Postoperative

Respiratory Failure
Dr.Anto Mathew
INTRODUCTION
• The success or failure of the surgery is defined not in the operating
room, but postoperatively, when the adverse effects of surgery may
first become apparent and when intercurrent complications may
jeopardize the patient’s recovery.

• A number of postoperative complications, such as

pneumonia,aspiration pneumonitis, and acute respiratory distress
syndrome(ARDS) may lead to respiratory compromise independent of
the patient’s pre surgical status.
IDENTIFICATION OF THE HIGH-RISK
PATIENT
• American Society of Anesthesiologists (ASA) class.
• Twenty-eight variables were identified that were independently
associated with increased risk
• COPD has been identified as an independent predictor of postoperative
respiratory failure.

• The use of preoperative pulmonary function testing to assess risk of

postoperative respiratory failure in COPD patients has been most closely
examined .

• Respiratory failure or death was for those patients with an FEV1 <40%while
the probability of avoiding these complications was 90% for those with an
FEV1 ≥40%.
• Patients with COPD scheduled for surgery should undergo a preparatory
pulmonary regimen intended to optimize lung function and minimize airway
secretions.

• This regimen should include smoking cessation, institution or intensification

of inhaled bronchodilator and inhaled corticosteroid therapy, and use of oral
antibiotics in the presence of purulent secretions or a “loose” cough.

• instructed on the use of incentive spirometry or cough and deep breathing

techniques prior to surgery.

• A short course of oral corticosteroids should be considered in patients who

have a significant bronchospastic component to their disease.
• Smoking has been shown to be a risk factor for postoperative pulmonary
complications.

• Effects of smoking include bronchial irritation with resultant excessive

airway secretions, impairment in mucociliary clearance, and elevation of
carboxyhemoglobin levels with consequent impairment in oxygen uptake
and tissue oxygen utilization.

• Require a minimum of 8 weeks of abstinence.

MEASURES TO REDUCE RISK
• surgical approach can be modified.
• Eg. use of a transverse abdominal incision appears to carry less risk than a
vertical midline incision.
• Cholecystectomy performed by laparoscopic technique is associated with
significantly less compromise in postoperative FEV1 and FVC and more
rapid recovery of lung function compared with the conventional open
approach.
• Use of video-assisted thoracoscopic surgery (VATS) in combination with
lobectomy, segmentectomy, or wedge resection appears to be well
tolerated by patients with severe lung disease, with only a 4% incidence of
respiratory failure and a 1% mortality rate documented, in a study of 100
consecutive patients with an FEV1 <35% predicted
Causes of Postoperative Respiratory Failure
Factors extrinsic to the lung
• Depression of central respiratory drive (anesthetics, opioids,sedatives)
• Phrenic nerve injury/diaphragmatic dysfunction
• Obstructive sleep apnea
• Factors intrinsic to the lung
• Atelectasis
• Pneumonia
• Aspiration of gastric contents
• Acute respiratory distress syndrome
• Volume overload/congestive heart failure
• Pulmonary embolism
• Bronchospasm/COPD
Depression of central respiratory drive (anesthetics, opioids,sedatives)

• GENERA L ANESTHESIA.

• whether by the inhaled or intravenous route, results in an almost immediate loss

of diaphragmatic and intercostal muscle tone, a cephalad shift of the diaphragm,
and a decrease in the transverse thoracic diameter.

• These dimensional alterations in thoracic volume result in a 20% reduction in

functional residual capacity (FRC) and in the development of compressive
atelectasis.

• CT during and after general anesthesia, patients develop crescent-shaped areas

of atelectasis in dependent areas of lung within 10 minutes of induction.
• A notable exception is ketamine, a drug that is unique in its maintenance of
respiratory muscle tone.

• The inhaled anesthetic agents in common usage are respiratory depressants that
blunt the response to both hypoxemia and hypercapnia.These agents depress the
ventilatory response to CO2 in a dosedependent fashion.

