PULMONARY EMERGENCIES

• BRONCHOSPASM• LARYNGOSPASM• PNEUMOTHORAX• HEMOTHORAX• PULMONARY EMBOLISM• MENDELSON SYNDROME• ACUTE RESPIRATORY DISTRESS SYNDROME• BRONCHOPNEUMONIA• RESPIRATORY FAILURE

BRONCHOSPASM

• Bronchospasm is an abnormal contraction of the smooth muscle of the bronchi, resulting in an acute narrowing and obstruction of the respiratory airway. A cough with generalized wheezing usually indicates this condition.

• Bronchospasm is a chief characteristic of asthma and bronchitis

BRONCHOSPASM

• Bronchospasm is a temporary narrowing of the bronchi (airways into the lungs) caused by contraction of the muscles in the lung walls, by inflammation of the lung lining, or by a combination of both.

• This contraction and relaxation is controlled by the autonomic nervous system. Contraction may also be caused by the release of substances during an allergic reaction.

• The bronchial muscle goes into a state of tight contraction (bronchospasm), which narrows the diameter of the bronchus. The mucosa becomes swollen and inflamed which further reduces the bronchial diameter.

BRONCHOSPASM

• addition, bronchial glands produce excessive amounts of very sticky mucus which is difficult to cough out and which may form plugs in the bronchus, further obstructing the flow of air.

• When bronchi become obstructed, greater pressures are needed to push air through them in order to meet the body's requirement for oxygen. This requires greatly increased muscular effort. Breathing during bronchospasm requires more effort than normal breathing

Causes and Risk Factors of Bronchospasm

• Excessive bronchial irritability is the root of asthma.

• Allergy. When foreign substances such as bacteria, viruses or toxic substances enter the body, one of the natural defenses is the formation of antibodies - molecules which combine with the foreign substances so as to render them harmless. This process is called immunity.

• The ones that commonly cause problems are animal dander, pollen, dusts, molds and foods. Inhalation of an allergen triggers bronchoconstriction.

Causes and Risk Factors of Bronchospasm

• Emotions. Psychological stress may trigger symptoms but asthma is not a psychosomatic disease.

• Upper Respiratory Infections.• When an asthmatic child has an upper respiratory

infection, asthma may be triggered. • Viral respiratory illnesses may produce their effect by

causing epithelial damage, producing specific Immunoglobulin E (IgE) antibodies directed against respiratory viral antigens and enhancing mediator release.

• Irritants. There is a wide variety of substances which irritate the nose, throat or bronchi. Cigarette smoke is one of the most common, but dust, aerosol sprays, and strong odors may serve as irritants

Symptoms of Bronchospasm

• Cough is a major symptom, and may be a more important symptom than wheezing in some asthmatic children, especially infants and toddlers.

• Wheezing and tightness in the chest are also very common.

Diagnosis of Bronchospasm

• Diagnosis is based upon the clinical exam in which wheezing, poor air flow and generalized signs of an asthma attack may be found. Chest x-ray may show little if any change from normal.

Treatment of Bronchospasm

• Beta2-agonists relax airway smooth muscle and may modulate mediator release from mast cells and basophils.

• Most beta-agonist drugs are prescription medications. albuterol (Proventil, Ventolin), bitolterol (Tornalate), isoetharine (Bronkometer), metaproterenol (Alupent), pirbuterol (Maxair), and terbutaline (Brethaire).

• While anti-inflammatory drugs, such as inhaled corticosteroids or cromolyn sodium, treat the underlying inflammation that causes the airways to react and narrow, beta-agonists only treat symptoms.

PNEUMOTHORAX

• a pneumothorax, or collapsed lung, is a potential medical emergency caused by accumulation of air or gas in the pleural cavity.

• A pneumothorax can occur spontaneously, or as the result of disease or injury.

