Common Post-operativePulmonary

ComplicationsThoracic Surgery

Dr.Hamdy5th year

Females of the 3rd group 2010

Prepared By

-Hind Abdulla Bagitiba

Mageda Ben Hidara--Shekha Bawazeer-Wafa Damnan

Introduction:. The IMPORTANCE

■More surgical ptient probably die of postoperative chest problems than anything else.

■ Such morbidity and mortality can be largely prevented by adequate pre-and postoperative care

■ Riskfactors are complex and multifactorial. A number of schema facilitate identification and ranking of high-risk patients.

Those variables are categorised broadly as procedure-related factors and patient-related factors .

pre oprative predisposing factor

1.Age of pt.2.Sex.

3.Smoking4.Chronic bronchitis

5.Dehydration.

Operative and post operative factors :

1.Anasthesia.2.Nature of operation.

3.Abdominal destention.4.Postoperative pain

.

Procedure-related factors Patient-related factors

1. Surgical site :-thoracic > upper Abdominal surgery .-Neurosurgery > peripheral surgery .2. Open Versus laparoscopic .3. Other types of surgery

(Neck,neurosurgery )4. General Anesthesia 5. Duration of surgery > 3 h6. Emergency surgery .7. Type of neuromuscular block (use of

pancuronium )8. Pain control with parenteral norcotic

vs analgesia .9. NG tube .

1. General health & nutritional status.- age > 65 y.-low albumin. -wt loss > 10%-Obesity (BMN > 27.5 kgm -2 ) .2. Impaired sensorium3. History of CVA .4. CHF5. RF6. Blood transfusion 7. Chronic steroid use8. Alcohol 9. Diabetes10. Chronic lung disease 11. Presence of chronic cough 12. Cigarette smoking 13. Abnormal chest radiograph .

Common complications:

1.Atelectasis .2.Aspiration pneumonia3. Bronchitis4.Bronchopneumonia5.Acute respiratory distress syndrome6. Lung Abscess .7.Pulmonary Embolism.

Atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion. Atelectasis is defined as diminished volume affecting all or part of a lung.

Classification of atelectasis :

1- acute atelectasis, the lung has recently collapsed and is primarily notable only for airlessness.

2- chronic atelectasis, the affected area is often characterized by a complex mixture of airlessness, infection, widening of the bronchi (bronchiectasis), destruction, and scarring (fibrosis)

3-Absorption Atelectasis If a large volume of nitrogen in the lungs is replaced with oxygen, the oxygen may subsequently be absorbed into the blood reducing the volume of the alveoli, resulting in a form of alveolar collapse known as absorption atelectasis

. Causes:

Atelectasis is divided physiologically into obstructive and nonobstructive causes:

1-Obstructive atelectasis:The primary cause of acute or chronic atelectasis is bronchial obstruction by the following: - Plugs of tenacious sputum . - Foreign bodies . - Endobronchial tumors . - Tumors, a lymph node, an aneurysm compressing the bronchi . - a bronchial distortion.

. b-Relaxation atelectasis…….. is caused by the following: Pleural effusion , Pneumothorax , A large emphysematous bullac-Compression atelectasis …….is caused by the following: - Chest wall, pleural, or intraparenchymal masses - L oculated collections of pleural fluidd-Adhesive atelectasis is caused by the following: - Acute respiratory distress syndrome - Smoke inhalation - Cardiac bypass surgery - Uremia. - Prolonged shallow breathinge-Cicatrization atelectasis …….is caused by the following: - Chronic tuberculosis - idiopathic pulmonary fibrosis - Fungal infections - Radiation fibrosisf -Replacement atelectasis - by tumor or fluid.

. . Pathophysiology:Obstructive atelectasis:Following obstruction of a bronchus, the circulating blood absorbs the gas in the peripheral alveoli, leading to retraction of the lung and an airless state within a few hours. In the early stages, blood perfuses the airless lung; this results in ventilation-perfusion mismatch and arterial hypoxemia. A filling of the alveolar spaces with secretions and cells may occur, thereby preventing complete collapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing the surrounding structures. The heart and mediastinum shift toward the atelectatic area, the diaphragm is elevated, and the chest wall flattens.If the obstruction is removed, any complicating postobstructive infection subsides and the lung returns to its normal state. If the obstruction is persistent and infection continues to be present, fibrosis develops and the lung becomes bronchiectatic .

