HYPOXEMIA IN THE IMMEDIATE POSTOPERATIVE PERIOD
Dr Ashima Sharma , NIMS.

FACTORS

BASIS

TREATMENT

ADDITIONAL REMARKS

1.UPPER AIRWAY OBSTRUCTION

Pharyngeal obstruction

• Posterior tongue displacement

• Soft tissue collapse

Simple maneuvers such as a chin lift, jaw thrust, and lateral decubitus positioning, as well as decreasing the level of sedation usually are successful in relieving pharyngeal obstruction. Oropharyngeal or nasopharyngeal airways are useful adjuncts.

Nasopharyngeal airways are better tolerated than oral airways at light levels of sedation because of less tendency to provoke a gag reflex. Careful insertion of nasal
airways is necessary to avoid creating a nosebleed

Laryngeal Obstruction

• Laryngeal Edema

Treatment of partial airway
obstruction resulting from airway edema includes head-up positioning to promote venous drainage, administering nebulized epinephrine and steroids. Treatment of severe airway edema may require emergency reintubation
or tracheostomy. Patients at risk for significant swelling should be evaluated (using direct or fiberoptic laryngoscopy) prior to extubation because they are at risk for complete airway
obstruction . Patients with significant obstruction should remain intubated until airway edema resolves.

Laryngeal or subglottic edema can create airway obstruction, especially in children because
of their smaller airway diameter and in patients recovering from neck. surgery.
The common practice of listening for an air leak after a positive pressure breath (with the endotracheal cuff deflated) is a reliable way to determine that extubation likely will be successful if a leak is present. However, a failed leak test does not preclude uneventful extubation.

• Laryngospasm     

Laryngospasm is a reflex resulting from prolonged glottis closure. Although the cords are adducted,
the primary obstruction is caused by tonic contraction of the laryngeal muscles and descent of the epiglottis over the laryngeal inlet.

Management consists of jaw thrust, positive-pressure ventilation,and possibly administration of iv propofol or a small dose of succinylcholine (0.1mg/kg).

Laryngospasm may be precipitated by the presence of an airway irritant such as secretions, blood, or a foreign body. It also can be caused by stimulation from an elongated uvula, may be sleep related, or may be stimulated by distal esophageal afferents

• Extrinsic Airway Compression-

Definitive treatment usually requires returning to the operating room for hematoma evacuation and exploration.

Neck hematomas can develop after carotid endarterectomy, thyroid or parathyroid surgery, or other neck surgery. A rapidly expanding hematoma can cause marked tracheal deviation and make emergency reintubation extremely difficult.

2. HYPOVENTILATION

Decreased Ventilatory Drive-  is characterized by an inappropriately low minute ventilation with resulting hypercapnia and
respiratory acidosis.

• Drug induced

The typical combination of inhaled anesthetics, opioids, and  benzodiazepines can depress both hypercarbic and hypoxic drive, resulting in hypoventilation.

Opioid-induced hypoventilation can be reversed by small incremental doses of naloxone (0.04–0.08 mg) while preserving some analgesia. Reversal usually occurs within 1–2 minutes and lasts for 30–60 minutes.
Flumazenil can reverse the sedative effects of BZD, but it does not reverse the depression of hypoxic drive.

A balance must be achieved between adequate analgesia and an acceptable level of respiratory depression.

Respiratory Muscle Insufficiency-

• Incomplete reversal

• Splinting of respiratory muscles.

• Extrathoracic causes⃰

Consider reintubation and extubation  under neuromuscular monitoring assessment.
Simple cases will benefit with CPAP and careful observation in OT till the ventilation becomes adequate.

Better analgesia (particularly that produced by neuraxial and intercostal blocks) facilitates
deep breathing and significantly reduces hypercapnia and hypoxemia.

Incentive spirometry, chest physiotherapy,
upright positioning, and continuous positive airway pressure may be effective therapeutic maneuvers.

The patient may exhibit discoordinated movements, generalized weakness, hypoxemia, or shallow breathing with incomplete reversal Residual block is more common in patients who receive long-acting muscle relaxants such as pancuronium and those not treated with reversal agents .

