Chest pain

From Wikipedia, the free encyclopedia Chest pain ICD-10 ICD-9 R07 786.5

Chest pain may be a symptom of a number of serious conditions and is generally considered a medical emergency. Even though it may be determined that the pain is non-cardiac in origin, this is often a diagnosis of exclusion made after ruling out more serious causes of the pain.

Contents
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1 Differential diagnosis o 1.1 Cardiovascular o 1.2 Pulmonary o 1.3 GI o 1.4 Chest wall o 1.5 Psychological o 1.6 Others 2 Diagnostic approach 3 Management 4 Epidemiology 5 References

[edit] Differential diagnosis

Causes of chest pain range from non-serious to serious to life threatening.[1] DiagnosisPro lists more than 440 causes on its website.[2]

[edit] Cardiovascular

Acute coronary syndrome o Unstable Angina Pectoris - requiring emergency medical treatment but not primary intervention as in a myocardial infarction. [3] o Myocardial infarction ("heart attack") Aortic dissection Pericarditis and cardiac tamponade Arrhythmia - atrial fibrillation and a number of other arrhythmias can cause chest pain.

Stable angina pectoris - this can be treated medically and although it warrants investigation, it is not an emergency in its strictest sense

[edit] Pulmonary

Pulmonary embolism Pneumonia Hemothorax Pneumothorax and Tension pneumothorax Pleurisy - an inflammation which can cause painful respiration

[edit] GI

Gastroesophageal reflux disease (GERD) and other causes of heartburn Hiatus hernia Achalasia, nutcracker esophagus and other neuromuscular disorders of the esophagus Functional dyspepsia

[edit] Chest wall

Costochondritis or Tietze's syndrome - a benign and harmless form of osteochondritis often mistaken for heart disease Spinal nerve problem Fibromyalgia Chest wall problems Radiculopathy Precordial catch syndrome - another benign and harmless form of a sharp, localised chest pain often mistaken for heart disease Breast conditions Herpes zoster commonly known as shingles Tuberculosis

[edit] Psychological

Panic attack Anxiety Clinical depression Somatization disorder Hypochondria

[edit] Others

Hyperventilation syndrome often presents with chest pain and a tingling sensation of the fingertips and around the mouth Da costa's syndrome Bornholm disease - a viral disease that can mimic many other conditions

Carbon monoxide poisoning Sarcoidosis Lead poisoning High abdominal pain may also mimic chest pain

[edit] Diagnostic approach

In the emergency department the typical approach to chest pain involves ruling out the most dangerous causes: heart attack, pulmonary embolism, thoracic aortic dissection, esophageal rupture, tension pneumothorax and cardiac tamponade. By elimination or confirmation the most serious causes, a diagnosis of the origin of the pain may be made. Often, no definite cause will be found and reassurance is then provided.[1] If acute coronary syndrome ("unstable angina") is suspected, many people are admitted briefly for observation, sequential ECGs, and determination of cardiac enzymes over time. On occasion, further tests on follow up may determine the cause. TIMI score performed at time of admission may help stratify risk. As in all medicine, a careful medical history and physical examination is essential in separating dangerous from trivial causes of disease, and the management of chest pain may be done on specialised units (termed medical assessment units) to concentrate the investigations. A rapid diagnosis can be life-saving and often has to be made without the help of X-rays or blood tests (e.g. aortic dissection). Occasionally, invisible medical signs will direct the diagnosis towards particular causes, such as Levine's sign in cardiac ischemia. Generally, however, additional tests are required to establish the diagnosis. A focus on recent health changes, family history (premature atherosclerosis, cholesterol disorders), tobacco smoking, diabetes and other risk factors is useful. Features of the pain suggest of cardiac ischaemia are describing the pain as heaviness; radiation of the pain to neck, jaw or left arm; sweating; nausea; palpitations; the pain coming upon exertion; dizziness; shortness of breath and a "sense of impending doom." On the basis of the above, a number of tests may be ordered:

X-rays of the chest and/or abdomen (CT scanning may be better but is often not available). Routine X-rays and CT may however not be needed.[4] An electrocardiogram (ECG) V/Q scintigraphy or CT pulmonary angiogram(when a pulmonary embolism is suspected) Blood tests: o Complete blood count o Electrolytes and renal function (creatinine) o Liver enzymes o Creatine kinase (and CK-MB fraction in many hospitals) o Troponin I or T (to indicate myocardial damage) o D-dimer (when suspicion for pulmonary embolism is present but low)

serum amylase to exclude acute pancreatitis

[edit] Management
In people with chest pain supplemental oxygen is not needed unless the oxygen saturations are less than 94% or there are signs of respiratory distress.[5][6] Entonox is frequently used by EMS personnel in the prehospital environment.[7] There is however little evidence about its effectiveness.[8][9]

[edit] Epidemiology
Chest pain is the presenting symptom in about 12% of emergency department visits in the United States and has a one year mortality of about 5%.

Chest trauma
From Wikipedia, the free encyclopedia

Chest trauma
Classification and external resources

A CT scan of a pneumothorax eMedicine MeSH med/2916 med/3658 D013898

Chest trauma (or thoracic trauma) is a serious injury of the chest. Thoracic trauma is a common cause of significant disability and mortality, the leading cause of death from physical trauma after head and spinal cord injury.[1] Blunt thoracic injuries are the primary or a contributing cause of about a quarter of all trauma-related deaths.[1] The mortality rate is about 10%.[2] Chest injuries were first described in detail in around 1600 BC in the ancient Egyptian Edwin Smith Papyrus.[3]

Contents

[hide]

1 Classification 2 Diagnosis 3 References 4 External links

[edit] Classification

A chest X-ray of a right sided pulmonary contusion associated with flail chest and subcutaneous emphysema Chest trauma can be classified as blunt or penetrating. Blunt and penetrating injuries have different pathophysiologies and clinical courses. Specific types of chest trauma include:

Injuries to the chest wall o Chest wall contusions or hematomas. o Rib fractures o Flail chest o Sternal fractures o Fractures of the shoulder girdle Pulmonary injury (injury to the lung) and injuries involving the pleural space o Pulmonary contusion o Pulmonary laceration o Pneumothorax o Hemothorax o Hemopneumothorax Injury to the airways o Tracheobronchial tear Cardiac injury o Pericardial tamponade o Myocardial contusion

Blood vessel injuries o Traumatic aortic rupture, thoracic aorta injury, aortic dissection And injuries to other structures within the torso o Esophageal injury (Boerhaave syndrome) o Diaphragm injury

[edit] Diagnosis
Most blunt injuries are managed with relatively simple interventions like tracheal intubation and mechanical ventilation and chest tube insertion. Diagnosis of blunt injuries may be more difficult and require additional investigations such as CT scanning. Penetrating injuries often require surgery, and complex investigations are usually not needed to come to a diagnosis. Patients with penetrating trauma may deteriorate rapidly, but may also recover much faster than patients with blunt injury.

An empyema (from Greek: ) is a collection of pus within a naturally existing anatomical cavity, such as the lung pleura. It must be differentiated from an abscess, which is a collection of pus in a newly formed cavity. In human medicine, empyema occurs in:

the pleural cavity (pleural empyema also known as pyothorax) the thoracic cavity the uterus (pyometra) the appendix (appendicitis) the meninges (subdural empyema) the joints (septic arthritis) the gallbladder the brain (subdural empyema)

Pleural empyema
From Wikipedia, the free encyclopedia

Pleural empyema
Classification and external resources ICD-10 ICD-9 J86 510

DiseasesDB MedlinePlus eMedicine MeSH

4200 000123 med/659 D016724

Pleural empyema (also known as a pyothorax[1] or purulent pleuritis) is an accumulation of pus in the pleural cavity. Most pleural empyemas arise from an infection within the lung (pneumonia), often associated with parapneumonic effusions. There are three stages: exudative, fibrinopurulent and organizing. In the exudative stage, the pus accumulates. This is followed by the fibrinopurulent stage in which there is loculation of the pleural fluid (the creation of pus pockets). In the final organizing stage, scarring of the pleural space may lead to lung entrapment.[2]

Contents
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1 Symptoms 2 Diagnosis 3 Treatment 4 References 5 External links

[edit] Symptoms

CT chest showing large right sided hydro-pneumothorax from pleural empyema. Arrows A: air, B: fluid

Encasement of the left lung by thick purulent exudate which is characteristic of pleural empyema. Symptoms of pleural empyema may vary in severity. Typical symptoms include: cough, fever, chest pain, sweating and shortness of breath.[2] Clubbing may be present in cases of a chronic nature. There is a dull percussion note and reduced breath sounds on the affected side of the chest. Other diagnostic tools include a blood white cell count, chest x-ray, CT scan, and ultrasonography.[2]

Progression to empyema over 2 weeks period.