• hypoxemic drive is markedly attenuated even at very low, subanesthetic

concentrations of the volatile agents.

• deposition of these agents in muscle and fat, concentrations sufficient to depress

hypoxic drive persist for several hours after termination of anesthesia.

• This can result in significant postoperative respiratory depression in patients with

chronic hypercapnia who are dependent on hypoxic ventilatory drive to breathe.
NEURAXIAL ANESTHESIA
• neuraxial anesthesia preserves diaphragmatic innervation and function.
• External intercostal muscle paralysis is induced by thoracic levels of
neuraxial anesthesia, but the level is generally two dermatomes below the
sensory level because of the lesser sensitivity of motor neurons to the
effects of the anesthetic agent.
• Hypoxic pulmonary vasoconstriction is unaffected by neuraxial anesthesia,
and the ventilatory response to CO2 is unimpaired, indeed the CO2
response may be heightened
• comparing general to neuraxial anesthesia detected a significant reduction
in 30-day mortality, venous thromboembolism, pneumonia, and respiratory
depression
 POSTOPERATIVE ANALGESIA
• Analgesia is important not only in ensuring patient comfort, but also in
mitigating the adverse effects of pain on respiratory function and airway
clearance.

• Inadequate pain relief can lead to splinting and patient reluctance to cough and
deep breathe;the end result is promotion of retained secretions, atelectasis,
hypoxemia, and, possibly, pneumonia.

• The risk may be slightly lower in association with the epidural as opposed to
parenteral route of administration.

• Morphine &fentanyl
IMPACT OF SURGERY ON
POSTOPERATIVE
PULMONARY FUNCTION
• UPPER ABDOMINAL SURGERY.
• Within 24 hours following upper abdominal surgery, vital capacity declines
by 50%. Although the vital capacity improves with time,marked
impairment persists for as long as 7 days after the surgery.
• In contrast, vital capacity falls by only 25% following lower abdominal
procedures; it returns to normal by the third postoperative day.
• This is because of development of diaphragmatic dysfunction, as reflected
in a reduction in trans diaphragmatic pressure with tidal respirations and in
a shift from abdominal to rib cage breathing
• Two main theories have been proposed to explain the observed impairment
in diaphragmatic function.

• One theory is that there is a primary alteration in diaphragmatic contractility

induced by local irritation, inflammation, surgical trauma, or pain.

• Diaphragmatic dysfunction results from diminished phrenic nerve

output,fav theory by inhibitory arc by pain
CARDIAC SURGERY
• Lung volumes decrease by approximately 30% after CABG; the return to
preoperative values may take several months.
• Lung function may decline to a greater degree when internal mammary
harvesting and grafting are employed.
• A number of factors have been implicated in the development of post-CABG
pulmonary dysfunction and atelectasis. Alterations in chest wall compliance and
motion may result from division of the sternum, harvesting of the internal
mammary artery, and traumatic injury to the costovertebral joints and first rib
induced by retraction.
• intraoperative injury to the left phrenic nerve and consequent diaphragmatic
paralysis or paresis
• The phrenic nerve is vulnerable to stretch and ischemic injury during sternal
retraction, dissection of the left internal mammary artery, or prolonged
distention of the pericardium.

• In addition, thermal injury to the nerve may occur with the cardioplegic
technique of instilling iced slush into the open pericardial sac.
CAUSES OF POSTOPERATIVE
RESPIRATORY FAILURE
• ATELECTASIS
• the most common pulmonary complication encountered in the surgical patient,
particularly following thoracic and upper abdominal procedures.
• The atelectasis is typically basilar and segmental in distribution,obscuring the
hemidiaphragms radiographically.
• A distinct and less common cause of postoperative atelectasis is plugging of
central airways by retained secretions. This problem is encountered in the
surgical patient whose efforts to clear secretions are compromised by
depressed consciousness, inadequate pain control, or a weak,ineffective
cough.
• When situated in a main stem bronchus, mucus plugs can result in
collapse of an entire lung; more distal obstruction leads to lobar collapse.