Limited chest expansion may be caused by pain (splinting) after thoracic and upper abdominal surgery, resulting in atelectasis and right-to-left shunting.

Obesity, gastric distension, and restrictive dressings on the chest or abdomen.

Acute or Chronic Lung Disease-  .

• mainly Obstructive diseases

• Restrictive diseases-

Management includes treating bronchospasm and airway inflammation, correcting hypoxemia and respiratory acidosis, clearing secretions, and removing/treating precipitating factors. The concerns for CO2 retention and respiratory depression
resulting from  administration of supplemental oxygen to patients with COPD have been overemphasized. In
all cases, correction of hypoxemia should take precedence over concerns for carbon dioxide retention.

Preexisting pulmonary disease is an important risk factor for developing postoperative pulmonary complications..

A decreased diffusion capacity may reflect the presence of underlying
lung disease such as emphysema, interstitial lung disease,
pulmonary fibrosis, or primary pulmonary hypertension.

3.DIFFUSION HYPOXIA

- refers to the rapid diffusion of nitrous oxide
into alveoli at the end of a nitrous oxide anesthetic. Nitrous oxide dilutes the alveolar gas and produces a transient decrease in PaO2and PaCO2.

In a patient breathing room air, the resulting decrease
in Pao2 can produce arterial hypoxemia while decreased Paco2 can depress the respiratory drive.
BLE 73–

Supplemental O2 after N2O is switched off ( for 5-10 minutes).

4. ASPIRATION

General anesthesia and surgery depress airway protective reflexes and predispose patients to aspiration. Gastric contents or objects such as dislodged teeth can enter the trachea during induction or emergence, and even after PACU admission.

Signs of significant aspiration include bronchospasm, hypoxemia, atelectasis, tachypnea, tachycardia,and hypotension.

Initial treatment of a significant aspiration consists of oropharyngeal suctioning, administration of bronchodilators for bronchospasm, and supplemental oxygen. Plans should be made for transfer of the patient to an ICU. Bronchoscopy may be beneficial to remove particulate matter from the tracheobronchial tree, but pulmonary lavage with large volumes of saline is generally believed to be detrimental. Mechanical ventilatory support with positive end-expiratory pressure may be necessary if hypoxemia is severe. Administration of empiric antibiotics for aspiration is not recommended unless the material aspirated has a high bacterial load, as with a small bowel obstruction. Steroids are not beneficial for treatment if administered after an aspiration has occurred.

In cases of mild or uncertain aspiration, close postoperative observation should be undertaken with continuous pulse oximetry monitoring and chest radiography. Patients with clinical evidence of aspiration who do not develop signs or symptoms (cough, wheeze, hypoxia on room air, or radiologic abnormalities)
within 2 hours of aspiration are unlikely to develop pulmonary complications.

5.PULMONARY EDEMA-

  is the accumulation of fluid in the interstitium and alveoli of the lungs that can hinder gas exchange.

• Negative pressure pulmonary edema-

 During upper airway obstruction, forceful inspiratory efforts against a closed glottis can result in large negative intrathoracic
pressures with an increased leftventricular preload and afterload. In addition, hypoxia and increased circulating catecholamine levels may elevate pulmonary and systemic vascularresistance, shift the intraventricular septum to the left, and cause left ventricular diastolic dysfunction.

• Cardiac pulmonary edema

 
results from increased pulmonary capillary pressure secondary to elevated left atrial pressure that may be precipitated by fluid overload, left ventricular dysfunction, or mitral valve disease.

• Transfusion-Related Lung Injury

Transfusion-related lung injury is typically manifested within 1 to 2 hours after the transfusion of plasma-containing blood products, including packed red blood cells, whole blood, fresh frozen plasma, or platelets.

Mainstays of treatment include supplemental oxygen, diuretics,
vasodilators, and mechanical ventilatory
support with positive end-expiratory pressure.

Evaluation by a cardiologist may be indicated when myocardial ischemia or acute valvular disease is considered to be the cause of the pulmonary edema.

Treatment is supportive and includes supplemental oxygen and drug-induced diuresis. Mechanical ventilation may be needed to support hypoxemia and respiratory failure. Vasopressors may be required to treat refractory
hypotension.