ETIOLOGY

• Spontaneously (most commonly in tall slim young males and in Marfan syndrome)

• Following a penetrating chest wound • Following Barotrauma to the lungs• Chronic lung pathologies including emphysema, asthma • Acute infections • Chronic infections, such as tuberculosis • Cancer • Rare diseases that are unique to women such as

Catamenial pneumothorax (due to endometriosis in the chest cavity) and lymphangioleiomyomatosis (LAM).

• Pneumothoraces are divided into tension and non-tension pneumathoraces.

Signs and symptoms

• Sudden shortness of breath, dry coughs, cyanosis (turning blue) and pain felt in the chest, back and/or arms are the main symptoms. In penetrating chest wounds, the sound of air flowing through the puncture hole may indicate pneumothorax, hence the term "sucking" chest wound.

• Subcutaneous emphysema is another symptom.• If untreated, hypoxia may lead to loss of consciousness

and coma.• In addition, shifting of the mediastinum away from the site

of the injury can obstruct the superior and inferior vena cava resulting in reduced cardiac preload and decreased cardiac output.

• Untreated, a severe pneumothorax can lead to death within several minutes.

Signs and symptoms

• Spontaneous pneumothoraces are reported in young people with a tall, skinny stature. There is a preponderance among males, possibly because men are in general taller than women. The reason for this association, while unknown, is hypothesized to be the presence of subtle abnormalities in connective tissue.

• Pneumothorax can also occur as part of medical procedures, such as the insertion of a central venous catheter (an intravenous catheter) in the subclavian vein or jugular vein. While rare, it is considered a serious complication and needs immediate treatment.

• Other causes include mechanical ventilation, emphysema and quite rarely other lung diseases (pneumonia).

Diagnosis

• The absence of audible breath sounds through a stethoscope can indicate that the lung is not unfolded in the pleural cavity. This accompanied by (higher pitched sounds than normal) to percussion of the chest wall is suggestive of the diagnosis. auscultation

• If the signs and symptoms are doubtful, an X-ray of the chest can be performed, but in severe hypoxia, or evidence of tension pneumothorax emergency treatment has to be administered first.

• .

Clinical treatment•

• Small pneumothoraces often are managed with no treatment other than repeat observation via Chest X-rays, but most patients admitted will have oxygen administered since this has been shown to speed resolution of the pneumothorax

• Pneumothoraces which are too small to require tube thoracostomy and too large to leave untreated, have been aspirated with a needle to remove the pressure, although this technique is usually reserved for tension pneumothoraces.

TREATMENT

• Larger pneumothoraces may require tube thoracostomy, also known as chest tube placement. If a thorough anesthetizing of the parietal pleura and the intercostal muscles is performed, the only major pain experienced should be either the injury that caused the pneumothorax or the re-expanding of the lung.

• The tip of the syringe that contains the anesthetic is now in the intercostal muscles. A proper and sizable injection should ensue.

• A tube is then inserted into the chest wall outside the lung and air is extracted using a simple one way valve

TREATMENT

• This allows the lung to re-expand within the chest cavity. This re-expansion usually lasts for approximately 15–30 seconds depending on the size of the pneumothorax and feels as if your breath has been taken away

• This response is normal and should pass fairly quickly. The pneumothorax is followed up with repeated X-rays.

• If the pneumothorax has resolved and there is no further air leak, the chest tube removed

Spontaneous pneumothorax

• The most common cause is chronic obstructive pulmonary disease (COPD). However, there are several other diseases that may also lead to spontaneous pneumothorax:

• Tuberculosis • Pneumonia • Asthma • Cystic fibrosis • Lung cancer • Interstitial lung disease • Marfan syndrome

HEMOTHORAX

• Cause and presentation• Its cause is usually traumatic, from a blunt or

penetrating injury to the thorax, resulting in a rupture of either of the serous membrane lining the thorax and covering the lungs.

• This rupture allows blood to spill into the pleural space, equalizing the pressures between it and the lungs. Blood loss may be massive in people with these conditions, as each side of the thorax can hold 30%-40% of a person's blood volume.