Right Middle Lobe Atelectasis. Frontal radiograph of the chest (left) demonstrates indistinctness of the right heart border (white arrow) and slight elevation of the right hemidiaphragm from volume loss. The lateral view of the chest (right) shows downward displacement of the minor fissure (red arrow) and slight upward bowing of the major fissure (black arrow), both bordering the increased triangular density of the atelectatic middle lobe

. . Clinical:

History:-may occur postoperatively following thoracic or upper abd.procedures.

symptoms and signs Determined by: - the rapidity with which the bronchial occluded

- the size of effected area. -the presence or absence of complicating infection.

Rapid bronchial occlusion with a large area of lung collapse causes pain on the affected side, sudden onset of dyspnea, and cyanosis. Hypotension, tachycardia, fever, and shock may also occur.

Slowly developing atelectasis may be asymptomatic or may cause only minor symptoms. Middle lobe syndrome often is asymptomatic, although irritation in the right middle and right lower lobe bronchi may cause a severe, hacking, nonproductive cough.The physical examination

dullness to percussion over the involved area and diminished or absent breath sounds. Chest excursion in the area is reduced or absent. The trachea and the heart are deviated toward the affected side.

Diagnosis

1_chest X-ray.appear as segmental,lobar and total collapse.2- C.T3-Bronchoscopy .

Management -Postoperative atelectasis is treated with adequate oxygenation and reexpansion of the lung segments. Supplemental oxygen should be titrated to achieve an arterial oxygen saturation of greater than 90%.-Severe hypoxemia associated with severe respiratory distress or hypoxemia should lead to intubation and mechanical support. Intubation not only provides oxygenation and ventilatory support, but also provides access for suctioning of the airways and facilitates performing bronchoscopy, if needed. The positive pressure and larger tidal volumes often help to reexpand collapsed lung segments.-Continuous positive airway pressure delivered via a nasal cannula or facemask may also be effective in improving oxygenation and reexpanding the collapsed lung.-Broad-spectrum antibiotics should be prescribed if evidence of infection is present, such as fever, night sweats, or leukocytosis.

. - Prophylactic maneuvers for reducing the incidence and magnitude of postoperative atelectasis in high-risk patients should be encouraged. These techniques are deep-breathing exercises, coughing exercises, and incentive spirometry. -For maximal benefit, prophylactic measures should be taught and instituted before surgery and used regularly, on an hourly basis, after surgery.

-Early ambulation of patients after surgery has also been found to be as effective as physical therapy.

*Chronic atelectasis is treated with segmental resection or lobectomy.

Radiograph showing right upper lobe atelectasis

. . Chest x-ray show Rt.lung opacity=compelet(total) collapsed lungWith shifting mediastinum and trachea to Rt.side also expansion in

Lf.lung as compensatory lung.

. . Chest X-ray show Rt.lower lobe opacityand no shifiting of mediastinum.

Aspiration Pneumonia. . Aspiration pneumonia results from inhalation of stomach contents or secretions of the oropharynx leading to LRTI . In many healthy adults, very small quantities of aspiration occur frequently but the normal defence mechanisms (cough, lung cilia) remove the material with no ill effects.

Causes & Types :

1-Chemical pneumonitis: chemical irritation of the lungs, which may progress to acute respiratory distress syndrome and/or bacterial infection. Acute aspiration of gastric contents into the lungs can produce an extremely severe and sometimes fatal illness. This has been termed Mendelson's syndrome and can complicate anaesthesia, particularly during pregnancy. 2-Obstruction: large volumes of aspirated material may lead to obstruction of the respiratory tract. 3-Bacterial infection: infection of the lower airways may lead to empyema, lung abscess, acute respiratory failure and acute lung injury. Persistent aspiration pneumonia is often due to anaerobes and it may progress to lung abscess or even bronchiectasis .

. N.B:The usual site for an aspiration pneumonia are the apical and posterior segments of the lower lobe of the right lung. If the patient is supine then the aspirated material may also enter the posterior segment of the upper lobes.