[edit] Diagnosis
Diagnosis is confirmed by thoracentesis; frank pus or merely cloudy fluid may be aspirated from the pleural space. The pleural fluid typically has a leukocytosis, low pH (<7.20), low glucose (<60 mg/dL), a high LDH (lactate dehydrogenase), elevated protein and may contain infectious organisms.[2]

[edit] Treatment

World War I photo showing removal of several ribs as described. Definitive treatment for pleural empyema entails drainage of the infected pleural fluid or pus. A chest tube may be inserted, often using ultrasound guidance. Intravenous antibiotics are given. Chest tubes in the setting of pleural empyema have a tendency to be clogged by the thick pus. To combat this problem, surgeons will often place one or more large bore chest tubes. Insufficient drainage of the pleural empyema, particularly in loculated empyema, can lead to re accumulation of pus and infected material, a worsening clinical picture, organ failure and even death. Thus managing chest tube function is particularly important in the treatment of a pleural empyema.[2] To improve the chest tube drainage, fibrinolytics and DNA enzyme can be given intrapleurally through the chest tube to break the fibrinous septation and to reduce the pus viscosity. Although these adjunct treatments are proven effective, its administration may cause rare but lifethreatening intrapleural hemorrhage and hypersensitivity reaction.[3] If this is insufficient, surgical debridement of the pleural space may be required. This is frequently done using video-assisted thoracoscopic techniques but if the disease is chronic, a limited thoracotomy may be necessary to fully drain the pus and remove the fibrinopurulent exudate from the lung and from the chest wall.[2] Occasionally, a full thoracotomy, formal decortication and pleurectomy are required. Rarely, portions of the lung have to be resected. An earlier form of treatment involved surgical removal of most of the ribs on the infected side of the thorax, causing a permanent collapse of the lung and obliteration of the infected pleural space. This would leave the patient with a large portion of the upper chest removed, giving the

impression that the shoulder had been detached from the body. Rarely performed today, the surgery was common during World War I. [4]

Chest tube
From Wikipedia, the free encyclopedia (Redirected from Thoracostomy tube)

Chest tube
Intervention

The free end of the Chest Drainage Device is usually attached to an underwater seal, below the level of the chest. This allows the air or fluid to escape from the pleural space, and prevents anything returning to

the chest. ICD-9-CM MeSH 34.04 D013907

Size of Chest Tube: Adult or Teen Male = 28-32 Fr Pp Adult or Teen Female = 28 Fr Child = 18 Fr Newborn = 12-14 Fr
[1]

A chest tube (chest drain or tube thoracostomy in British medicine or intercostal drain) is a flexible plastic tube that is inserted through the side of the chest into the pleural space. It is used to remove air (pneumothorax) or fluid (pleural effusion, blood, chyle), or pus (empyema) from the intrathoracic space. It is also known as a Blau drain or an intercostal catheter.

Contents
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1 Indications 2 Contraindications 3 Technique 4 Chest Drainage Canister 5 Complications 6 References 7 External links

[edit] Indications

Pneumothorax: accumulation of air in the pleural space Pleural effusion: accumulation of fluid in the pleural space o Chylothorax: a collection of lymphatic fluid in the pleural space o Empyema: a pyogenic infection of the pleural space o Hemothorax: accumulation of blood in the pleural space o Hydrothorax: accumulation of serous fluid in the pleural space

[edit] Contraindications

Contraindications to chest tube placement include refractory coagulopathy, lack of cooperation by the patient, and diaphragmatic hernia. Additional contraindications include scarring in the pleural space (adhesions)