Prognosis

• If left untreated, the condition can progress to a point where the blood accumulation begins to put pressure on the mediastinum and the trachea, effectively limiting the amount that the heart's ventricles are able to fill. The condition can cause the trachea to deviate, or move, toward the unaffected side.

Signs and symptoms• Tachypnea • Dyspnea • Cyanosis • Decreased or absent breath sounds on affected side • Tracheal deviation • Dull resonance on percussion • Unequal chest rise • Tachycardia • Hypotension • Pale, cool, clammy skin • Possibly subcutaneous emphysema • Narrowing pulse pressure

Management

• A hemothorax is managed by removing the source of bleeding and by draining the blood already in the thoracic cavity.

• Blood in the cavity can be removed by inserting a drain (chest tube) in a procedure called a tube thoracostomy. Patients should recover swiftly after this. However, if the cause is rupture of the aorta in , the intervention by a thoracic surgeon is mandatory.

• Thrombolytic agents have been used

LARYNGOSPASM

• Is a reflex closure of the vocal cords that may occur in anesthetized patients when the vocal cords are irritated by secretions or when a patient experiences apainful stimulus

• Total occlusion due to laryngospasm is characterized by absence of sound because is no air movement

TREATMENT OF LARYNGOSPASM

• Is by application of the head-tilt-jaw-thrust maneuver while applying positive airway pressure by means of a face mask connected to a delivery system containing 100% oxygen

• If laryngospasm persists despite this treatment and signs of arterial oxygen desaturation develop it is imperative to administer a shortacting muscle relaxant intravenously such as succinylcholine 0,2-0,5 mg/kg

PULMONARY EMBOLISM

• Pulmonary embolism (PE) is a blockage of the pulmonary artery or one of its branches, usually occurring when a deep vein thrombus (blood clot from a vein) becomes dislodged from its site of formation and travels, or embolizes, to the arterial blood supply of one of the lungs. This process is termed thromboembolism.

PULMONARY EMBOLISM

• Common symptoms include difficulty breathing, chest pain on inspiration, and palpitations. Clinical signs include low blood oxygen saturation (hypoxia), rapid breathing (tachypnea), and rapid heart rate (tachycardia).

• Severe cases of untreated PE can lead to collapse, circulatory instability, and sudden death

PULMONARY EMBOLISM

• Diagnosis is based on these clinical findings in combination with laboratory tests and imaging studies.

• While the gold standard for diagnosis is the finding of a clot on pulmonary angiography, CT pulmonary angiography is the most commonly used imaging modality today.

PULMONARY EMBOLISM

• The most common sources of embolism are proximal leg deep venous thrombosis (DVTs) or pelvic vein thromboses. Any risk factor for DVT also increases the risk that the venous clot will dislodge and migrate to the lung circulation, which happens in up to 15% of all DVTs.

• The conditions are generally regarded as a continuum termed venous thromboembolism (VTE).

• The development of thrombosis is classically due to a group of causes named Virchow's triad (alterations in blood flow, factors in the vessel wall and factors affecting the properties of the blood). Often, more than one risk factor is present.

PULMONARY EMBOLISM

• Factors in the vessel wall: of limited direct relevance in VTE

• Factors affecting the properties of the blood (procoagulant state):

• Estrogen-containing hormonal contraception • Genetic thrombophilia (factor V Leiden,). • Acquired thrombophilia (

antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria

TREATMENT

• Treatment is typically with anticoagulant medication, including heparin and warfarin.

• Severe cases may require thrombolysis with drugs such as tissue plasminogen activator (tPA) or may require surgical intervention via pulmonary thrombectomy

Surgical management

• Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently.

• Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.

MENDELSON SYNDROME

• Mendelson's syndrome is chemical pneumonia caused by aspiration during anaesthesia, especially during pregnancy.

MENDELSON SYNDROME

• Mendelson's syndrome is characterised by a reaction following aspiration of gastric content during general anaesthesia due to abolition of the laryngeal reflexes.

