fever, and ARDS.
  13. Features of minor pulmonary embolism include chest pain, pleural friction rub with signs of consolidation or crepitations, cough, and hemoptysis.
  1. Chest X-ray: Usually normal, pleural effusion, pulmonary edema, and atelectasis.
  2. Pulmonary angiogram: It gives definitive diagnosis. Hemodynamic studies can be performed while catheters are in situ.
  3. Electrocardiogram: Acute cor pulmonale and right heart strain.
  4. Arterial blood gas analysis: Decreased PaO2, increased PaCO2, and respiratory acidosis. Increased A/a gradient even with an FiO2 of 100%.
  5. Serum lipase: Increased in fat embolism.14
  6. Serum lactate dehydrogenase: Increased.
  7. Lung scan: Low uptake of 131I with normal chest X-ray is very suggestive of embolism.
  8. Total blood count.
  9. Coagulation studies.
  10. Hemodynamic monitoring: Sudden increase in pulmonary artery pressure.
  11. Examination of urine.
  12. Examination of sputum.
  1. Cardiopulmonary support
    1. IV central line
    2. Volume expanders to improve cardiac output
    3. Oxygen therapy
    4. Mechanical ventilation: IPPV
    5. External cardiac massage and IPPV in cases of sudden cardiac arrest
    6. Inotropic drugs: Isoprenaline and dopamine
    7. Reversal of metabolic acidosis: 8.4% sodium bicarbonate
    8. Heparin
    9. Diuretics
    10. Steroids.
  2. Definitive treatment
    1. Embolectomy: Pulmonary artery embolectomy is only indicated in cases of massive emboli. Cardiopulmonary bypass should be used.
    2. Anticoagulants: Heparin decreases clotting ability of blood and thus prevents thromboembolus.
    3. Systemic fibrinolytic therapy: Streptokinase or urokinase is used to hasten resolution of emboli. It is best effective when the clot is less than 3 days old. But it may cause uncontrolled bleeding and cardiac 15arrhythmias. The therapy needs laboratory control with thrombin clotting time. Streptokinase therapy is contraindicated in cases of internal bleeding and history of cerebrovascular accident, hemorrhagic diathesis and severe hypertension. Relative contraindications may include asthma, allergic patients, pregnancy, elderly patients, inflammatory bowel disease, etc.
  3. In cases with air embolus, the patient should be placed on left side in head down position, so air will float into the right atrium.
    • Aspiration of the air from right atrium can be done through a central line inserted into right atrium.
  4. Treatment of acute massive pulmonary embolism:
    1. External cardiac massage
    2. Oxygen therapy
    3. Heparin IV
    4. Treatment of acidosis
    5. Definitive measures:
      1. Anticoagulants
      2. Fibrinolytic therapy
      3. Surgical intervention.
  5. Prophylaxis:
    1. Anticoagulant therapy: Heparin may be indicated.
    2. Inferior vena cava interruption may be indicated in some cases to prevent further emboli. It is usually done with a transvenous umbrella filter or with surgically placed clip on the vessel. It is indicated in cases of recurrent emboli, septic emboli, critically ill patients, and when heparin therapy is not possible.
Pneumothorax is usually defined as the presence of air in the pleural space from an injury of chest wall or more 16commonly from an air leak of the lung. There may be either connection of the atmosphere to the pleural space or rupture of alveolus into the pleural cavity.
  1. Chest injury: Penetrating chest injury, fracture of ribs, and lung laceration.
  2. Spontaneous rupture of emphysematous bullae.
  3. IPPV with PEEP.
  4. Rupture of esophagus, damage to a bronchus or trachea.
  5. Regional block of nerves or surgery in close proximity to pleural cavity.
  6. Barotrauma.
  7. During laparoscopy (due to CO2 insufflation).
  8. Following diagnostic procedures like bronchoscopy, esophagoscopy, pleurocentesis, lung biopsy, liver biopsy, and following CVP line placement.
