Pertussis (Whooping Cough)

Definition
Pertussis (Whooping Cough) is an acute disease of the respiratory tract. Found in children younger than 5 years, especially in children age 2-3 years.

Cause
Pertussis is caused by gram-negative Bordetella Pertussis.

Clinical Overview
These symptoms occur 1-2 weeks after contact with the infected person and preceded by an incubation period of 7-14 days. Typically, the disease lasts for 6 weeks or more. That is why the disease is called cough hundred days.
On his way, pertussis includes several stages, namely:

• Kataralis which marked the onset of a mild cough, especially at night, accompanied by mild fever and runny nose. This stage lasts 1-2 weeks. In the catarrhal stage indistinguishable from that caused by a viral respiratory infection
• Second is the spasmodic stage lasts 2-4 weeks. Symptoms, cough more often, people with sweat, and blood vessels in the face of wide-neck. Long coughing attack usually ends with a distinctive high-pitched sound (whooping caugh) and accompanied by vomiting. Subconjunctival frequent bleeding and / or epistaxis. Nails and lips become blue because the blood of patients a lack of oxygen. Beyond the attacks, the patient looked healthy.
• In the next stage, namely convalescence, going for two weeks. Symptoms, cough subsided and the patient gradually began to increase appetite.

Diagnosis

• Increased serum IgA specific Bordatella pertussis
• Detected Bordatella pertussis from nasopharyngeal specimens
• Nasopharyngeal swab culture was found Bordatella pertussis

Management

• Pertussis treatment aimed at infecting with appropriate antibiotics, such as erythromycin 30-50 mg / kg 4 times daily.
• Codeine for cough may be given 0.5 mg / year / time.
• Pertussis can be prevented by immunization of DPT (Diphtheria-Pertussis-Tetanus). This immunization is given three times in a row in infants aged three, four, five months.

Rating: 4.5

Cough - Causes and Complications

Cough Reflex
Cough reflex consists of five main components, ie, cough receptors, afferent nerve fibers, central cough, nervous system and efferent effectors. A cough begins with a stimulus on cough receptor. These receptors are non-myelinated nerve fibers in the form of finely located both inside and outside the thoracic cavity. Located within the thoracic cavity, among others, contained in the larynx, trachea, bronchi and the pleura. Will decrease the number of receptors on the branches of a small bronchus, and a large number of receptors found in the larynx, trachea, carina and bronchus branching region. The receptors are also found even in the ear canal, stomach, hilum, paranasalis sinus, pericardial and diaphragm.
The most important afferents exist in the branch of the vagus, which excitatory flow of the larynx, trachea, bronchus, pleura, stomach, and also stimulate the ear through the Arnold branch of n. Vagus. Trigeminal nerve stimulation of the sinus paranasalis channeling, channeling glosofaringeus nerve stimulation of the pharynx and channel phrenic nerve stimulation of the pericardium and diaphragm.

Causes of Cough
Cough in outline can be caused by excitatory as follows:
Inflammatory stimuli such as mucosal edema with a lot of tracheobronchial secretions.
Mechanical stimuli such as foreign body in airway foreign body such as the respiratory tract, post nasal drip, retention of bronchopulmonary secretions.
Temperature stimuli such as cigarette smoke (an oxidant), heat / cold, gas inhalation.
Psychogenic stimuli.

Some causes of cough

• Irritant

- Cigarettes
- Smoke
- SO2
- Gas in the workplace

• Mechanical

- Retention of bronchopulmonary secretions
- Foreign body in respiratory tract
- Post nasal drip
- Aspiration

• Obstructive Pulmonary Disease

- Chronic Bronchitis

- Asthma

- Emphysema

- Firbrosis cystic

- Bronchiectasis

• Restrictive Lung Disease

- Pneumoconiosis
- Diseases of collagen
- Granulomatous Disease

• Infection

- Acute Laryngitis

- Acute Brochitis

- Pneumonia

- Pleurisy

- Pericarditis

• Tumor

- Laryngeal tumors

- Lung Tumors

• Psychogenic
• Other

Complications of Cough
At the time of coughing intrathoracic pressure rises to 300 mmHg. Pressure elevation is required to produce an effective cough, but this can lead to complications in the lungs, musculoskeletal, cardiovascular system and central nervous system.

Pneumomediastinum may arise in the lung, may also occur pneumoperitonium and pneumoretropritonium but this is very rare. Another complication was pneumothorax and emphysema, complications muskuloskletal, broken ribs, ruptured abdominal rectus muscle. Cardiovascular complications may include bradycardia, subconjungtiva vein laceration, nose and anus as well as cardiac arrest.

In the central nervous system can occur cough syncope, due to increased intrathoracic pressure occurs reflex vasodilation of systemic arteries and veins. This leads to decreased cardiac output and sometimes berkibat low arterial pressure resulting in loss of consciousness. Syncope occurred a few seconds after the paroxysmal cough.

Can also occur among other constitutional symptoms of insomnia, fatigue, decreased appetite, vomiting, elevated body temperature and headaches. Another complication is urinary incontinence, hernias and prolapse of the vagina.

Cough - Definition and Mechanisms

Cough
Cough is a symptom of the most common disease in which the prevalence was found in about 15% in children and 20% in adults. One out of ten patients who visited the doctor's office each year has a chief complaint of cough. Coughing can cause bad feelings, sleep disorders, affecting daily activities and reduce quality of life.

Cough is a complex physiological reflex that protects the lung from mechanical trauma, chemical and temperature. Coughing is also a natural defense mechanism of lung airway to keep it clean and open to the street:
Prevent the entry of foreign objects into the respiratory tract.
Remove foreign objects or abnormal secretions from the respiratory tract.
Coughing becomes physiologically when perceived as a nuisance. Such a cough is often a sign of a disease within or outside the lungs and sometimes are the early symptoms of a disease. Cough may be very significant on the transmission of disease through the air (air-borne infection). Cough is one of the symptoms of respiratory tract diseases in addition to tightness, wheezing, and chest pain. Often the cough is a problem faced by physicians in their daily work. The reason is very diverse and the introduction of the pathophysiology of cough would be very helpful in establishing the diagnosis and prevention of people with coughs. Research shows that in patients with acquired chronic cough 628 cough up to 761 times / day. Patients with pulmonary TB coughs number about 327 times / day and patients with influenza-even up to 154.4 times / day.
Epidemiological studies have shown that many chronic cough associated with smoking. Twenty-five percent of those who smoked 1 / 2 pack / day will have to cough, while the patients who smoked one pack per day will be found to be approximately 50% of chronic cough. Most of the heavy smokers who smoked 2 packs / day will complain of chronic cough. Large-scale research in the U.S. also found that 22% of non-smokers also suffer from cough, among others, caused by chronic diseases, air pollution and others. Coughing can also cause various complications such as pneumothorax, pneumomediastinum, headache, fainting, disc herniation, inguinal hernia, broken ribs, bleeding subkonjungtiva, and urinary incontinence.