[edit] Technique
The insertion technique is described in detail in an article of the NEJM.[2] The free end of the tube is usually attached to an underwater seal, below the level of the chest. This allows the air or fluid to escape from the pleural space, and prevents anything returning to the chest. Alternatively, the tube can be attached to a flutter valve. This allows patients with pneumothorax to remain more mobile. British Thoracic Society recommends the tube is inserted in an area described as the "safe zone", a region bordered by: the lateral border of pectoralis major, a horizontal line inferior to the axilla, the anterior border of latissimus dorsi and a horizontal line superior to the nipple[citation needed]. More specifically, the tube is inserted into the 5th intercostal space slightly anterior to the mid axillary line.[3] Chest tubes are usually inserted under local anesthesia. The skin over the area of insertion is first cleansed with antiseptic solution, such as iodine, before sterile drapes are placed around the area. The local anesthetic is injected into the skin and down to the muscle, and after the area is numb a small incision is made in the skin and a passage made through the skin and muscle into the chest. The tube is placed through this passage. If necessary, patients may be given additional analgesics for the procedure. Once the tube is in place it is sutured to the skin to prevent it falling out and a dressing applied to the area. Once the drain is in place, a chest radiograph will be taken to check the location of the drain. The tube stays in for as long as there is air or fluid to be removed, or risk of air gathering. Chest tubes can also be placed using a trocar, which is a pointed metallic bar used to guide the tube through the chest wall. This method is less popular due to an increased risk of iatrogenic lung injury. Placement using the Seldinger technique, in which a blunt guidewire is passed through a needle (over which the chest tube is then inserted) has been described.

[edit] Chest Drainage Canister

A chest drainage canister device is typically used to drain chest tube contents (air, blood, effusions). There are generally three chambers. The first chamber is a collecting chamber. The second is the "water seal" chamber which acts as a one way valve. Air bubbling through the water seal chamber is usual when the patient coughs or exhales but may indicate, if continual, a pleural or system leak that should be evaluated critically. It can also indicate a leak of air from the lung. The third chamber is the suction control chamber. The height of the water in this chamber determines the negative pressure of the system. Bubbling should be kept a gentle bubble to limit evaporating the fluid. Increased wall suction does not increase the negative pressure of the system. Newer systems are designed not to need the water seal chamber, so there is not a column of water that can spill and mix with blood, mandating the replacement of the

canister. Even newer systems are smaller and more ambulatory so the patient can be sent home for drainage if indicated.

[edit] Complications
Major complications are hemorrhage, infection, and reexpansion pulmonary edema. Chest tube clogging can also be a major complication if it occurs in the setting of bleeding or the production of significant air or fluid. When chest tube clogging occurs in this setting, a patient can suffer from pericardial tamponade, tension pneumothorax, or in the setting of infection, an empyema. All of these can lead to prolonged hospitilization and even death. To minimize potential for clogging, surgeons often employ larger diameter tubes. These large diameter tubes however, contribute significantly to chest tube related pain. Even larger diameter chest tubes can clog.[4] In most cases, the chest tube related pain goes away after the chest tube is removed, however, chronic pain related to chest tube induced scarring of the intercostal space is not uncommon. In recent years surgeons have advocated using softer, silicone Blake drains rather than more traditional PVC conventional chest tubes to address the pain issues. Clogging and chest tube occlusion issues have been a problem, including reports of life threatening unrecognized bleeding that occurs in the chest due to an occluded or clogged drain.[5] Thus when a chest tube is inserted for whatever reason, maintaining patency is critical to avoid complications. Injury to the liver, spleen or diaphragm is possible if the tube is placed inferior to the pleural cavity. Injuries to the thoracic aorta and heart have also been described. Minor complications include a subcutaneous hematoma or seroma, anxiety, shortness of breath (dyspnea), and cough (after removing large volume of fluid). Subcutaneous emphysema indicates backpressure created by a clogged drain or insufficient negative pressure.

[edit]

Pneumonia
From Wikipedia, the free encyclopedia For other uses, see Pneumonia (disambiguation).