Types of Pneumothorax
  1. Simple pneumothorax: Minor leak of air causing mild degree of lung collapse. Leak usually seals and air is absorbed. No chest tube drainage is needed.
  2. Open pneumothorax: Leak has a free communication with the atmostphere either through a bronchopleural fistula or a wound in chest wall.
  3. Closed pneumothorax: Air accumulates in closed intrathoracic cavity and there is no communication with the atmosphere. A valve system at the leak can occur when the air can enter, but cannot escape leading to tension pneumothorax. This causes shifting of mediastinum and displacement of major vessels. Venous return to the heart decreases and cardiovascular collapse results. It can cause sudden death.17
Clinical Features
  1. History of chronic bronchitis, asthma, chronic obstructive airway disease, emphysema, lung cyst, and bronchopleural fistula.
  2. History of chest injury and fracture of ribs.
  3. Chest pain, agitation, apprehension, shortness of breath, cough, and shoulder pain.
  4. In severe cases nausea/vomiting, syncope, and shock.
  5. Closed pneumothorax:
    1. Dyspnea, tachypnea, and cyanosis.
    2. Diminished breath sounds over the affected site.
    3. Hypoxemia.
  6. Open pneumothorax: Added findings are:
    1. Open injury at affected site.
    2. Sucking sound on inspiration at affected site.
    3. Subcutaneous emphysema.
  7. Tension pneumothorax: Added findings are:
    1. Asymetric movement of chest.
    2. Deviation of trachea to unaffected side.
    3. Reduced venous return.
    4. Tachycardia, low blood pressure, and shock.
    5. Heart sounds muffled.
  1. Chest X-ray: It is most helpful to detect pneumothorax. In tension pneumothorax there are features of mediastinal shift, tracheal deviation and area of air without lung markings.
    • An apical pneumothorax may show a cap of air and it should be carefully observed. It should also be determined whether there is fluid indicating hemopneumothorax. Pre-existing lung disease can also be ascertained.18
  2. Hemodynamic monitoring: Cardiac output, pulmonary wedge pressure, and central venous pressure may need monitoring.
  3. Pulmonary function tests: Decreased lung function.
  4. CT scan of chest.
  1. Identification of patients at risk of pneumothorax.
  2. Nitrous oxide should be avoided in such cases.
  3. CVP lines should be placed carefully.
  4. Ventilation with high pressure should be avoided. Patients with long-term IPPV need regular chest X-ray to exclude pneumothorax.
  5. Regional block or surgery very close to pleural cavity needs extra caution.
  1. Closed pneumothorax:
    1. If pneumothorax is small and less than 20%, usually no treatment is needed.
    2. Re-expansion of the lung should be promoted.
      • Insertion of an intercostal catheter attached to an underwater seal. It is usually done under local anesthesia into the axillary area. Escape of the air should be slow, otherwise sudden changes in intrapleural pressure can cause acute pulmonary edema and rapid mediastinal shift may cause problems. Serial X-rays of chest will assess the re-expansion of the lungs. Frequent assessment of breath sounds is also needed.
    3. Chest drainage should be assessed.
    4. Serial arterial blood gas analysis and chest X-ray are always helpful.19
  2. Open pneumothorax:
    1. This is a more serious condition. In addition to the measures for simple closed pneumothorax, the wound needs careful attention. Sterile occlusive dressing over the wound is always helpful. But if a tension pneumothorax develops, the wound will be uncovered and insertion of chest tube is indicated. Tension pneumothorax can be diagnosed by tracheal deviation, jugular vein distension and acute respiratory distress.
  3. Tension pneumothorax:
    1. Early recognition is most important.
    2. In acute emergency situation, needle decompression using a 14–16 gauge needle at the second intercostal space, midclavicular line on affected side is most indicated.