Definition
Cough in Latin called tussis is a reflex that can occur suddenly and often repeated that aims to help clear mucus from the respiratory tract of, irritants, foreign particles and microbes. Coughing can happen voluntarily or involuntarily.
Coughing is a reflex action in the respiratory tract that is used to clean the upper airways. Chronic cough lasts more than 8 weeks are common in the community. Causes include smoking, exposure to cigarette smoke, and exposure to environmental pollutants, especially particulates.

Mechanism of Occurrence of Cough
Cough starts from a cough receptor stimulation. These receptors are non-myelinated nerve fibers in the form of finely located both inside and outside the thoracic cavity. Located within the thoracic cavity, among others, contained in the larynx, trachea, bronchus, and pleura. Will decrease the number of receptors on the branches of a small bronchus, and a large number of receptors in the can in the larynx, trachea, carina and bronchus branching region. The receptors are also found even in the ear canal, stomach, hilum, paranasalis sinus, pericardial, and diaphragm.

Mechanism Of Cough

Afferent fibers are the most important branch of the vagus on the drain stimuli from larynx, trachea, bronchus, pleura, stomach, and also stimulation of the ear through the Arnold branch of the vagus. Trigeminal nerve stimulation of the sinus paranasalis channel, glosofaringeus nerve, excitatory channel of the pharynx and channel phrenic nerve stimulation of the pericardium and diaphragm.

By excitatory afferent fibers was taken to the cough center located in the medulla, near the center of the respiratory and vomiting centers. Then from here by afferent fibers of the vagus, phrenic nerve, intercostal and lumbar nerves, the trigeminal nerve, facial nerve, nerve hipoglosus, and others headed to the effector. These effector standing of the muscles of the larynx, trachea, bronchi, diaphragm, intercostal muscles, and others. In the area of ​​this effector mechanism of cough ensued.

Phase of Cough

Basically the mechanism of cough can be divided into four phases, namely:


1. Phase irritation
Irritation of one sensory vagus nerve in the larynx, trachea, large bronchi, or afferent fibers from the pharyngeal branch glosofaringeus nerve can cause coughing. Coughing also arise when the cough receptors in the lining of the pharynx and esophagus, pleural cavity and external ear canal is stimulated.

2. Phase of inspiration
In the inspiration phase of the glottis is wide open due to reflex muscle contraction abduktor aritenoidea cartilage. Inspiration occurs in and quickly, so the air quickly and in large quantities into the lungs. This is accompanied terfiksirnya rib due to muscle contraction under the thorax, abdomen and diaphragm, so that the lateral dimension enlarged breasts lead to increased lung volume. The entry of air into the lungs by the number of lots of benefits that will strengthen the expiratory phase resulting in faster and stronger and reduce the air cavity is closed so as to produce a potential cleaning mechanism.

3. Compression phase
This phase begins with the closing of the glottis due to contraction of the adductor muscle aritenoidea cartilage, glottis closed for 0.2 seconds. In this phase the intrathoracic pressure rises to 300 cmH2O to place an effective cough. Pleural pressure remained elevated for 0.5 seconds after the glottis open. Coughing can occur without glottis closure because of expiratory muscles to increase intrathoracic pressure although the glottis remains open.

4. Expiratory phase / expulsion
In this phase the glottis opens suddenly due to active contraction of expiratory muscles, so there was spending large amounts of air at high speed accompanied by spending foreign objects and other materials. Movement glottis, respiratory muscles and the branches of the bronchus is important in the mechanism of cough phase and this phase of cough is actually happening. Cough sound varies greatly due to vibration secretions in the respiratory tract or the vibration of vocal cords

Cough - Causes and Complications
Management of Cough

Pulmonary Edema

Definitions

Edema, in general, means swelling. This typically occurs when fluid from the inside of blood vessels leak out of blood vessels into surrounding tissues, causing swelling. This can occur because of too much pressure in blood vessels or there is not enough proteins in the blood stream to hold the liquid in the plasma (part of blood that does not contain any blood cells).
Pulmonary Edema is the term used when edema occurs in the lungs. The area immediately outside of the small blood vessels in the lung occupied by air pockets are very small, called alveoli. This is where oxygen from the air through which blood is taken by, and carbon dioxide in the blood released into the alveoli to exhaled out. Normal alveoli have very thin walls that allow air exchange, and liquids are usually kept away from the walls of the alveoli-dindig unless it loses its integrity.
Pulmonary edema is an accumulation of fluid in the lungs due to sudden increase in intravascular pressure. Pulmonary edema is due to the flow of fluid from the blood into the space next to interstisial pulmonary alveoli of the lungs, exceeding the liquid back into the blood stream or through lymphatic channels.
Pulmonary edema is a condition caused by excess fluid in the lungs. This fluid collects in the air sacs in the lungs of many, making it difficult to breathe. In most cases, heart problems cause pulmonary edema. But fluid can accumulate due to other reasons, including pneumonia, exposure to certain toxins and drugs, and sports or live at high altitude.
Pulmonary edema is the term used when edema occurs in the lungs. Pulmonary edema is a condition caused by excess fluid in the lung.

Causes
1. Imbalance of Starling Forces:

a) Increased pulmonary capillary pressure:

• Increased pulmonary venous pressure in the absence of left ventricular dysfunction (mitral stenosis).
• Increased pulmonary venous pressure secondary because of impaired left ventricular function.
• Increased pulmonary capillary pressure secondary because of increased pulmonary artery pressure (over-perfusion pulmonary edema).

b) Decrease in plasma oncotic pressure.

• Hypoalbuminemia secondary because of kidney disease, liver, protein-losing enteropaday, dermatological diseases or nutritional diseases.

c) Increased negative pressure intersisial:

• Taking too fast pneumothorax or pleural effusion (unilateral).
• A highly negative pleural pressure due to acute airway obstruction in conjunction with an increase in end-expiratory volume (asthma).

d) Increased oncotic pressure intersisial.

• Until now there has been no example of a trial or clinic.

2. Changes in alveolar-capillary membrane permeability (Adult Respiratory Distress Syndrome)

a) Pneumonia (bacteria, viruses, parasites).
b) The material inhaled toxic (phosgene, ozone, chlorine, smoke, Teflon ®, NO2, etc.).
c) Foreign material in the circulation (snake venom, bacterial endotoxins, alloxan, alpha-naphthyl Thiourea).
d) Aspiration of gastric acid.
e) Acute radiation pneumonitis.
f) Material endogenous vasoactive (histamine, kinin).
g) Disseminated intravascular coagulation.
h) Immunology: hypersensitivity pneumonitis, drug nitrofurantoin, leukoagglutinin.
i) Shock Lung therefore outside the thoracic trauma.
j) Bleeding Acute Pancreatitis.

3. Lymphatic insufficiency:

a) Post Lung Transplant.
b) Lymphangitic carcinomatosis.
c) fibrosing lymphangitis (silicosis).

4. Not known / not clear

a) High Altitude Pulmonary Edema.
b) Neurogenic Pulmonary Edema.
c) Narcotic overdose.
d) Pulmonary embolism.
e) Eclampsia
f) Post cardioversion.
g) Post Anesthesia.
h) Post Cardiopulmonary Bypass.