• postoperative atelectasis may lead to severe hypoxemia and respiratory

distress. The magnitude of hypoxemia is dictated by the extent of
atelectasis, the presence and severity of underlying lung disease, and the
integrity of the hypoxemic pulmonary vasoconstrictive response.

• Careful examination of the patient, however, will reveal an absence of

breath sounds over the involved lung, providing an important clue to the
presence of central airway obstruction and obviating pursuit of other
considerations, such as pulmonary embolism
• Treatment of respiratory failure due to atelectasis is
• combined goals of adequate oxygenation and re expansion of lung segments.
• Supplemental oxygen should be titrated to achieve an arterial oxyhemoglobin
saturation of at least 90%.
• Refractory hypoxemia, severe respiratory distress, progressive hypercapnia, or
inability of the patient to clear copious airway secretions should prompt
immediate intubation and mechanical ventilator support.
• facilitates performance of bronchoscopy should it be necessary.
• the positive pressure and large tidal volumes delivered by the ventilator are
often effective in rapidly re-expanding collapsed lung segments.
• Fiberoptic bronchoscopy is commonly employed in the treatment of serious
atelectasis but evidence suggests that it may be no more effective than standard
chest physiotherapy
• discontinue vasoactive drugs with the potential to influence the pulmonary
vascular bed; examples include nitrates, nitroprusside, calcium channel
blockers, angiotensinconverting enzyme inhibitors, and hydralazine.

• Mucolytics, such as N-acetyl cysteine, are commonly administered in an

effort to promote clearance of tenacious secretions.

• Maneuvers to promote periodic full lung expansion, including intermittent

positive pressure breathing (IPPB), cough and deep breathing exercises,
and incentive spirometry, have been developed in an attempt to prevent or
mitigate the severity.
PNEUMONIA
• Pneumonia is the third most common postoperative infection and the most lethal,
with an associated mortality rate of 20% to 50%.
• The type of surgery heavily influences the risk of developing pneumonia in the
postoperative period. In particular, the risk is greatest following abdominal aortic
aneurysm repair, thoracic and upper abdominal procedures, head and neck
surgery, and neurosurgical procedures.
• advanced age, chronic steroid use, current or recent smoking, COPD, low serum
albumin level,impaired sensorium, and dependent preoperative functional status.
• The presence of a nasogastric tube and the use of gastric acid–suppressive
medications, commonly employed interventions in postoperative patients, have
been cited as risk factors for nosocomial pneumonia in general.
• mechanically ventilated patients have a 6- to 21-fold increased risk of
pneumonia compared with nonventilated patients
• organisms may reach the lower respiratory tract by several routes, micro aspiration
of orpharyngeal secretions appears to be the predominant mechanism in the
pathogenesis of nosocomial pneumonia.
• Oropharynx.
• stomach as an additional source of bacteria in the development of nosocomial
pneumonia. While the acidic milieu of the stomach normally inhibits bacterial
growth, the common use of H2-blockers and antacids as stress ulcer prophylaxis
overrides this natural barrier and promotes gastric colonization with gram-negative
enteric organisms.
• Gastro esophageal reflux, a common feature of the critically ill patient, permits
bacteria-laden gastric contents to enter the respiratory tract either directly or by first
colonizing the oropharynx.
• This route of migration has been confirmed by recovery of technetium-99m-labeled
gastric contents in endobronchial secretions and by the demonstration in some
patients that organisms cultured from the airways first appeared in the stomach.
• Impairment of the mucociliary escalator due to recent cigarette smoking or
underlying COPD, weak and ineffective cough, and use of immunosuppressive
medications (e.g., corticosteroids), favor the proliferation of organisms and the
development of pneumonia.
• postoperative atelectasis predisposes to pneumonia by entrapping bacteria.