    3. Insertion of chest tube with underwater drain must be done once the emergency is over.
  4. Other supportive measures:
    1. Adequate oxygenation: Airway clearance
    2. Prevention of infection: Antibiotics
    3. Pain relief: Analgesics
    4. Monitoring of vital signs.
  5. Definitive surgical intervention may be needed in cases of:
    1. Bilateral pneumothorax
    2. If pneumothorax remains open
    3. Recurrent pneumothorax.
  1. Hypoxemia
  2. Hypotension and shock
  3. Cardiac arrhythmias
  4. Venous or arterial gas embolism
  5. Cardiac arrest.20
Aspiration Pneumonitis
Aspiration pneumonitis is characterized by destruction of surfactant producing cells resulting atelectasis and damage to pulmonary capillary endothelium causing intravascular fluid leaks into the lungs due to the aspiration of gastric fluid into the lungs.
Predisposing Factors
  1. Common in children, elderly patients, obstetric pateints, patients with full stomach and vomiting prone type of patients.
  2. Patients with impaired laryngeal reflexes, altered level of consciousness, anesthesia of larynx and pharynx, muscle weakness or paralysis, acute intoxication of alcohol.
  3. Patients with incompetent gastroesophageal junction: Hiatus hernia, previous esophageal surgery.
  4. Passive regurgitation and active vomiting.
  1. It is mostly due to massive aspiration of gastric contents. Severity of lung damage depends on pH, volume, and distribution of the aspirated material into the lungs. Aspiration of food matters may also be a factor. Aspiration of hypertonic solutions, irritating food matters, infected materials, and foreign bodies may also be responsible.
  2. Initially reflex airways closure, alteration of surfactant, interstitial and alveolar edema, obstruction of smaller airways, intrapulmonary shunts, increased lung water, and loss of pulmonary compliance. All these lead to hypoxemia.21
  3. Highly acidic material causes loss of alveolar capillary permeability, severe inflammation, edema, hemorrhage and necrosis of airways and lung parenchyma. Excessive lung damage causes loss of intravascular volume, hypotension, and shock.
  4. Critical pH value of the aspirate is 2.5; above pH 2.5, the response is mostly similar to that of distilled water; pH below 1.5, pulmonary damage is maximum.
  5. Volume of the aspirate is also a factor. The critical volume of the aspirate is 25 ml. The volume more than 25 ml causes much damage.
  6. Infected aspirate material causes infection and lung abscess, empyema or necrotising bacterial pneumonia can occur.
Clinical Features
  1. It will depend on the character and type of aspirate, volume, pH, and distribution of the aspirate in lung parenchyma.
  2. Particulate aspirate may cause airway obstruction, severe hypoxemia, and even cardiorespiratory arrest.
  3. Small infected material may not show any symptoms initially; but, later on, there may be features of lung abscess and lobar pneumonia.
  4. Aspiration of gastric contents with a pH less than 2.5 and volume more than 25 ml cause chemical burns and aspiration pneumonitis. There may be bronchospasm, dyspnea, tachypnea, cyanosis, hypotension, wheezing, and crepitations. Arterial hypoxemia is the main feature.
  5. Due to obstruction and atelectasis, there is shunting of arteriolar blood with a widening of alveolar arterial oxygen gradient. Noncardiogenic pulmonary edema, adult respiratory distress syndrome will result. There 22are decreased pulmonary compliance, ventilation perfusion defect and significant intrapulmonary shunting.
  1. Chest X-ray: May remain normal for first 6–12 hours after aspiration. Later, patchy pneumonitis with irregular soft mottled densities in the peripheral lung fields. Atelectasis may also be there.
  2. Arterial blood gas analysis: Hypoxemia, hypercarbia, and acidosis.
  3. Total blood count.
Prophylactic Measures
  1. Aspiration pneumonitis is most common at the time of induction of anesthesia. So adequate preparation is essential. Preanesthetic fasting for 4–6 hours is needed. General anesthesia should be avoided in patients with full stomach.
  2. Laryngeal competence may be decreased for 4–8 hours following extubation. Thus, adequate care is needed during early postoperative period.
  3. Patients at risk should be identified and adequate precautions should be taken. Patients with gravid uterus, intra-abdominal injury, intestinal obstruction, etc. may have gastric emptying time much longer.