Classification
Based on the cause, is divided into 2 pulmonary edema, cardiogenic and non-cardiogenic. It is important to know because its treatment is very different. Cardiogenic Pulmonary Edema due to Left Heart Terrible any reason. Acute Cardiogenic Pulmonary Edema is caused by the presence of Acute Left Heart Sucks. But with the precipitation factors, may occur also in patients with Chronic Left Heart Sucks.

» Cardiogenic pulmonary edema
Edema, cardiogenic pulmonary edema is caused by abnormalities in the heart organ. For example, the heart does not work properly as the heart pumps are not good or strong the heart is not pumping anymore.
Cardiogenic pulmonary edema resulting from high pressure in blood vessels of the lungs caused by poor heart function. Congestive heart failure caused by poor cardiac pump function (coming from a variety of causes such as arrhythmias and diseases or weakness of the heart muscle), heart attacks, or heart valves can lead to abnormal accumulation of more than the usual amount of blood in blood vessels of the lungs. This can, in turn, causes the fluid from the blood vessels are pushed out into the alveoli when the pressure is growing.

» Non-cardiogenic pulmonary edema
Non-cardiogenic pulmonary edema is that edema is usually caused by the following:

• Acute respiratory distress syndrome (ARDS). In ARDS, the integrity of the alveoli become compromised as a result of an underlying inflammatory response, and this menurus on a leaky alveoli that can be filled with fluid from blood vessels.
• A potentially serious condition caused by severe infections, trauma, lung injury, inhalation of toxins, lung infections, smoking cocaine, or radiation to the lungs.
• Renal failure and inability to remove fluid from the body can cause a buildup of fluid in blood vessels, resulting in pulmonary edema. In people with advanced kidney failure, dialysis may be necessary to remove excess body fluids.
• High altitude pulmonary edema, which can occur due to a rapid rise to high altitudes over 10,000 feet.
• Traumatic brain, bleeding in the brain (intracranial hemorrhage), severe seizures, or brain surgery can sometimes result in accumulation of fluid in the lungs, causing neurogenic pulmonary edema.
• Lung expanding rapidly can sometimes lead to a re-expansion pulmonary edema. This may occur in cases when a collapsed lung (pneumothorax) or large amounts of fluid around the lungs (pleural effusion) was issued, resulting in rapid expansion of the lung. This can result in pulmonary edema only on the affected side (unilateral pulmonary edema).
• Rarely, overdose on heroin or methadone can lead to pulmonary edema. An overdose of aspirin or the use of high doses of aspirin can lead to chronic aspirin intoxication, especially in the elderly, which may cause pulmonary edema.
• Other causes are less frequent than non-cardiogenic pulmonary edema may include pulmonary embolism (blood clot that had walked into the lungs), acute lung injury related to transfusion or transfusion-related acute lung injury (TRALI), some infections -viral infection, or eclampsia in pregnant women.

Pathophysiology
Pulmonary edema occurs when the alveoli are filled with excess fluid that seeps out of blood vessels in the lungs instead of air. This can cause problems with gas exchange (oxygen and carbon dioxide), resulting in difficulty breathing and poor blood pengoksigenan. Occasionally, this can be referred to as "water in the lungs" when describing this condition in patients. Pulmonary edema can be caused by many different factors. He can be connected in heart failure, called cardiogenic pulmonary edema, or linked to other causes, referred to as non-cardiogenic pulmonary edema.

Clinical Manifestations
The most common symptoms of pulmonary edema is shortness of breath. This is probably a gradual onset if the process develops slowly, or he may have a sudden onset in cases of acute pulmonary edema. Other common symptoms may include fatigue, shortness of breath develop faster than normal with usual activities (Dyspnea on Exertion), rapid breathing (tachypnea), dizziness, or weakness.
Low blood oxygen levels (hypoxia) may be detected in patients with pulmonary edema. Furthermore, upon examination of the lungs with a stethoscope, the doctor may hear abnormal lung sounds, rales or crackles crate (short boiling sounds disjointed, which corresponds to the muncratan fluid in the alveoli during breathing).
Clinical manifestations Pulmonary Edema specifically also divided into 3 stages:
Stage 1.
The existence of small blood vessels distended and prominent lung would improve gas exchange in lungs and slightly increase the capacity of diffusion of CO gas. Complaints at this stage may just be a shortness of breath while working. Physical examination is also not clearly found abnormalities, except maybe the inspiration for ronkhi at the time of opening of the closed airway during inspiration.
Stage 2.
At this stage intersisial pulmonary edema. Limit pulmonary blood vessels become blurred, so too the hilum also become blurred and interlobularis thickened septa (Kerley B lines). By accumulation of fluid in the loose network of inter-sisial, will further reduce the small airways, especially in the basal area because of the influence of gravity. Might also occur bronkhokonstriksi reflex. Often there is takhipnea. Although this is a sign of impaired left ventricular function, but takhipnea also help pump lymph flow is slowed so that the buildup of fluid intersisial. On examination there was little change in spirometry alone.
Stage 3.
At this stage of alveolar edema. Severely impaired gas exchange, hypoxemia and hypocapnia occur. Patients seem very crowded with reddish frothy cough. Vital capacity and other lung volume decreased markedly. Occurs right-to-left intrapulmonary shunt. Patients usually suffer from hypocapnia, but in severe cases can occur hypercapnia and acute respiratory acidemia. In this situation morphine has to be used with caution (Ingram and Braunwald, 1988).
Pam edema that occurs after acute myocardial infarction is usually due to capillary pulmonary hypertension. However, experiments on dogs that do arteriakoronaria ligation, pulmonary edema occurred despite normal pulmonary capillary wedge pressure, which can be prevented with indomethacin administration before. It is estimated that by inhibiting cyclic nucleotide phosphodiesterase or cyclooxygenase to reduce edema 'secondary to increased pulmonary alveolar-capillary permeability; on human beings still requires further research. Sometimes patients with acute myocardial infarction and pulmonary edema, capillary wedge pressure normal lungs; this is probably due to the slow clearance of edema fluid radiographically although pulmonary capillary pressure has gone down or alternatively in some patients an increase in alveolar-capillary permeability secondary lung because of the contents sekuncup low as in cardiogenic shock lung.

Diagnosis Supports
»Physical Examination

• Central cyanosis. Shortness of breath by breath sounds like a frothy mucus.
• Ronchi loud in the basal lung wet and then took up almost the entire lung field, sometimes accompanied by dry and expiratory Ronchi which extends a result of bronchospasm so-called cardiac asthma.
• Tachycardia with S3 gallops.
• Murmur when valve abnormalities.

»Electrocardiography. Can sinus tachycardia with left atrial hypertrophy or atrial fibrillation, depending on the cause of heart failure. Preview infarction, left ventricular hypertrophy or arrhythmias can be found.
»Laboratory

• Low pO2 blood gas analysis, pCO2 initially low and then hypercapnia.
• Enzymes cardiospesific increase if the cause of myocardial infarction.
• Blood routine, urea, creatinine, electrolytes, urinalysis, thoracic images, ECG, cardiac enzymes (CK-MB, Troponin T), coronary angiography.