• The main clinical features, which may become evident within two to five hours after anaesthesia, consist of cyanosis, dyspnea,pulmonary wheeze,crepitante rales, , , rhonchi, decreased arterial oxygen tension , and , associated with a high BP.

• Pulmonary edema can cause sudden death or death may occur later from pulmonary complications. It occurs predominantly in association with obstetric anesthesia.

Treatment

• The risk may be reduced by administering Ranitidine.

ACUTE RESPIRATORY DISTRESS SYNDROME

• ARDS is a severe lung disease caused by a variety of direct and indirect issues. It is characterized by inflammation of the lung parenchyma leading to impaired gas exchange with concomitant systemic release of causing inflammation, hypoxemia and frequently resulting in multiple organ failure.

• This condition is often fatal, usually requiring mechanical ventilation and admission to an intensive care unit.

• A less severe form is called acute lung injury (ALI).

ARDS

• ARDS was defined as the ratio of arterial partial oxygen tension (PaO2) as fraction of inspired oxygen (FiO2) below 200 mmHg in the presence of bilateral on the chest x-ray.

• These infiltrates may appear similar to those of left ventricular failure, but the cardiac silhouette appears normal in ARDS. Also, the pulmonary capillary wedge pressure is normal (less than 18 mmHg) in ARDS, but raised in left ventricular failure.

• A PaO2/FiO2 ratio less than 300 mmHg with bilateral infiltrates indicates acute lung injury (ALI). Although formally considered different from ARDS, ALI is usually just a precursor to ARDS.

ARDS

• ARDS is characterized byAcute onset • Bilateral infiltrates on chest radiograph • Pulmonary artery wedge pressure < 18 mmHg

(obtained by pulmonary artery catheterization), if this information is available; if unavailable, then lack of clinical evidence of left ventricular failure suffices

• if PaO2:FiO2 < 300 mmHg acute lung injury (ALI) is considered to be present

• if PaO2:FiO2 < 200 mmHg acute respiratory distress syndrome (ARDS) is considered to be present

ARDS

• ARDS can occur within 24 to 48 hours of an injury or attack of acute illness. In such a case the patient usually presents with shortness of breath, tachypnea, and symptoms related to the underlying cause, i.e. shock.

• ARDS is classically associated with hypoxemia, petechiae in the axillae and neurologic abnomalities such as mental confusion

• Long term illnesses can also trigger it, eg malaria. The ARDS may then occur sometime after the onset of a particularly acute case of the infection.

ARDS

• An arterial blood gas analysis and chest X-ray allow formal diagnosis by inference using the aforementioned criteria. Although severe hypoxemia is generally included, the appropriate threshold defining abnormal PaO2 has never been systematically studied.

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

TREATMENT

• Acute respiratory distress syndrome is usually treated with mechanical ventilation in the Intensive Care Unit. Ventilation is usually delivered through oro-tracheal intubation, or tracheostomy whenever prolonged ventilation (≥2 weeks) is deemed inevitable.

• The possibilities of are limited to the very early period of the disease or, better, to prevention in individuals at risk for the development of the disease (atypical pneumonias, pulmonary contusion, major surgery patients

TREATMENT

• Appropriate antibiotic therapy must be administered as soon as microbiological culture results are available.

• Empirical therapy may be appropriate if local microbiological surveillance is efficient. More than 60% ARDS patients experience a (nosocomial) pulmonary infection either before or after the onset of lung injury.

• The origin of infection, when surgically treatable, must be operated on. When sepsis is diagnosed, appropriate local protocols should be enacted

ARDS TREATMENT

• Pressure Regulated Volume Control

• The overall goal is to maintain acceptable gas exchange and to minimize adverse effects in its application.

• Three parameters are used: PEEP (positive end-expiratory pressure, to maintain maximal recruitment of alveolar units), mean airway pressure (to promote recruitment and predictor of hemodynamic effects) and plateau pressure (best predictor of alveolar overdistention).