Pathogens :

Pathogens of community acquired aspiration pneumonia are often the normal flora of the oropharynx including:

- streptococcus pneumoniae - staphylococcus aureus .

pathogens of nosocomial aspiration pneumonia include:-Oral anaerobes - as above -Gram-positive cocci, e.g. Peptostreptococcus spp

Risk factors:

In the absence of a tracheo-oesophageal fistula, significant aspiration usually occurs only during periods of impaired consciousness, with reflux oesophagitis with an oesophageal stricture, or in bulbar palsy.

. . Presentation/clinical picture :

SymptomsNon-specific symptoms, e.g. fever, headache, nausea, vomiting,

anorexia, myalgia, weight loss CoughDyspnoeaPleuritic chest painPurulent sputum

Signs may include: - tachycardia, tachypnoea, - decreased breath sounds and dullness to percussion over areas of consolidation, pleural friction rub - Severe infection may lead to hypoxia and septic shock

. . Investigations

Lab.: Blood count: neutrophil leucocytosis Electrolytes and renal function: dehydration, electrolyte imbalanceBlood culture

Blood gases Culture of sputum:

Many aspiration pneumonias are mixed aerobic-anaerobic infections.Chest x-ray:

-Right middle and lower lung lobes are the most common sites.

N.B : Aspiration when upright may cause bilateral lower lung infiltrates. Right upper lobe often shows consolidation in alcoholics who aspirate in the prone position.

Lung CT and bronchoscopy are only very occasionally required

. . Management

1- Mechanical obstruction: removal of object normally by bronchoscopy. Tracheal suction if seen early.

2-Intubation with positive pressure ventilation may be required. 3-Bacterial infection of lower airways :

-Initial empirical antibiotic therapy while awaiting culture results. -Hospital acquired aspiration pneumonia: a suitable combination in patients who have not already recently been treated with these antibiotics is cefuroxime plus metronidazole.

4-The role of steroids is uncertain and not of proven benefit.

Typical findings on chest radiographs are bilateral opacities in the middle or lower lung zones

Aspiration of gastric acid to bilateral dependent lungs in 60-year-old man with fever and loss of consciousness. Chest CT images (2-mm collimation, lung window setting) show extensive bilateral airspace consolidation, mainly in dependent portions of lungs.

Chest CT scan with intravenous contrast in a patient with mixed Streptococcus milleri and anaerobic empyema following aspiration pneumonia, 3 days following thoracostomy and intrapleural fibrinolysis

BronchitisIs inflammation of the mucous membranes of the bronchi, the airways

that carry airflow from the trachea into the lungs. Bronchitis can be classified into two categories, acute and chronic, each of which has unique etiologies, pathologies, and therapies.

Type:-Acute : often develops during the course of an upper respiratory

infection(URI) such as the common cold or influenza About 90% of cases of acute bronchitis are caused by viruses.

-Chronic : type of chronic obstructive pulmonary disease , is characterized by the presence of a productive cough that lasts for 3 months or more per year for at least 2 years. Chronic bronchitis most often develops due to recurrent injury to the airways caused by inhaled irritants. Cigarette smoking is the most common cause, followed by air pollution and occupational exposure to irritants, and cold air.

..Symptom..- cough with or without the production of sputum, mucus that is

expectorated (coughed up) from the respiratory tract -sore throat, runny nose, nasal congestion (coryza), low-grade fever,

pleurisy, malaise- occurs during the course of an acute viral illness such as the common

cold or influenza .

General physical signs:

-Barrel chest (increased anteroposterior diameter)-Diaphragm appears lower and flatter-Paradoxical inward movement of the lower ribs and visible interspaces during inspiration-Sternum appears elevated-The liver may become palpable as it is displaced downwards due to overinflation.-The breath sounds have a longer expiratory phase and their may be decreases air entry.-Other added sounds that may be heard on auscultation include, rhonchi and crackles.

. . Red Circled Area Shows the Location of Acute Bronchitis

. . Treatment:

Acute bronchitis is primarily symptomatic. - (NSAIDs) may be used to treat fever and sore throat.

- Decongestants can be useful in patients with nasal congestion, -expectorants may be used to loosen mucus and increase expulsion of sputum. -Cough suppressants may be used if the cough interferes with sleep or is bothersome, although coughing may be useful in expelling sputum from the airways. Even with no treatment, most cases of acute bronchitis resolve quickly.