Photo thoracic Pulmonary edema is typically diagnosed by chest X-ray. Radiograph (X-ray) a normal chest consists of a centralized area that offends white heart and major blood vessels plus the bones of the vertebral column, with the lung fields showed as areas darker on each side, which surrounded by the bone structures of the chest wall.
X-ray chest with a typical pulmonary edema may show more white Tampakan in both lung fields than usual. The cases are more severe than pulmonary edema may show opacification (bleaching) is significant in the lung with minimal visualization of the lung fields are normal. Bleaching represents filling of the alveoli as a result of pulmonary edema, but it may provide minimal information about the possible underlying causes.

»Overview Radiology found:

• Widening or thickening of the hilum (hilar vascular dilatation)
• Increased lung pattern (more than 1 / 3 lateral)
• Vascular cranialization
• Bleak hilum (the limit is not clear)
• Interstitial fibrosis (descriptions such as granulomas, small granulomas or miliary nodules)

»Preview the cause of heart failure echocardiography: valve abnormalities, ventricular hypertrophy (hypertension), Segmental wall motion abnormally (CHD), and generally found left ventricular dilatation and left atrium.

»Measurement of plasma B-type natriuretic peptide (BNP)

Other diagnostic tools used in assessing the underlying cause of pulmonary edema include the measurement of plasma B-type natriuretic peptide (BNP) or N-terminal pro-BNP. This is the marker proteins (hormones) that will arise in the blood caused by the stretching of the heart chambers. The increase of BNP nanograms (a billionth of a gram) per liter larger than a few hundred (300 or more) is very high suggesting cardiac pulmonary edema. On the other hand, the values ​​are less than 100 are essentially rule out heart failure as the cause.

»Pulmonary artery catheter (Swan-Ganz)

Pulmonary artery catheter (Swan-Ganz) is a long, thin tube (catheter) is inserted into large veins of the chest or neck and advanced through the room - right side of the heart chamber and placed into the pulmonary capillaries or pulmonary capillaries (branch -small branches of blood vessels of the lungs). This tool has the ability to directly measure the pressure in the pulmonary vessels, called pulmonary artery wedge pressure. Wedge pressure of 18 mmHg or higher is consistent with cardiogenic pulmonary edema, while wedge pressure of less than 18 mmHg usually support non-cardiogenic cause of pulmonary edema. Swan-Ganz catheter placement and interpretation of data is done only at the intensive care unit (ICU).

Differential Diagnosis 

• Pulmonary embolism.
• Asthma Bronchiale

Management

• Semi-Fowler position.
• Oxygen (40-50%) to 8 liters / minute if necessary with a mask.
• If deteriorated (patients increasingly congested, takipneu, Ronchi added, can not be maintained PaO2 ≥ 60 mmHg with O2 concentration and high flow, CO2 retention, hypoventilation, or unable to adequately reduce the edema fluid), then performed endotracheal intubation, suctioning and ventilators.
• Infusion emergency. Monitor blood pressure, ECG monitor, pulse oximetry if available.
• Sublingual or intravenous nitroglycerin. Peroral nitroglycerin 0.4 to 0.6 mg every 50-10 minutes. If the systolic blood pressure> 95 mmHg may be given intravenous nitroglycerin starts dose of 3-5 ug / kg.
• If it does not give satisfactory results it can be given IV Nitroprusid starting dose of 0.1 ug / kg / minute if they do not respond to nitrate, the dose is increased to obtain clinical improvement or until systolic blood pressure of 85-90 mmHg in patients who had had blood pressure normal or can be maintained as long as adequate perfusion to vital organs.
• Morphine sulfate 3-5 mg iv, may be repeated every 25 minutes, a total dose of 15 mg (best avoided).
• Diuretics Furosemide 40-80 mg IV bolus dose may be repeated or increased every 4 hours or continued drip continue to achieve urine output of 1 ml / kg / hour.
• If necessary (blood pressure drop / mark hypoperfusion): Dopamine 2-5 ug / kg / min or dobutamine 2-10 ug / kg / min to stabilize hemodynamics. The dose may be increased according to clinical response or both.
• Thrombolytic or revascularization in patients with myocardial infarction.
• Ventilator in patients with severe hypoxia, acidosis / does not work with oxygen.
• Operations on the complications of acute myocardial infarction, such as regurgitation, VSD, and ventricular wall rupture / corda tendinae.

Tags : pulmonary edema definition, pulmonary oedema, flash pulmonary edema, acute pulmonary edema, pulmonary edema symptoms, pulmonary edema causes, pulmonary edema treatment, lung edema, altitude pulmonary edema,

Respiratory Failure

Respiratory failure is the inability of the respiratory system to maintain normal blood oxygenation (PaO2), elimination of carbon dioxide (PaCO2) and pH Adequate ventilation problem caused by diffusion or perfusion.
Respiratory failure is inadequate gas exchange to hypoxia, hypercapnia (increased arterial carbon dioxide concentration), and acidosis.
Respiratory failure occurs when the exchange of O2 to CO2 in the lungs can not maintain the rate of O2 consumption and CO2 formation in the body's cells causing pO2 <> 2> 45 mmHg (hypercapnia) (Smeltzer, C Susane, 2001)


Causes / Etiology
1. The central nervous system depression

Resulting in respiratory failure due to inadequate ventilation. Respiratory centers that control breathing, located below the brain stem (pons and medulla) so slow and shallow breathing.

2. Primary neurological disorder

May hamper respiratory function. Impulses arising in the respiratory center spreads through the nerves that extend from the brainstem to the spinal nerves continue to receptors on the respiratory muscles. Diseases of the nervous disorders such as spinal cord, the muscles of respiration or neuromuslular meeting that occurs on breathing will greatly affect ventilation.

3. Pleural effusion, Pneumothorax and Hemothorax

It is a condition that interferes with ventilation through the inhibition of lung expansion. This condition is usually caused by defect underlying lung, pleural disease or trauma and injury and can cause respiratory failure.

4. Trauma

Caused by motor vehicles can be a cause of respiratory failure. Accidents resulting in head injuries, unconscious and bleeding from the nose and mouth can lead to upper airway obstruction and respiratory depression. Hemothorax, Pneumothorax and rib fractures may occur and possibly causing respiratory failure. Flail chest may occur and can lead to respiratory failure. The treatment is to correct the underlying pathology.

5. Acute pulmonary disease

Pneumonia caused by bacteria and viruses. Bronchial asthma, Atelectasis,Pulmonary embolism and pulmonary edema are some other conditions that cause respiratory failure.