Pulmonary edema is characterized by a rapid onset of copious pink
fluid with bubbles due to acute fluid filtration into the lung, and capillary failure resulting in alveolar hemorrhage and hemoptysis.

A careful physical examination, CXR,ECG and ABG are useful for diagnosis.

A complete blood cell
count is obtained with the onset of symptoms, it is possible to document an acute drop in theWBC count ,reflecting the sequestration of granulocytes within the lung and exudative fluid.

6.PULMONARY EMBOLISM-

Thrombosis is triggered by venous stasis, hypercoagulability, and vessel wall inflammation (Virchow’s triad).

Under pathologic conditions, thrombi escape the normal fibrinolytic system, propagate in the deep veins of the lower
extremities and pelvis, and then dislodge and embolize blocking pulmonary
vessels.

Treatment of PE is supportive (volume
infusion, vasopressors, and mechanical ventilation) because anticoagulation
or thrombolytic therapy often is not an option in the immediate postoperative period.
Inhaled nitric oxide has been given experimentally to reverse pulmonary vasospasm.
In patients with severe hypoxemia or hypotension, emergency pulmonary embolectomy may be required.
Insertion of an inferior vena cava filter may be  beneficial to prevent further embolism in patients in whom anticoagulation is contraindicated.

A patient with a massive PE may present with hypotension, severe hypoxemia, cardiogenic shock, or cardiac arrest. ECG may reveal signs of
right ventricular strain but may be entirely normal in previously healthy patients, and the CXR is often normal. Chest CT has become the primary diagnostic imaging modality to evaluate suspected PE. Alternate imaging modalities include a ventilation– perfusion lung scan, MRI, ECHO and pulmonary angiography.

7.PNEUMOTHORAX

is the accumulation of
gas within the pleural space.

It can result from surgical entrance into the pleural space during thoracic, upper abdominal, or retroperitoneal surgery,
tracheostomy, or surgery on the chest wall or neck. Other causes important in postoperative period are rupture of blebs or bulla or barotrauma from positive-
pressure ventilation, and as a complication of procedures such as central
line placement, thoracentesis, or upper
extremity neural blockade.

If a tension pneumothorax is suspected&hemodynamic or respiratory status is compromised, then decompression should be performed immediately, without waiting for confirmation of the diagnosis by CXR. A 14-
gauge angiocath can be placed through the chest wall in the 2nd second Intercostal space at the midclavicular line or the 4th  intercostal space at the midaxillary line. The needle is removed, and the catheter is held securely in position until a tube thoracostomy can be performed.
A rush of released air and
immediate improvement in respiratory and hemodynamic status should occur when decompression is successful.

A tension pneumothorax occurs when the site of pulmonary air leak forms a one-way valve, allowing airflow into the pleural space during inspiration but  preventing its elimination during expiration.
The rapid unilateral increase in intrathoracic pressure can be life
threatening because it can produce a contralateral mediastinal shift with a rapid deterioration in gas exchange, diminished cardiac output, and marked hemodynamic instability. Diminished
or absent chest sounds on auscultation may be present over one hemithorax.

8.VENTILATION-PERFUSION MISMATCH AND SHUNT-

Hypoxic pulmonary vasoconstriction refers to the attempt of normal lungs to optimally match ventilation and perfusion.

In the PACU, the residual effects of inhaled anesthetics and vasodilators such as nitroprusside and
dobutamine used to treat systemic hypertension or improve hemodynamics will blunt HPV and contribute to arterial hypoxemia

This response constricts vessels in poorly ventilated regions of the lung and directs pulmonary blood
flow to well-ventilated alveoli.

9.INCREASED VENOUS ADMIXTURE -

Increased venous admixture typically refers to low cardiac output
states. It is due to the mixing of desaturated venous blood with
oxygenated arterial blood.
.

Normally, only 2% to 5% of cardiac output is shunted through the lungs, and this shunted blood with
a normal mixed venous saturation has a minimal effect on PaO2.

In low cardiac output states, blood returns to the heart severely
desaturated. Additionally, the shunt fraction increases significantly in conditions that impede alveolar oxygenation, such as pulmonary edema and atelectasis. Under these conditions, mixing of desaturated shunted blood with saturated arterialized blood decreases PaO2