Bronchopneumonia

.bronchopneumonia one of pneumonia classics.. As Post-operative pulmonary complication came as asequel to bronchitis and atelectasis.. Microorganism pneumococci ,staph.pseudomonas , H.influenza.

Bronchopneumonia….characterized by

1- multiple area of patchy consolidation ( an exudative patchy ) of lung parenchyma due to terminal bronchiolitis with consolidation of peribronchial alveoli.2-there is profound toximea.

Clinical picture:

As pneumonia >>>Acute onset of fever, cough, chills, pleuritic pain shortness of breath.Intensity varies with the etiological agent.

Investigation : most important are >>

-Chest X-ray reveals multiple areas of patchy mottling.- Sputum culture will reveal the responsible organisms.

Prevention

1.preoperative breathing exercises and stopping of smoking for one month pre-operatively.2.treatment of any pre-existing chest infection prior to surgery.3.reduction of obesity.4.adequate endotrachial aspiration at the end of surgery.5.pain control.6.adequate postoperative hydration.7.early treatment of atelectasis.

. Treatment

1.once diagnosis is made the treatment is immediate physiotherapy and antibiotics.2.bronchoscopic removal of secretion may be required.

Multifocal central linear and patchy opacities

High-resolution CT image at the level of the lower lung zone shows centrilobular nodular and branching opacities (tree-in-bud pattern) (straight arrows), airspace nodules (curved arrows), focal areas of consolidation and ground-glass opacities. The areas of consolidation have the size and shape consistent with involvement of one or more adjacent lobules (lobular pneumonia). The patient was a 39-year-old man with acute myelogenous leukemia and bacterial bronchopneumonia.

. .

This is an example of bronchopneumonia. Notice how the bottom-front of the lung is darker than the rest of the lung. Usually this part of the lung will be heavier than the more normal, pink lung to the left. You will need to sample the darker tissue of this lung to find out the cause of the bronchopneumonia.

Acute respiratory distress syndrome

. . Acute respiratory distress syndrome (ARDS), also known as respiratory distress syndrome (RDS) or adult respiratory distress syndrome (in contrast with IRDS) .

Define: The acute respiratory distress syndrome (ARDS) is an acute and severe

form of microvascular lung injury which is frequently seen in ICU.

characterized by diffuse capillary leak resulting in wet lung and a constellation of features secondary to it.

-This syndrome is associated with a multitude of clinical conditions which primarily damage the lung or secondarily as part of a systemic disorder.

Pathogenesis :ARDS is supposed tobe due to activity of platelets,neutrophils &

macrophages release of O2 free radicals , which cause :

-endothelial damage -oedema of lung tissue -↑ cap.permeability & Neutrophils & RBCs move inside the Alveoli , -O2 diffusion impaired

defects occurs in the 3 aspects of respiratory process:1. Ventilation. 2. Perfusion .

3. Diffusion .

. . Pathology :Mac.pic:

lung wt ↑ greatly & hemorrhagic patchy in epithelial surface.Mic.pic:

↑ oedema & hemorrhage , Alveolar oedema , perialveolar hemorrhage , ↑ intravascular fat globules & fibrin plugs .

..Cause ..

Indirect lung injury Direct lung injury

-Sepsis-Pancreatitis

-Prolonged hypothermia-Massive blood transfusion

-Multiple trauma-DIC -↑ICP

-Fat embolism

-Aspiration of gastric contents-Inhalation injury due to burns

or toxins-Airway/Chest Infection

-Near drowning-Trauma and lung contusion

-Prolonged mechanical ventilation

Clinical pictuer

-ARDS can occur within 24 to 48 hours of an injury.-ARDS patients usually presents with :

shortness of breath, Tachycardia tachypnoea cyanosis perpheral VD occasionally confusion.Bilateral fine inspiration crackles .

. . Diagnosis..

1- routine test ( CBC ,RFT , LFT ,clotting profile ,ESR &CRP )2-ABG ------------------ severe hypoxemia (PaO2 < 50 mmHg)

hypocapnia (at least in the early phase), 3-chest X-ray

Plain chest X-rays are sufficient to document bilateral alveolar infiltrates in the majority of cases.