Signs and Symptoms
Sign
a. Failed total breath

• The flow of air in the mouth, the nose is not heard / felt
• In spontaneous breathing movements supra visible retraction between the ribs and clavicles and no development of the chest on inspiration

b. Partial failure of breath

• The sound of gargling extra breathing, snoring, growing and wheezing
• There is a chest retraction

Symptoms
a. Hypercapnia is an increase in CO2 levels in the body more than 45 mmHg
b. Hypoxaemia occurs tachycardia, restlessness, sweating or cyanosis or decreased pO2

Pathophysiology
Breath failed there are two kinds of acute respiratory failure and chronic respiratory failure in which each individual has a sense of bebrbeda. Acute respiratory failure is failing breath that arise in patients whose lungs are structurally and functionally normal before disease arises. While chronic respiratory failure is occurring in patients with chronic lung diseases such as chronic bronchitis, emphysema and black lung disease (disease of coal miners.) Patients experiencing tolerance to hypoxemia and hypercapnia that worsens gradually. Acute respiratory failure after lung usually re origin stage. In chronic respiratory failure structure of natural lung damage is irreversible.
Indicators of respiratory failure has been the frequency of respiratory and vital capacity, normal respiratory frequency is 16-20 times/mnt. When more than 20x/mnt action taken to give a ventilator because of "breathing work" to be high so that the resulting fatigue. Vital capacity is a measure of ventilation (normal 10-20 ml / kg).
Failed breath is the most important causes of inadequate ventilation where there is upper airway obstruction. Respiratory centers that control breathing are located below the brain stem (pons and medulla). In the case of patients under anesthesia, head injury, stroke, brain tumors, encephalitis, meningitis, hypoxemia and hypercapnia have the ability to suppress the respiratory center. So that breathing becomes slow and shallow. In the postoperative period with anesthesia can occur breathing is inadequate because there are agents that suppress breathing to the effect issued or to enhance the analgesic effect of opiad. Pneumonia or lung disease can lead to acute respiratory failure.

Examination Supports
a. Examination of arterial blood gases

Hypoxemia
Lightweight: PaO2 <80 mmHg
Medium: PaO2 <60 mmHg
Weight: PaO2 <40 mmHg
Examination of arterial blood gases is important to determine the presence of respiratory acidosis and respiratory alkalosis, as well as to determine whether the client is experiencing metabolic acidosis and metabolic alkalosis or both on a client who had long suffered respiratory failure. In addition, this examination is also very important to know and evaluate the progress of oxygenation therapy or treatment given to the client.

b. Chest X-ray examination

Based on the photo thoracic PA / AP and lateral fluoroscopy as well as data obtained will be many such as the occurrence of hyperinflation, pneumothorax, pleural effusion, and lung tumors.

c. Measurement of lung function

The use of spirometers can make us determine if there is obstructive pulmonary disorder.
d. ECG

The existence of pulmonary hypertension can be seen on the ECG is characterized by elevated P wave changes in leads II, III, and aVF, as well as an experienced cardiac right ventricular hypertrophy. Ischemia and cardiac arrhythmias are common in disorders of ventilation and oxygenation.

e. Sputum examination

Noteworthy is the color, odor, and consistency. If it is necessary to culture and sensitivity test against germs that cause. If there is found the blood lines in sputum (blood strekaed), probably caused by bronchitis, bronchiectasis, pneumonia, pulmonary tuberculosis, and malignancy. Sputum pink and frothy may be due to pulmonary edema. For a lot of sputum containing blood, the more often a sign of pulmonary or lung malignancy.

 Treatment

• Oxygen therapy. Low velocity oxygen delivery: Venturi mask or nasal prong
• Mechanical ventilator with continuous positive airway pressure (CPAP) or PEEP
• Inhalation nebulizer
• Chest physiotherapy
• Monitoring of hemodynamic / cardiac
• Drugs: Brokhodilator and Steroids
• Nutritional support as needed

The principle of handling Respiratory Failure

1. Secretions are not detained (ineffective cough): adequate hydration, expectorant, aerosols, assisted cough, aspiration with a catheter, suction bronchoscopy, aspiration with endotracheal tubes.
2. Hypoxemia: is oxygen therapy gradually with frequent blood gas monitoring.
3. Hypercapnia: Respiratory stimulation (drug overdose), avoid sedation, artificial ventilation through the ET tube.
4. Respiratory tract infections: Antibiotics, given preferably after culture results are obtained and the test sensitivity to germs that cause.
5. Bronchospasm: bronchodilator drugs.

Tags : Respiratory Failure, Acute Respiratory Failure, Type Respiratory Failure, Respiratory Heart Failure, Chronic Respiratory Failure, Respiratory Failure Symptoms, Hypercapnic, Hypercapnic Respiratory Failure, Respiratory Distress

Pulmonary Embolism

Pulmonary embolism is the obstruction of one or more pulmonary artery by a thrombus originating from somewhere. (Brunner and Suddarth)
Pulmonary embolism (PE) is a blockage of the main artery of the lung or one of its branches by a substance That has Travelled from elsewhere in the body through the bloodstream (embolism). (Wikipedia)

Causes
Most cases of pulmonary embolism according to Brunner and Suddarth caused by
1. Blood clot
2. Air bubble
3. Fat
4. Tumor cells

Pulmonary Embolism (PE)

Overview
Causes
Clinical Manifestations
Pathophysiology
Diagnostic Examination
Investigations
Complication
Medical Management

Clinical Manifestations
The symptoms of pulmonary embolism depends on the size of the thrombus and the area of ​​the pulmonary artery is clogged by a thrombus. The symptoms may be nonspecific. Chest pain is the most common symptom and usually has a sudden onset and is pleuritic. Subternal sometimes can and can mimic angina pectoris or myocardial infarction. Dyspnea is the second most common symptom is followed by tachypnea, tachycardia, nervousness, cough, diaphoresis, hemoptysis, and syncope.
Massive embolism of the pulmonary artery bifurcation clog could cause actual dyspnea, substernal pain sudden, rapid and weak pulse, shock, syncope and sudden death.
Multiple small embolism can get stuck in the terminal pulmonary arteries, resulting in multiple small infarcts in the lungs. Clinical picture may resemble bronchopneumonia or heart failure. (Brunner and Suddarth)

Pathophysiology
When the thrombus blocking some or all pulmonary arteries, enlarged alveolar space loss due to the area, although they keep getting ventilation, receive little or no blood flow at all. In addition a number of substances that are released from the clot and cause the blood vessels constrict bronchiolus. This reaction in seimbangi ventilation perfusion imbalance, resulting in decreased O2 and increased CO2 levels.
Hemodynamic consequence is an increase in pulmonary vascular resistance due to decrease in size of pulmonary vascular net-nets., Causing an increase in pulmonary artery pressure and ultimately improve the working right ventricle to maintain pulmonary blood flow. When the right ventricle needs exceed the capacity, it will happen right ventricular failure that leads to a decrease in systemic blood pressure and shock. (Brunner and Suddarth)

Diagnostic Examination
Diagnostic examination of pulmonary embolism according to Brunner and Suddarth, are:
1. Chest X-rays
Chest radiograph in pulmonary embolism is usually normal but may shows a pneumo-constriction, infiltrates, atelectasis, elevation diagfragma the position of the sick, or dilation of the arteries and ​​pleural effusion.
2. ECG
ECG usually shows sinus tachycardia, atrial flutter or fibrillation and right axis deviation possible, or right ventricular strain.
3. Impedance Plethysmography
Plethysmography impedance performed to determine the presence of deep venous thrombosis.
4. Arterial blood gas
Arterial blood gases on pulmonary embolism may show hypoxemia and hipokapnea.