• fever, leukocytosis, purulent sputum, and radiographic infiltrates has

traditionally defined the presence of pneumonia.

• Cultures of sputum and tracheal aspirates are poorly reflective of the bacterial
flora of the distal airways, since these specimens are contaminated by
colonizing organisms in the oropharynx and upper respiratory tract.

• diagnostic certainty, bronchoscopic sampling of the distal airways using a sterile

sheathed brush or bronchoalveolar lavage has been advocated.
• most common organisms isolated in cases of postoperative pneumonia are gram-
negative bacteria and Staphylococcus aureus.
Preventative strategies.
• abstinence from cigarette smoking for a minimum of 8 weeks prior to elective
surgery.

• Following surgery, nasogastric and endotracheal tubes should be removed as soon

as possible.

• Postoperative analgesia must be titrated to permit the patient to comfortably and

vigorously cough, but excessive sedation impairing protection of the airway and
enhancing the risk of aspiration must be avoided.

• maintenance of a semierect position has been shown to diminish the aspiration of

gastric contents and the incidence of pneumonia.
• selective digestive decontamination (SDD)

• intended to prevent or diminish the magnitude of gram-negative colonization of

the aerodigestive tract.

• typically consist of some combination of antibiotics applied topically to the

oropharynx, instilled into the stomach as a slurry, and/or administered
systemically.
ACUTE RESPIRAT ORY DISTRESS
SYNDROME
• ARDS is defined by the constellation of hypoxemic respiratory failure, diffuse
pulmonary infiltrates, and the absence of clinical evidence of elevated left atrial
pressure.
ASPIRATION OF GASTRIC CONTENTS.
• Acute lung injury and is an important cause of ARDS in the surgical patient.
• It is the third leading cause of anesthesia-related deaths, accounting for 10% to
30% of fatal outcomes.
• mechanisms of glottic closure and cough, which normally protect the airway, are
compromised.
• Blunting of consciousness,
• Insufflation of air into the stomach during induction may cause gastric
distention and promote vomiting.
• Reflux of gastric contents is facilitated by medication-induced relaxation of
the lower esophageal sphincter, placement of the patient in a supine
position, and manipulation of the bowel during abdominal procedures.
• upper airway reflexes-remain significantly impaired for up to 2 hours,
residual glottic dysfunction for up to 8 hours following removal of the tube.
• Acidic gastric contents introduced into the airways are rapidly disseminated
throughout the bronchial tree and lung parenchyma, producing an almost
instantaneous chemical burn.
• acid aspiration triggers a more delayed inflammatory response,with release of
inflammatory cytokines and recruitment of neutrophils into the lung. The result
is injury to the alveolar–capillary membrane, with flooding of the interstitium
and airspaces by proteinaceous edema fluid.
• Surfactant levels drop due to both direct acid denaturation and diminished
production, leading to alveolar instability and atelecta
• The magnitude of lung injury is directly related to the pH and volume of
aspirated material. Initial studies in animals suggested that a pH of less than 2.5
and a volume in excess of 0.4 mL/kgs.
The diagnosis of aspiration
• witnessed vomiting or recovery of gastric contents from the airways.
• Massive aspiration presents with fever, tachypnea, and diffuse rales developing
within several hours of the event.
• Wheezing is appreciated in approximately one-third of patients and may be due
either to obstruction of airways by particulate matter or, more commonly, to
reflex bronchospasm.
radiographic patterns.
(1) extensive bilateral consolidation resembling diffuse pulmonary edema;
(2) widespread, but discrete, patchy infiltrates involving dependent areas of lung;
(3) focal consolidation usually localized to one or both lung bases
• The treatment of respiratory failure secondary to aspiration issupportive
and includes mechanical ventilatory strategies.