ARDS TREATMENT

• The ARDS Clinical Network, or ARDSNet, completed a landmark trial that showed improved mortality when ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg. Low tidal volumes (Vt) may cause hypercapnia and atelectasis due to their inherent tendency to increase dead space.

• . Plateau pressure less than 30 cm H2O was a secondary goal,

ARDS TREATMENT

• Positive end-expiratory pressure

• Positive end-expiratory pressure (PEEP) must be used in mechanically-ventilated patients in order to contrast the tendency to collapse of affected alveoli.

ARDS TREATMENT

• Prone position• Distribution of lung infiltrates in acute respiratory

distress syndrome is non-uniform. Repositioning into the prone position (face down) might improve oxygenation by relieving atelectasis and improving perfusion. However, although the hypoxemia is overcome there seems to be no effect on overall survival

• Fluid management• Several studies have shown that pulmonary

function and outcome are better in patients that lost weight or was lowered by diuresis or fluid restriction

ARDS TREATMENT

• Corticosteroids• The initial regimen consists of methylprednisolone

2 mg/kg daily. After 3-5 days a response must be apparent. In 1-2 weeks the dose can be tapered to methylprednisolone 0.5-1.0 mg daily. Patients with ARDS do not benefit from high-dose corticosteroids

• Nitric oxide• Inhaled nitric oxide (NO) potentially acts as

selective pulmonary vasodilator. Rapid binding to hemoglobin prevents systemic effects. It should increase perfusion of better ventilated areas.

ARDS

• Pulmonary: barotrauma (volutrauma), pulmonary embolism (PE), pulmonary fibrosis, ventilator-associated pneumonia (VAP).

• Gastrointestinal: hemorrhage (ulcer), dysmotility, pneumoperitoneum, bacterial translocation.

• Cardiac: arrhythmias, myocardial dysfunction. • Renal: acute renal failure (ARF), positive fluid balance. • Mechanical: vascular injury, pneumothorax (by placing

pulmonary artery catheter), tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube.

• Nutritional: malnutrition (catabolic state), electrolyte deficiency.

ARDS

• Mechanical ventilation, sepsis, pneumonia, shock, aspiration, trauma (especially pulmonary contusion), major surgery, massive transfusions, smoke inhalation, drug reaction or overdose, fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy may all trigger ARDS

• . Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients. Pneumonia and sepsis may be either causes or complications of ARDS.

• The mortality rate varies from 30% to 85.

RESPIRATORY FAILURE

• describe inadequate gas exchange by the respiratory system, with the result that arterial oxygen and/or carbon dioxide levels cannot be maintained within their normal ranges.

• A drop in blood oxygenation is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia.

• The normal reference values are: oxygen PaO2 > 60 mmHg, and carbon dioxide PaCO2 < 45 mmHg.

RESPIRATORY FAILURE

• respiratory failure is defined as hypoxaemia without hypercapnia, indeed the CO2 level may be normal or low. It is typically caused by a ventilation/perfusion mismatch; the air flowing in and out of the lungs is not matched with the flow of blood to the lungs.Basic defect in type 1 respiratory failure is failure of oxygenation characterized by: PaO2-low(<60mmhg) PaCO2_normal/low(</=49mm hg) PA-aO2-increased This type is caused by conditions that affect oxygenation like:

• Parenchymal disease(V/Q mismatch) • Diseases of vasculature and shunts: right to left shunt,

ARDS, pneumonia

BRONCHOPNEUMONIA

• Bronchopneumonia is more likely than lobar pneumonia to be associated with Streptococcus.[3]

• The bronchopneumonia pattern has been associated with hospital-acquired pneumonia, and with specific organisms such as Staphylococcus aureus, Klebsiella, E. coli, and Pseudomonas.[4]

• In bacterial pneumonia, invasion of the lung parenchyma by bacteria produces an . This response leads to a filling of the alveolar sacs with exudate. The loss of air space and its replacement with fluid is called consolidation. In bronchopneumonia, or lobular pneumonia, there are multiple foci of isolated, acute consolidation, affecting one or more pulmonary lobes.