Investigations
Diagnostic examination that is often found on client pulmonary embolism as proposed by Doenges, M. E. (2000) the following:

1. Lung scan (ventilation / perfusion scan) can show abnormal perfusion pattern in the area of ​​ventilation or absence of ventilation and perfusion.
2. Pulmonary angiography: the presence of defects or cutoff in the absence of arterial blood in the distal blood flow.
3. Chest X-ray: often normal (especially in the subacute state), but may show a shadow of blood clots, damage to blood vessels, elevation of the diaphragm on the affected area of ​​pleural effusion, infiltration consolidation.
4.  ABGs: PaO2 may indicate a decrease, Paco, (hypoxemia, hipokapnea) and elevation of pH (respiratory alkalosis), especially if severe pulmonary obstruction.
5. Complete blood: may show increased HT (hemoconcentration) increased red blood cell polistemia.
6.  ECG : May be normal or show changes in the right ventricle that identify disorders, such as changes in ST segment or T waves, axis deviation / right bundle branch block (RBBB), tachycardia and dysrhythmias often occur.

Complication
Complications resulting from pulmonary embolism are:
1. Respiratory failure,
2. Acute right heart failure, and
3. Hypertension

Medical Management
According to Brunner and Suddarth (2001) The goal of treatment is to destroy (lyse) embolism pmbentukan existing and prevent new ones. Treatment of pulmonary embolism can include a variety of modalities:

1. Anticoagulant therapy. Anticoagulation therapy include heparin, warfarin sodium has traditionally become the primary method to cope with acute deep vein thrombosis and pulmonary embolism.
2. Thrombolytic therapy. Thrombolytic therapy include urokinase, streptokinase may also be used in dealing with pulmonary embolism, especially in highly disturbed paien. Thrombolytic therapy destroys thrombus or emboli faster and restore hemodynamic function of the pulmonary circulation is greater, because reducing pulmonary hypertension and improve perfusion, oxygenation, and cardiac output.
3. Common action to improve the status of respiratory and vascular. Common actions undertaken to improve the status of respiratory and vascular patients. Oxygen therapy is given to correct hypoxia and to eliminate pulmonary vascular vasoconstriction and pulmonary hypertension and reduced.
4. Surgical intervention.  Surgical intervention is carried out embolectomy lung, but embolectomy may be indicated in the following conditions:

a. if patients had persistent hypotension, shock, and severe heat
b. if very high pulmonary artery pressure
c. if the angiogram showed obstruction of the pulmonary blood vessels.
Embolectomy pulmonary require thoracotomy with cardiac pulmonary bypass technique

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Atelectasis

Atelectasis is a common acute restrictive disease occurs, include the collapse of lung tissue or lung functional unit. Atelectasis is a common problem post-surgery clients.
Atelectasis is incomplete lung expansion at birth (neonatorum atelectasis) or collapse before fully developed alveoli, which are usually found in adults that is atelectasis acquired.

Atelectasis is shriveling, some or all of the lung caused by blockage of the airways (bronchi and bronchioles) or by very shallow breathing.
Pulmonary Atelectasis is a state or part of the lung who have developed resistance to perfect that developing lung aeration or completely filled with air.
As a basic picture of atelectasis is radiologically in the lung volume reduction both lobaris, segmental or whole lung, with the consequent lack of aeration, thus giving more gloomy shadow (high density) with the withdrawal of the mediastinum towards the atelectasis, whereas the diaphragm is pulled up and broke ribs narrowed.

Types of Atelectasis
Based on the Factors Causing 
1.  Atelectasis Neonatorum

Many occur in premature infants, in which the respiratory center in the brain is not mature and respiratory movement is still limited. Precipitating factors including childbirth complications that cause hypoxia intrauteri.
At autopsy, the lungs appear collapsed, bluish red, non-crepitant, tender and alastis. The typical lung is not able to expand in the water. Histologically, lung alveoli have a baby, with a small alveolar spaces of uniform, covered with thick septa dindingin that looks shriveled. Epithelial cabbage prominem melaposi cavity and the alveoli often contained granular edapan protein mixed with amniotic debris and air cavity. Neonatorum atelectasis on the system, respiratory distress, have been previous discussion

2. Acquired atelectasis or Learned

Atelectasis in adults, including intrathoracic disorders that cause collapse of the air space, which previously has been developed. So divided into absorption atelectasis, compression, contractions and spotting. This term involves a lot of the basic mechanisms that lead to lung collapse or on the distribution of these changes.

• Altelectasis absorption occurs if the respiratory tract completely blocked so that air can not enter the distal parenchyma. The air that has been available is gradually entering the blood stream, accompanied by the collapse of the alveoli. Depending on the level of airway obstruction, the entire lung, a lobe of a complete, or spotting segments can be involved. The most common cause of the collapse of absorption is bronchial obstruction by a mucus blockage. This often occurs after surgery. Bronchial asthma, bronchiectasis and chronic bronchitis and acute, can also cause acute and chronic obstruction. Can also cause acute and chronic obstruction, can also cause obstruction due to blockage mukopurulen materials. Sometimes the obstruction caused by foreign body aspiration or blood clots, especially in children or during oral surgery or anesthesia. Airways may also be too stoppers by tumors, especially bronchogenic carcinoma with enlarged lymph nodes (as in tuberculosis, for example) and by vascular aneurysms.

• Compression atelectasis most often associated with fluid accumulation of blood or air in the pleural cavity, which mechanically causes lung collapse beside him. This is a frequent occurrence in the pleural effusion from any cause, but perhaps most often associated with heart trouble hidrotoraks on congestion. Pneumothorax may also cause compression atelectasis in patients with bed rest and the patient with ascites, atelectasis basal position of the diaphragm causes a higher rate.

• Contraction atelectasis occurs when changes in pulmonary and pleural fibrosis which inhibits ekspensi and enhance resilience to expiration.

• Atelectasis spots shall mean the existence of small elapsed from lung collapse, as occurs in multiple obstruction of bronchioles due to secretion or exudate respiratory distress syndrome in both adults and infants. In a few cases, atelectasis occurs because certain that accompanies pathogenesis clear to the chest wall.

Atelectasis acquired (acquired) may be acute or chronic. Usually arise because of the relatively acute blockage of mucus, which becomes manifest as sudden shortness of breath occur. Indeed, events of acute breathlessness in 48 hours after a surgical procedure, it is almost always diagnosed as atelectasis. The important thing is atelectasis can be diagnosed early and appropriate happens reekspensi of the affected lung, due to the collapse parenchyma forbid the menunggagi susceptible to infection. Persistent atelectasis lung segments may be an important part to the occurrence of bronchogenic carcinoma who quietly.