4- pulmonary artery catheter to measuer pulmonary capillary preasuer .serious reduction in PCWP < 18 mmHg.

5-CT scanning leads to more accurate images of the pulmonary parenchyma in ARDS, it has little utility in the clinical management of patients with ARDS, and remains largely a research tool.

Dx. Chareteria:1-acute onset 2-CXR:bilateral infiltrates 3-PCWP<19 mmgh4-refractory hypoxeamia ĕ PaO2 : FiO2 < 200

N.B

ALI (Acute Lung Injury )

is the term used for patients with significant hypoxemia (PaO2/FiO2 ratio of <300)

ARDS

is the term used for a subset of ALI patients with severe hypoxemia (PaO2/FiO2 ratio of <200)

.. management..management of Acute Respiratory Distress Syndrome generally focuses on: a) preventing iatrogenic lung lesions, b) reducing water in lungs and, c) maintaining tissue oxygenation………………………………………..SO,

1- Pt admit to ( ICU ) .2-Treatment of the underlying cause is imperative.

3-Respiratory support :1-Early continuous positive airway pressure (CPAP) …40-60% O2

2- Mechanical ventilation: indicated for PaO2 <62.4 mmgh 4- Circulation support :

-hemodynamic circulation monitoring ĕ arterial line & Swan-Ganz catheter.

-fluid management ( I.V line & UOP ).-medication : Dobutamine , VD & bl.transfusion .

5- sepsis : use empirical Braod-spectrum antibiotic & do cultuer&sensvite test.6-Surfactant therapy -controlled clinical trial has

shown a significant mortality benefit of exogenous surfactant in ARDS.8- nutritional support : TPN .

. . Anteroposterior (AP) portable chest radiograph in a patient who had been in respiratory failure for 1 week with the diagnosis of acute respiratory distress syndrome. This image shows an endotracheal tube, a left subclavian central venous catheter in the superior vena cava, and bilateral patchy opacities in mostly the middle and lower lung zones.

. . . Prognosis:

=Even with optimal therapy mortality is 60%.

=Patients who recover have almost normal pulmonary function. Some diffusion defect can be residual

. Chest X-ray showing bilateral air emphysema in the pectoral muscles (sunburst sign) and above the clavicles in a ventilated patient with ARDS after blunt chest

trauma. There are bilateral residual basal pneumothoraces (lucent crescents above the diaphragm) despite the presence of patent chest drains.

. . 65 year old male who received induction chemotherapy for AML developed hypoxemic respiratory failure and was intubated. His PaO2 while receiving 100% oxygen was 55. An echocardiogram was normal. CT shows bilateral diffuse ground glass infiltrates.

• CT scan of the chest show widespread patches of interstitial and bilateral alveolar infiltrates in both lung fields, which, compared to cardiogenic pulmonary oedema, mostly involve peripheral and less parahilar regions.

Lung abscess. .Is necrosis of the pulmonary tissue and formation of cavities (more than 2 cm) containing necrotic debris or fluid caused by microbial infection.

Causes:

Conditions contributing to lung abscess :-Aspiration of oropharyngeal or gastric secretion -Septic emboli -Necrotizing pneumonia -Vasculitis: Wegener's granulomatosis -Necrotizing tumors: 8% to 18% are due to neoplasms the squamous

carcinoma of the lung is the commonest. Organisms :

-Anaerobic : Peptostreptococcus, Bacteroides, -Aerobic : Staph, Klebsiella, Haemophilus, Pseudomonas,, E. coli, Strept,

Mycobacteria -Fungi: Candida, Aspergillus -Parasites: Entamoeba histolytica,

. .Symptom..most of the patients have had symptoms for at least 2 weeks , patients

typically have:1- an intermittent febrile course2- weight loss, general malaise, and night sweats3- productive cough4- Initially, foul sputum is not observed in the course of the infection,

after cavitations occurs, putrid expectorations are quite prevalent.5- The odor of the breath and sputum of a patient with an anaerobic

lung abscess is often quite pronounced and noxious and may provide a clue to the diagnosis.