BRONCHOPNEUMONIA

• should be noted that although these two patterns of pneumonia, lobar and lobular, are the classic anatomic categories of bacterial pneumonia, in clinical practice the types are difficult to apply, as the patterns usually overlap. Bronchopneumonia (lobular) often leads to lobar pneumonia as the infection progresses.

• From the clinical standpoint, far more important than distinguishing the anatomical subtype of pneumonia, is identifying its causative agent and accurately assessing the extent of the disease

BRONCHOPNEUMONIA

• lobular pneumonia is a type of pneumonia characterized by multiple foci of isolated, acute consolidation, affecting one or more pulmonary lobes.

• It is one of two types of bacterial pneumonia as classified by gross anatomic distribution of consolidation (solidification), the other being lobar pneumonia

Type 2

• Type 2 respiratory failure is caused by increased airway resistance; both oxygen and carbon dioxide are affected. Defined as the build up of carbon dioxide that has been generated by the body.

• The underlying causes include:• Reduced breathing effort (in the fatigued patient) • Increased resistance to breathing (such as in

asthma) • A decrease in the area of the lung available for

gas exchange (such as in emphysema).

Causes

• •

• Chest X-ray showing ARDS• Pulmonary dysfunction

– Asthma – Emphysema – Chronic Obstructive Pulmonary Disease – Pneumonia – Pneumothorax – Pulmonary contusion– Hemothorax – Acute Respiratory Distress Syndrome (ARDS) is a specific

and life-threatening type of respiratory failure. – Cystic Fibrosis

Causes

• Cardiac dysfunction – Pulmonary edema – Cerebrovascular Accident – Arrhythmia – Congestive heart failure – Valve pathology

• Other – Fatigue due to prolonged tachypnoea in

metabolic acidosis – Intoxication with drugs (e.g. morphine,

benzodiazepines) that suppress respiration. – Neurological Disease – Toxic Epidermal Necrolysis

TREATMENT

• •

• Mechanical Ventilator• Emergency treatment follows the principles of

cardiopulmonary resuscitation.• Treatment of the underlying cause is required.

Endotracheal intubation and mechanical ventilation may be required.

• Respiratory stimulants such as doxapram may be used, and if the respiratory failure resulted from an overdose of sedative drugs such as opioids or benzodiazepines, then the appropriate antidote such as naloxone or flumazenil will be given.

Ventilation/perfusion ratio

• In respiratory physiology, the ventilation/perfusion ratio (or V/Q ratio) is a measurement used to assess the efficiency and adequacy of the matching of two variables"V" - ventilation - the air which reaches the lungs

• "Q" - perfusion - the blood which reaches the lungs

Ventilation

• Gravity and lung’s weight act on ventilation by increasing pleural pressure at the base (making it less negative) and thus reducing the alveolar volume. However at these smaller volumes the alveoli are more compliant (more distensible) and so capable of wider oxygen exchanges with the external environment. On the other side the apex, though showing a higher oxygen partial pressure, ventilates less efficiently since its compliance is lower and so smaller volumes are exchanged.

Perfusion

• The impact of gravity on pulmonary perfusion expresses itself as the hydrostatic pressure of the blood passing through the branches of the pulmonary artery in order to reach the apical and basal district of the lung, acting respectively against or synergistically with the pressure developed by the right ventricle. Thus at the apex of the lung the resulting pressure can be insufficient for developing a flow (which can be sustained only by the negative pressure generated by venous flow towards the left atrium) or even for preventing the collapse of the vascular structures surrounding the alveoli, while the base of the lung shows an intense flow due to the higher resulting pres

VENTILATION/PERFUSION

• The V/Q ratio can be measured with a ventilation/perfusion scan.

• An area with no ventilation (and thus a V/Q of zero) is termed "shunt." An area with no perfusion (and thus a V/Q of infinity) is termed dead space