• Bronchoscopy is indicated only when large airway obstruction by

particulate matter is suspected on the basis of a localized wheeze or lobar
atelectasis.

• Administration of systemic corticosteroids in the treatment of aspiration

pneumonitis have been inconclusive
MEASURES TO PREVENT
• overnight fasting prior to elective surgery.
• up to one-third of patients will maintain a gastric volume in excess of 0.4
mL/kg (approximately 25–30 mL in the average adult), and up to three-
quarters will have a gastric pH below 2.5.
• Administration of H2-blockers and proton-pump inhibitors can effectively
raise the pH and reduce the volume of gastric contents, suggesting a
potentially appealing strategy.
• During induction, manual pressure should be applied to the cricoid cartilage
and maintained until the endotracheal tube is in proper position and the cuff is
inflated.
• Postoperatively, extubation should be performed only when consciousness
and the gag reflex +
POSTPNEUMONECTOMY PULMONARY EDEMA
• Mechanisms that have been advanced include hyperinflation and volutrauma
resulting from single lung ventilation, endothelial injury due to hyperperfusion
of the remaining lung, disruption of lymphatic drainage, and ischemia
reperfusion injury.
CARDIOPULMONARY BYPASS.
• CPB activates a number of inflammatory pathways that could lead to acute
lung injury.
• mechanical shear stress and exposure to the artificial surfaces of the bypass
circuit.
• In addition, an increased expression of cell surface adhesion molecules has
been demonstrated, which may promote neutrophil binding to pulmonary
endothelium and release of proteolytic enzymes and reactive oxygen species.
• The central role played by neutrophils in causing acute lung injury following
CPB is supported by several lines of evidence:
(1) bronchoalveolar lavage fluid from patients undergoing CPB contains an
increased number of neutrophils;

(2) plasma levels of neutrophil elastase and myeloperoxidase are increased;

(3) inhibition of neutrophil activation with pentoxiphylline as well as neutrophil

depletion attenuate the degree of pulmonary dysfunction.

• A number of other inflammatory mediators are released in association with

CPB, including complement, proinflammatory cytokines, and prostaglandins
AMIODARONE
• Amiodarone-induced pulmonary toxicity usually presents as a subacute
illness characterized by cough, dyspnea, fever, and patchy pulmonary
infiltrates.

• drug was initiated as prophylaxis or treatment for atrial arrhythmias.

• suggested that exposure to high levels of supplemental oxygen may be a

contributing factor.
TRANSFUSION-RELATED ACUTE LUNG
INJURY
• transfusion of blood and blood products has been linked to the development of
acute lung injury >15 units/24 hours.
• Acute lung injury can also be associated with the transfusion of a single unit of
blood or blood components, an entity known as “transfusion-related acute lung
injury” (TRALI).
• acute development of hypoxemia and bilateral radiographic opacities during or
within 6 hours of a completed transfusion,.
• Donor plasma that contains high titer antiHLA antibodies that bind recipient
leukocytes.
• The leukocytes aggregate in the pulmonary vasculature and release mediators
that increase capillary permeability-develops pulmonary edema,b/l interstitial
on chest xray
 ACUTE EXACERBATIONS OF PULMONARY FIBROSIS
• Patients with idiopathic pulmonary fibrosis (IPF) can experience sudden and
dramatic respiratory decompensation in the absence of identifiable precipitants.
• an exacerbation of IPF, this phenomenon is characterized by acutely worsening
hypoxemia in association with new bilateral ground-glass opacities or
consolidation on chest CT.
• histological hallmark is diffuse alveolar damage, superimposed on underlying
usual interstitial pneumonia.
• The mechanism by which surgical manipulation of the lung could cause an
exacerbation is currently speculative.
• Mortality associated with postoperative acute exacerbations is high, 50% to 100%.
• Steroids and other immunosuppressive agents are commonly initiated but there is
no compelling evidence for efficacy.
• Lung transplantation may be an option in selected cases.
PHRENIC NERVE INJURY AND DIAPHRAGMATIC DYSFUNCTION