Based on the extent of atelectasis

1. Massive atelectasis, on one lung
2. One lobe, branching main bronchus

Based on the location of atelectasis

1. Atelectasis lobaris down: if there is dilobaris down the left lung, it will be hidden behind the shadow of the heart and the PA chest x-ray only diaphragm showed a high position.
2. Atelectasis lobaris center-right (right middle lobe). Often caused by inflammation or suppression of the bronchi by the enlarged lymph nodes.
3. Atelectasis lobaris top (upper lobe): provide high-density shadow fissure interlobaris withdrawal sign up and trachea toward atelectasis.
4. Segmental atelectasis: sometimes hard to recognize in the photo thoraj PA, it is necessary to shoot with other positions such as lateral, oblique (obligue), which shows the money is disguised as a withdrawal interlobularis fissure.
5. Lobularis atelectasis (plate like / local atelectasis). If a blockage occurs in the small bronchi for some segments of the lung, there will be a shadow of a thin horizontal, usually lower lung field that is often difficult to distinguish from the process of fibrosis. Because only a small portion of lung is affected, then there is usually no complaints.
6. Atelectasis in the right lung upper lobe. These include the collapse of the anterior, superior and medial. On PA chest x-ray indescribable with minor fissure and the superior part of the shift dial. On the lateral image, the major fissure moves forward, while the minor fissure can also experiencing a shift towards a superior.

Etiology
Etiology of atelectasis is the most that is two intrinsic and extrinsic.
1. Atelectasis intrinsic etiology is as follows:

• BBronchi are blocked, the blockage can be derived in the bronchi such as bronchial tumors, foreign bodies, fluid secretion is massive. And bronchial obstruction due to suppression of tumor outside the bronchus such as around the bronchi, the enlarged gland.
• Intraluminar airway inflammation that causes the buildup of mucus secretions.
• Extra pulmonary pressure, usually caused by pneumothorax, pleural fluid, elevation of the diaphragm, abdominal herniation tool into thoracic cavity, thoracic tumors such as tumors of the mediastinum.
• Paralysis or paresis of respiratory motion, will cause the development of the lungs are not perfect, for example in cases of poliomyelitis and other neurological disorders. Impaired breathing motion will affect the smooth bronchial secretions and this expenditure will lead to blockage of the bronchus that ended with the situation worsens atelectasis.
• Barriers to respiratory motion by pleural abnormalities or trauma to the thoracic pain, state expenditures will also inhibit bronchial secretions that can aggravate the occurrence of atelectasis

2. Etiology extrinsic atelectasis:

• Pneumothorax
• Tumors
• Enlarged lymph nodes.
• Anesthesia  / Surgery
• Bed rest the long run without change of position
• Shallow Breathing
• Lung disease

Symptoms
Atelectasis can occur slowly and cause only a mild shortness of breath. Patients with medial lobe syndrome may have no symptoms at all, although many who suffer from short cough.
Symptoms can include:
• Respiratory problems
• Chest pain
• Cough
If accompanied by an infection, may develop a fever and increased heart rate, sometimes to shock (very low blood pressure).
Clinical symptoms vary widely, depending on the cause and extent of atelectasis. In general, atelectasis that occurs in tuberculosis, lymphoma, neoplasm, asthma and diseases caused by infection such as bronchitis, bronchopneumonia, and other pain-rarely cause obvious clinical symptoms, unless there is obstruction in the main bronchus. If the area of atelectsis was large and occurred very rapidly going to happen dipsneu with a pattern of rapid and shallow breathing, tachycardia and frequent cyanosis, high temperatures, and if continued will lead to loss of consciousness or shock. On percussion dim and perhaps also normal compensation in case of emphysema. In an extensive atelectasis, atelectasis involving more than one lobe, noisy breathing will weaken or no sound, usually obtained differences thoracic wall motion, the motion between the ribs and diaphragm. On percussion of the heart and mediastinum may limit will be shifted, the position of the diaphragm may be elevated.

Pathophysiology
After the blockage occurs suddenly bronchial peripheral blood circulation will be absorbed by the air of the alveoli, which will lead to respiratory failure and withdrawal of the lung within a few minutes, this is without desebabkan an infection. The lungs will shrink in the complex. In early levels, blood perfused lungs will lack the air that causes arterial hypocsemia. If the capillary and tissue hypoxia lead to the emergence of transudates in the form of gas and fluid and pulmonary oedema. Expenditures transudates of alveoli and cells is a complete prevention of collapse of lung atelectasis. However in case of diaphragm collapse extensive experience exaltation, chest wall pain, and this will affect the change of location of the heart and mediastinum.
Congested due to a variation of the central stimulus change respiration and cerebral cortex. The stimulus comes from the chemoreceptors in areas where there are extensive atelectasis causing less pressure or O2 from the lungs and respiratory muscles, lungs where oxygen deficiency is not met and the additional work of breathing. May the blood flow in areas of atelectasis is reduced. CO2 pressure is usually normal or should be down slightly from the rest of the lung parenchyma hyperventilation are normal.

Diagnosis
Diagnosis based on clinical symptoms and results of physical examination. Chest X-rays will show the existence of air-free areas in the lungs. To determine the cause of the blockage may be necessary CT - scan or fiber-optic bronchoscopy.
Collapse can be diagnosed by the presence of:

Increased density and pulmonary blood vessels are clustered
Change the location of the hilum or fissure (upwards or downwards). In normal circumstances where the lower right hilum of the left hilum
Shift of the trachea, mediastinum or fissures interlobaris toward the collapsed lung
The remaining lung can be highly developed (over-expanded) and thus become hipertranslusen.

Radiological Picture
Lung atelectasis can be said to have when all / most of the lung to deflate, there will be a homogeneous shadow on the sides of it, to heart and went to the department's trachea and the diaphragm lifted. When only one lobe of the atelaktasis caused by bronchial obstruction, may appear two characteristic abnormalities. The first abnormality is a shadow of a homogeneous than the deflated lobe itself, which will occupy a smaller space than when it develops at all.
A right upper lobe collapse would appear as an opaque area at the top, with a limit that is strictly concave beneath the clavicle near the fissures caused by the raised horizontalis.
The left upper lobe usually includes Lingula when deflated, and the resulting image is less firm without the firm lower limit. But in the lateral projection would seem a tongue-shaped shadow with a peak near the diaphragm; anteriorly, it may be up to the sternum, or may be separated by a translucent area of ​​the lungs caused by a slip right next to them and the sternum posterior shadow It has a clear boundary with concave boundary caused by large fissures are pushed to the front.
A middle lobe will cause a shadow that is not firmly on the anterior projection, but may blur the line than the right heart, in the lateral projection it will appear as a ribbon-shaped shadow extending from the hilum to the angle of the sterno-diafragmatikus. Strict upper limits established by the nearest horizontalis fissures, whereas the concave rear boundary by a major fissure is pushed forward.
Lower lobe is deflated causing a triangular-shaped shadow, with the lateral border of the firm that ran downward and outward from the hilum to the diaphragm. Therefore it is usually located behind the heart shadow, he can only be seen when the radiograph is good. On the lateral projection image may be blurred at all, but its presence usually gives three images; thoracic vertebrae at the bottom will look more gray than black than the vertebrae next to the middle; the posterior than the shadow of the left diaphragm will not be seen; and finally, vertebrae in the back area below the heart shadow will be less black than the translucent area behind the sternum.
The symptoms of the other characteristics are the consequence rather than vascular shadows have become blurred in the general opacity than lobes that do not contain air, while the shadows of blood vessels in the other lobe is more dispersed because it fills a larger volume. Hilar blood vessels on the affected side will show a disease and not a lateral convexity concafitas as in the normal state at the place where the group rather than the upper lobe artery basal met in addition, the hilum will be smaller than on the other side, while blood vessels of the lungs will be more dispersed, so per unit area will look much less than on the other side (normal). Only there will be little or no relative translucency, because of capillary flow increases, whereas the tracheal pressure or elevation of the diaphragm and heart are usually a little switch only slightly in the direction of the deflated lobe of the collapse than the lower lobe, or more often as not at all on the upper lobe collapse rather than.
Prevention & Treatment of Atelectasis