6- Hemoptysis may occasionally follow the expectoration of putrid sputum.

following staphylococcal suppurative pneumonia in infants and children lack the typical indolent recurrent course of the more common postaspiration infections. S tart with abrupt & more threatening (chills, fever, tachycardia, tachypnea, and unremitting production of putrid sputum. )

The sputum is rarely without odor because an anaerobic infection has no indolent course

. .Sings .. The physical findings are similar to those of pneumonia, with or without

a pleural effusion. Auscultation may reveal coarse rhonchi and absent breath sounds. Clubbing of the fingers is sometimes noted.

..Diagnosis..1-The diagnosis of a typical lung abscess can usually be confirmed based on history and physical examination findings2-Laboratory studies: high ESR ,CRP

Evaluation of expectorated sputum is the first step in the diagnosisPerform a Gram stain and culture and special staining for acid-fast bacteria and fungi .

Transtracheal of Transbronchial(via bronchoscopy) aspirates can also be cultured. Fibre optic bronchoscopy is often performed to exclude obstructive lesion.3-Chest Xray and other imaging studies : Abscess is often unilateral and single involving posterior segments of the upper lobes and the apical segments of the lower lobes as these areas are gravity dependent when lying down. Presence of air-fluid levels implies rupture into the bronchial tree or rarely growth of gas forming organism.

.a-chest X-ray show cavitation in Rt.mid zone of lung.B -meadiastinum CT-scan show hyperdense area with hypodense referred to air-fluid levelc-reptured cavity

. .Management..

1-Broadspectrum antibiotic to cover mixed flora is the mainstay of treatment.

2-postural drainage are also important. 3-Surgical procedures are required in selective patients for drainage or

pulmonary resection .4-Pulmonary physiotherapy .

. . This lung abscess is a build-up of fluid near the lung (A). To drain it, the patient is placed on his or her side, and an incision is made (B). A rib is exposed (C) and cut (D). The fluid in the abscess is suctioned (E), and the incision is closed around a temporary drainage tube (F).

. . This is an example of a lung abscess that is connected to the rib cage

Pulmonary Embolism:

. A pulmonary embolus clogs the artery that provides blood supply to part of the lung. The embolus not only prevents the exchange of oxygen and carbon dioxide, but it also decreases blood supply to the lung tissue itself, potentially causing lung tissue to die (infarct).

A pulmonary embolus is one of the life-threatening causes of chest pain and should always be considered when a patient presents to a healthcare provider with complaints of chest pain and shortness of breath.

. .Cause ..thrombus cause ;The most important clinically identifiable risk factors for DVT and PE are a prior history of DVT or PE, recent surgery or pregnancy, prolonged immobilization, or underlying malignancy.

Reduced mobility Burns Obesity

Old age Malignancy Acute medical illness

Behçet disease ,(CHF) ,Myocardial infarction ,Polycythemia ,SLE ,Ulcerative colitisTrauma/major surgery Pregnancy

Oral contraceptives Drug abuse (intravenous [IV] drugs)

Hemolytic anemias Heparin-associated thrombocytopenia Bleeding disorder .Venous stasis Warfarin (first few days of therapy)

. . Non-thrombus causes of pulmonary embolus are rare but include:

-fat emboli from a broken femur, -an amniotic fluid embolus in pregnancy-in some cases, tumor tissue from cancer

The presentation is the same as that of a blood clot, caused by blockage of part of the arterial tree of the lung .

..Pathophysiology..

The pathophysiology of pulmonary embolism. Although pulmonary embolism can arise from anywhere in the body, most commonly it arises from the calf veins. The venous thrombi predominately originate in venous valve pockets (inset) and at other sites of presumed venous stasis. To reach the lungs, thromboemboli travel through the right side of the heart. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.

Thrombosis in the veins is triggered by venostasis, hypercoagulability, and vessel wall inflammation. These 3 underlying causes are known as the Virchow triad. All known clinical risk factors for DVT and PE have their basis in one or more elements of the triad .

.

.. History..

(PE) is a common condition presenting to the emergency department. A study evaluating patients with potential pulmonary embolism showed 7.2% to be positive for the thromboembolism.

..Symptoms..