• Thermal injury causes both demyelination and axonal degeneration of the

nerve, with slowing of conduction and impaired activation of the
diaphragm.
• The use of topical cooling techniques has fallen out of favor largely
because of this potential complication.
• the phrenic nerves can also be injured by traction, ischemia, use of
diathermy, or transection during sternal retraction and harvesting of the
internal mammary arteries.
• The detection of inspiratory thoracoabdominal paradox – an inward movement
of the abdominal wall with simultaneous expansion of the thorax – is an
important bedside clue to the presence of bilateral diaphragmatic paralysis and is
best evoked in the supine position.
• Unilateral diaphragmatic paralysis can be readily diagnosed by fluoroscopic
inspection, which reveals paradoxical upward movement of the affected
hemidiaphragm with a maximal inspiratory effort (“sniff ”).
• inspiration, the abdominal muscles relax and the hemidiaphragms descend
briefly, potentially creating the false impression that they are functional.
Because of this,fluoroscopy may not be confirmatory in these patients.
• Ultrasound has emerged as a simple bedside test for assessing diaphragmatic
function.
• Thickening of the diaphragm with inspiration reflects diaphragmatic shortening
and failure to observe this sign is indicative of diaphragmatic paralysis.10mm
• The gold standard for confirmation of phrenic nerve injury
iselectrophysiological testing.

• The phrenic nerve is stimulated transcutaneously in the neck, and the

diaphragmatic electromyogram (EMG) is recorded by surface electrodes placed
in the seventh intercostal space at the costochondral junction.

• The prognosis for patients with thermal or traction injury of the phrenic nerve is
favorable; recovery is typically complete,

• In symptomatic patients with unilateral diaphragmatic paralysis due to

transection of the phrenic nerve, surgical placation of the flaccid hemidiaphragm
may lead to improved pulmonary function and successful liberation from
mechanical ventilation
PULMONARY EMBOLISM
• increased risk of PE accompanies a number of surgical procedures, including
upper abdominal, neurosurgical, cardiac, major urological, and lower
extremity orthopedic procedures
• The patient is often dyspneic, and tachypnea and tachycardia are observed on
physical examination. However, these features are common in many
postoperative patients because of pain and atelectasis.
• evidence of acute cor pulmonale:distended neck veins, a parasternal heave,
right-sided third heart sound, and accentuation of the pulmonic component of
the second heart sound.
• “S1Q3T3” pattern or new right bundle branch block.
• CT angiography
• anticoagulation with heparin forms the mainstay of therapy for the
otherwise stable patient.
• insertion of an inferior vena cava filter is generally advised in this setting
and should be considered mandatory when anticoagulation is
contraindicated.
• Several interventional radiological techniques – thrombus fragmentation,
suction embolectomy, and intraembolic infusion of low-dose thrombolytics
– as well as surgical embolectomy are alternative considerations in the
deteriorating patient for whom systemic thrombolytics are either
contraindicated or unsuccessful.
OBSTRUCTIVE SLEEP APNEA
• is characterized by repetitive upper airway obstruction during sleep, resulting in
arterial desaturation, hypercapnia, and arrhythmias

• alterations in oropharyngeal anatomy that commonly accompany obesity and

OSA, orotracheal intubation at the time of induction may be difficult.

• The use of anesthetics, opioids, and sedatives diminishes the activity of the
upper airway dilator musculature and concurrently dampens respiratory arousal
mechanisms that can terminate obstructive apneas.
• Ideally, shorter acting anesthetic agents should be employed. Intraoperative use
of opioids should be minimized.

• Application of continuous positive airway pressure (CPAP) immediately after

extubation should be considered

• Nonopioid analgesics should be used in an attempt to avoid or minimize use of

opioids in the postoperative period.
Thank you.