Tags : Atelectacsis, atelectasis causes, atelectasis causes, atelectasis symptoms, define atelectasis, what is atelectasis, pulmonary atelectasis, atelectasis pathofisiology

Acute respiratory distress syndrome (ARDS)

Acute respiratory distress syndrome(ARDS)

Overview
Etiology
Risk Factors
Pathophysiology
Clinical Manifestations
Diagnostic Examination
Therapeutic Management
Complication
Medical Management

Acute respiratory distress syndrome (ARDS) or also known as Respiratory Distress Syndrome (RDS) is an immature development of the respiratory system or an inadequate amount of surfactant in the lung. RDS is said to be hyaline membrane disease (HMD).
Respiratory Distress Syndrome (RDS) is the immature development of the respiratory system or an inadequate amount of surfactant in the lung. RDS is said to be hyaline membrane disease (HMD).

ARDS formerly most commonly signified adult respiratory distress syndrome to differentiate it from infant respiratory distress syndrome in premature infants. However, as this type of pulmonary edema also occurs in children, ARDS has gradually shifted to mean acute rather than adult. The differences with the typical infant syndrome remain(Wikipedia)



Etiology
Associated with gestational age, the younger the infant, the higher the risk of RDS so that makes the immature development of the respiratory system or an inadequate amount of surfactant in the lung.
RDS there are two times more in males than females, incidence increased in infants with certain factors, such as: maternal diabetes who gave birth to a baby less than 38 weeks, perinatal hypoxia, was delivered by cesarean section.
ARDS develops as a result of dangerous conditions or the occurrence of lung tissue injury either directly or indirectly.

Risk Factors
1. Direct trauma to the lung

• Viral Pneumonia, Bacterial Pneumonia, Fungal Pneumonia
• Contusio lung
• Aspiration of gastric fluid
• Inhalation of excessive smoke
• Inhalation of toxin
• Inhaling high concentrations of O2 in a long time

2. Indirect Trauma

• Sepsis
• Shock
• DIC (Dissemineted intravascular coagulation)
• Pancreatitis
• Uremia
• Drug Overdose
• Idiophatic (unknown)
• Surgery of the old Cardiobaypass
• Blood transfusions are a lot of
• PIH (Pregnand Induced Hipertension)
• Improved ICT
• Radiation therapy

Pathophysiology
Various theories have been found as the cause of this disorder. Formation surtaktan lung substance is not perfect in the lungs, is one theory that many embraced. Surfactant is a substance that plays a role in lung development and is a complex consisting of proteins, carbohydrates and fats. The main compound substance is lecithin. This substance began to be formed at 22-24 weeks of pregnancy and reached a maximum at 35 week. The role of surfactant is to lower alveolar surface tension so it does not happen to collapse and be able to withstand the functional residual air at the end of expiration. Deficiency of surfactant substance found in hyaline membrane disease causes the lung to maintain stability wherever disturbed. Alveoli would come back every end-expiratory collapse, so for the next breath it takes a negative intrathoracic pressure accompanied yanglebih great inspiration stronger effort. Lung collapse will cause disruption of ventilation to hypoxia, CO2 retention and acidosis. Hypoxia will lead to:
1. decreased tissue oxygenation, anaerobic metabolism that would occur with the accumulation of lactic acid and other organic acids that cause metabolic acidosis in infants.
2. apitel capillary endothelial damage and alveolar ducts and that will lead to transudation into the alveoli and the subsequent formation of fibrin and fibrin together with the necrotic epithelial tissues form a layer called the hyaline membrane. Acidosis and atelectasis also cause disruption of blood circulation to and from the heart. Similarly, pulmonary blood flow will decrease and this will result in reduced formation of surfactant substance.

Clinical Manifestations
1. Rapid breathing (takipneu)
2. Nostril breathing
3. Clients complain of difficulty breathing, retractions and cyanosis
4. Cyanosis in line with hypoxemia
5. An increasing number of respiratory
6. On auscultation of breath sounds there may be additional
7. Systemic hypotension (peripheral pallor, edema, delayed capillary refill longer than 3 to 4 seconds)
8. Decrease in urine output
9. Decreased breath sounds with ronkhi
10. Takhikardi at the time of the occurrence of acidosis and hypoxemia

Diagnostic Examination
1. Chest X-ray

• Retikulogranular diffuse pattern with air bronkhogram overlapping each other.
• Signs of central lung, heart border is difficult to see, inflation is a bad lung.
• Chances are kardoimegali when other systems are also exposed (infants of diabetic mothers, hypoxia, congestive heart failure)
• Shadow of a large thymus
• Bergranul bronkhogram evenly on the air, which indicates severe disease if present in the first few hours.

2. Arterial blood gas showed respiratory and metabolic acidosis is a decrease in pH, PaO2 decreased and PaCO2 increased, decreased HCO3.
3. Complete blood count
4. Perubahabn electrolytes, tends to decrease levels: calcium, sodium, potassium and serum glucose.


Complication

1. Pneumothorax
2. Pneumomediastinum
3. Hypotension
4. The decline of urine
5. Acidosis
6. Hyponatremia
7. Hipernatremi
8. Hypokalemia
9. Disseminated intravascular coagulation (DIC)
10. Convulsions
11. Intraventricular hemorhagi
12. Secondary infections
13. Murmur

Therapeutic Management

• Administration of oxygen
• Maintain adequate nurtrisi
• Maintain a neutral ambient temperature
• Diet 60 kcal / kg per day (adjust with the existing protocols) with amino acids sufficient to prevent endogenous protein catabolism and ketoacidosis.
• Keep the pO2 within normal limits
• Intubation if necessary with positive pressure ventilation

Medical Management

Tags : ARDS, RDS, Acute Respiratory Distress, Adult Respiratory Distress Syndrome, respiratory failure, acute respiratory failure, What Is Respiratory Distress,