  4. Proper pharyngeal pack is needed following endotracheal intubation. Cuff must be efficient.
  5. Nasogastric suction at frequent intervals is often helpful.
  6. Some drugs like anticholinergic drugs, ganglion blocking drugs, opioids, thiopentone, tricyclic 23antidepressant drugs, etc. may reduce the lower esophageal sphincter pressure and increase the tendency to gastroesophageal reflux.
  7. Position of the patient is important. The patient should be placed in a position in which the tracheobronchial tree is at downward angle.
  8. Neutralization of gastric contents may be tried by some drugs:
    1. Magnesium trisilicate gel.
    2. Sodium citrate.
    3. H2 receptor blocking agents: Cimetidine, ranitidine, famotidine, etc.
    4. Metoclopramide is helpful in reducing gastric volume as it shortens the gastric emptying time. It also reduces the incidence and severity of vomiting.
  9. Vomiting-prone type of patients should also be identified. Antiemetic drugs like prochlorperazine, ondansetron, etc. may be given.
Massive aspiration of gastric contents should be detected early and managed immediately.
  1. Head down tilt.
  2. Tracheobronchial toilet. Lavage and suction may be needed to remove particulate material.
  3. Bronchoscopic suction.
  4. Adequate oxygenation: IPPV with 100% oxygen and PEEP.
  5. Ventilatory support: PEEP or continuous positive airway pressure may be helpful to maintain adequate oxygenation and normalize blood gas defects.
  6. Hydrocortisone instillation in tracheobronchial tree is often helpful.
  7. Bronchodilator drugs to relieve bronchospasm. Albuterol by metered dose inhaler may be effective.24
  8. Steroids IV may be beneficial.
  9. Broad-spectrum antibiotics.
  10. IV infusion of fluids: Overinfusion should be avoided.
  11. Diuretics should be used with sensible precautions.
  12. Monitoring of intrapulmonary shunt, wedge pressure and cardiac output is essential in critically ill patients. Pulmonary artery wedge pressure monitoring is often helpful.
  13. Monitoring of vital signs and blood gas analysis should be routine.
  14. Frequent lung assessment is also needed.
  1. Pneumonia
  2. Sepsis
  3. Adult respiratory distress syndrome.
Upper Airway Obstruction
Upper airway obstruction is a serious life-threatening condition that requires rapid evaluation of the patient and simultaneous therapy to provide adequate oxygenation and ventilation. Prompt recognition of the patient's condition is the most important for planning the patient care without wasting time.
Common Causes
Laryngospasm, foreign bodies, trauma, tumors, epiglottitis, Ludwig's angina, odontogenic abscess, peritonsillar abscess, tonsillar enlargement, laryngotracheitis, diphtheria, burns, inhalation injury, foreign body aspiration, hemorrhage into the neck, intraoral hemorrhage, damage to recurrent laryngeal nerves, collapsing trachea, etc.25
Clinical Features
Inability to phonate either partial or complete, rocking movement of the chest with inadequate air exchange, tracheal tug, flaring of nostrils, increased respiratory movements, cyanosis, inspiratory stridor.
Arterial blood gas analysis is helpful in diagnosing hypoventilation.
  1. Expiratory wheezing is common in small lower airway obstruction.
  2. Noisy auditory signs are commonly associated with partial airway obstruction.
Step by step guidelines for management of upper airway obstruction:
  1. Adequate airway should be either established or maintained. Head tilt and chin lift should be tried.
  2. Mask ventilation may be needed.
  3. Endotracheal intubation should be done only if necessary.
  4. If mask ventilation and intubation fail, transtracheal oxygenation is helpful. Transtracheal ventilation should not be done.
  5. Tracheostomy in extreme cases.
  6. Associated cardiovascular instability should be treated when ventilation is established.
  7. Lastly the exact cause of hypoventilation should be diagnosed and additional management is based on etiology.
  1. The expert help experienced in difficult airways may be needed.26
  2. Tracheostomy set and intubation equipment may be needed. Indirect laryngoscopy or fiber optic nasopharyngolaryngoscope should always to cautious.