1- chest pain, chest wall tenderness,2- back pain, shoulder pain, upper abdominal pain, 3-syncope4- hemoptysis,

5-shortness of breath, 6-painful respiration, new onset of wheezing, or cardiac arrhythmia.

predictive value for pulmonary embolism were as follows:1-Previous history of VTE 2-Surgery within the previous 4 weeks 3-Estrogen use currently 4-Active or metastatic cancer 5-Immobilization6-Non – cancer-related thrombophilia 7-Pleuritic chest pain 8-Family history of venous thromboembolism

..Singe.. The physical examination variables from the models that had a statistically significant predictive value for pulmonary embolism were as follows:13

-Unilateral leg swelling -Hypoxemia (saturation <95%) -Pulse >94 beats per minute

Massive pulmonary embolism (PE) causes hypotension due to acute cor pulmonale, but the physical examination findings early in sub-massive PE may be completely normal.

..Diagnosis..

- D-dimer. If the test result is negative, this can rule out DVT and PE.- Chest X-ray, although this can often be normal.- Computed tomography pulmonary angiography (CTPA). A dye is

injected into your veins so that they show up on the X-ray image. This is the main imaging test that doctors use to diagnose pulmonary embolism.

- C.T.- Isotope lung scanning - this test can see how much blood is getting into

your lungs. It's sometimes done before a CTPA.- An U/S of your legs, to look for DVT.

. Westermark's sign (dilation of pulmonary vessels c possible cut-off sign) are exceedingly rare, especially if the patient presents soon after the onset of symptoms

 

. . 58-year-old woman with suspected pulmonary embolism. Pulmonary angiogram of the right pulmonary artery obtained shortly after injection of contrast reveals an embolism within the right lower lobe pulmonary artery (arrow).

41-year-old woman with chronic pulmonary embolism. Axial CT image of the chest demonstrating a mass extending outside the vessel wall with a large filling defect involving the left main pulmonary artery and extending into all sub-

branches.

Ventilation-perfusion scan showing a perfusiondefect (left) in the absence of a ventilation defect (right) in theright upper lobe, indicating a pulmonary embolism

. .Management.. ..

The therapeutic approaches to pulmonary embolism includeanticoagulation, thrombolysis and physical removalof the embolus by open operation or embolectomy.

1- AnticoagulationThe majority of patients with pulmonary embolism aretreated with anticoagulation therapy alone. A large bolus dose of heparin (10,000-15,000 units) should be administered initially and thereafterheparin is administered as a continuous infusion at adose to maintain the APTT between 50 and 80 s. Continuousinfusion up to 1500 units/h may have to be given.Uncomplicated pulmonary emboli may be safely treatedwith subcutaneous low-molecular-weight heparin, administeredonce or twice daily. Warfarin therapy can beinstituted early and there is no advantage in continuingheparin therapy for 7 or 10 days.

Warfarin therapy is continuedfor 6 months but in patients who have idiopathicpulmonary embolism or those who suffer recurrent pulmonaryembolism lifelong anticoagulation is indicated.

. . 2-Thrombolytic therapyThrombolytic therapy results in greater improvementand normalization of the haemodynamic responses topulmonary emboli than heparin alone. Thrombolytictherapy should be considered in all patients with anestablished diagnosis of pulmonary embolism withhaemodynamic compromise. However, there are manycontraindications to its use Streptokinase, urokinase and t-PA are the three agent sused for thrombolysis. Allergic reactions may occur withStreptokinase and it should be avoided if the patient had.

3-Pulmonary embolectomyAttempts to remove pulmonary emboli by thoracotomyand direct operation on the pulmonary arteries(Trendelenburg procedure), with or without bypass, are associated with a high mortality from uncontrollable pulmonary parenchymal haemorrhage. More recently, pulmonaryemboli have been aspirated from the pulmonary arteries using a special steerable cup catheter introduced via the femoral vein and steered through the right heartinto the pulmonary artery. The embolus is suctioned into the cup and the whole apparatus is withdrawn through the femoral venotomy. Several passages may be required to clear an embolus and a filter should be left in the vena cava at the end of the procedure to prevent recurrent embolism.

This technique should be considered in haemodynamically unstable patients in whom thrombolytic therapy is contraindicated. With improved skill and advances in interventional radiology, better outcomes from massive pulmonary emboli are reported .

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