  3. Close monitoring of vital signs is essential.
  4. General supportive care.
Airway Burn
Airway burn can occur due to thermal or chemical injury to mucosa of airway extending from nose/mouth to alveoli. Thermal injury is usually due to inhalation of hot gases/vapors, or directly from fire and/or smoke. During laser surgery the endotracheal tube can ignite and cause airway burn. Faulty inspired gas heater or humidifier may also be responsible.
Clinical Features
All patients in closed space fires usually suffer from inhalation injury particularly in burns of face and neck, involvement of proximal airway can cause rapid edema and obstruction. Soft tissue swelling of the face, oropharynx, glottis, and trachea is common. There may be carbon deposits in the nasopharynx and oropharynx, expectorated carbonaceous sputum, wheezing, respiratory insufficiency, hypoxemia and increased carbon monoxide level in blood. There are decreased arterial PO2 and O2 saturation, decreased pulmonary compliance, pulmonary edema, bronchospasm and eventually leading to adult respiratory distress syndrome (ARDS). Management should include administration of 100% oxygen, early intubation and mechanical ventilation and general supportive care.
In cases of laser-ignited endotracheal fire:
  1. Ignition or burning of the tube may be seen27
  2. Smell of burning, smoke, and flames
  3. Fire can extend to breathing circuit.
  1. Patient should be disconnected from the breathing circuit. Flow of oxygen should be stopped through the tube.
  2. The damaged tube should be taken out.
  3. Mask ventilation with 100% oxygen.
  4. Reintubation is tried, if possible.
  5. Mechanical ventilation with PEEP.
  6. Steroids.
  7. Supportive care.
  8. Prevention:
    1. Use of protected endotracheal tube (laser-proof).
    2. Cuff should be filled with colored water or saline.
    3. Avoid nitrous oxide.
    4. Careful monitoring.
In cases with overheated gases/vapors:
  1. Breathing circuit becomes hot.
  2. High rise of patient's body temperature.
  3. High temperature alarm sounds may be heard.
  4. Management should include:
    1. Remoral of heater/humidifier from the circuit.
    2. Careful evaluation.
    3. Maintain adequate oxygenation.
    4. Steroids.
    5. Fiber optic bronchoscopy, when the condition is stable.
    6. General supportive care.
Flail Chest
Flail chest can result from direct high energy force over the chest wall. Broken ribs are very painful and cause splinting 28with ventilation-perfusion mismatching. Flail segment commonly involves anterior or lateral rib fractures, posterior rib fractures usually do not cause flail segment due to good stability provided by muscles. Usually two or more ribs are fractured in two or more sites. Paradoxical motion of that chest wall segment is often present. Flail segments can also cause inefficient ventilation and atelectasis.
Blunt force of injury mostly cause pulmonary contusion. In such cases hemoptysis and atelectasis can occur. Pneumothorax and hydrothorax can also result. Associated other injuries particularly abdominal injuries may be present. Diagnosis is confirmed by chest X-ray.
  1. Assess the patient very carefully. There may be shock and respiratory distress. Labored breathing, increased respiratory rate, low oxygen saturation and PaO2< 60 min Hg indicate respiratory insufficiency.
  2. In presence of shock and/or respiratory insufficiency endotracheal intubation and IPPV with 100% O2 are indicated. In patients with positive pressure ventilation paradoxical movement of chest wall segment may not be seen. Continuous positive airway pressure (CPAP) is often helpful.
  3. Pain control is most important:
    1. Systemic opioids by continuous infusion.
    2. Patient controlled anesthesia.
    3. Regional anesthesia: Epidural block.
    4. Intercostal nerve blocks.
  4. Close monitoring particularly pulse oximetry and continuous end-tidal CO2 is needed.
  5. General supportive care provides pulmonary hygiene and physiotherapy (cough-deep breathing).