Pneumonia
Classification and external resources

A chest X-ray showing a very prominent wedgeshaped bacterial pneumonia in the right lung. ICD-10 ICD-9 DiseasesDB MedlinePlus eMedicine MeSH J12, J13, J14, J15, J16, J17, J18, P23 480-486, 770.0 10166 000145 topic list D011014

Pneumonia is an inflammatory condition of the lungespecially affecting the microscopic air sacs (alveoli)associated with fever, chest symptoms, and a lack of air space (consolidation) on a chest X-ray.[1][2] Pneumonia is typically caused by an infection but there are a number of other causes.[1] Infectious agents include: bacteria, viruses, fungi, and parasites.[3] Typical symptoms include cough, chest pain, fever, and difficulty breathing.[4] Diagnostic tools include x-rays and examination of the sputum. Vaccines to prevent certain types of pneumonia are available. Treatment depends on the underlying cause with presumed bacterial pneumonia being treated with antibiotics. Although pneumonia was regarded by William Osler in the 19th century as "the captain of the men of death", the advent of antibiotic therapy and vaccines in the 20th century have seen radical improvements in survival outcomes. Nevertheless, in the third world, and among the very old, the very young and the chronically ill, pneumonia remains a leading cause of death.[5]

Contents
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1 Classification 2 Signs and symptoms 3 Cause o 3.1 Bacteria

3.2 Viruses 3.3 Fungi 3.4 Parasites 3.5 Idiopathic 4 Pathophysiology o 4.1 Viral o 4.2 Bacterial 5 Diagnosis o 5.1 Imaging o 5.2 Microbiology o 5.3 Differential diagnosis 6 Prevention o 6.1 Vaccination o 6.2 Environmental o 6.3 Other 7 Management o 7.1 Bacterial o 7.2 Viral o 7.3 Aspiration 8 Prognosis o 8.1 Clinical prediction rules o 8.2 Pleural effusion, empyema, and abscess o 8.3 Respiratory and circulatory failure 9 Epidemiology o 9.1 Children 10 History 11 Society and culture 12 References

o o o o

Classification
Main article: Classification of pneumonia Pneumonitis refers to lung inflammation; pneumonia refers to pneumonitis, usually due to infection but sometimes non infectious, that has the additional feature of pulmonary consolidation.[6] Pneumonia can be classified in several ways. It is most commonly classified by where or how it was acquired (community-acquired, aspiration, healthcare-associated, hospitalacquired, and ventilator-associated pneumonia),[7] but may also be classified by the area of lung affected (lobar pneumonia, bronchial pneumonia and acute interstitial pneumonia),[7] or by the causative organism.[8] Pneumonia in children may additionally be classified based on signs and symptoms as non-severe, severe, or very severe.[9]

Signs and symptoms

Main symptoms of infectious pneumonia People with infectious pneumonia often have a productive cough, fever accompanied by shaking chills, shortness of breath, sharp or stabbing chest pain during deep breaths, confusion, and an increased respiratory rate.[10] In the elderly, confusion may be the most prominent symptom.[10] The typical symptoms in children under five are fever, cough, and fast or difficult breathing.[11] Fever, however, is not very specific, as it occurs in many other common illnesses, and may be absent in those with severe disease or malnutrition. Additionally, a cough is frequently absent in children less than 2 months old.[11] More severe symptoms may include: central cyanosis, decreased thirst, convulsions, persistent vomiting, or a decreased level of consciousness.[11] Symptoms frequency in pneumonia[12] Some causes of pneumonia are associated with classic, Symptom Frequency but non-specific, clinical characteristics. Pneumonia 7991% caused by Legionella may occur with abdominal pain, Cough 90% diarrhea, or confusion,[13] while pneumonia caused by Fatigue Streptococcus pneumoniae is associated with rusty Fever 7175% colored sputum,[14] and pneumonia caused by Shortness of breath 6775% Klebsiella may have bloody sputum often described as Sputum 6065% "currant jelly".[12] Chest pain 3949% Physical examination may sometimes reveal low blood pressure, a high heart rate, or a low oxygen saturation. Examination of the chest may be normal, but may show decreased chest expansion on the affected side. Harsh breath sounds from the larger airways that are transmitted through the inflamed lung are termed bronchial breathing, and are heard on auscultation with a stethoscope. Rales (or crackles) may be heard over the affected area during inspiration. Percussion may be dulled over the affected lung, and increased, rather than decreased, vocal resonance distinguishes pneumonia from a pleural effusion.[10] Struggling to breathe, confusion, and blue-tinged skin are signs of a medical emergency.

Cause

Pneumonia is primarily due to infections, with less common causes including irritants and the unknown. Although more than one hundred strains of micro organisms can cause pneumonia, only a few are responsible for most cases. The most common types of infectious are viruses and bacteria with it being less commonly due to fungi or parasites. Mixed infections with both viruses and bacterial may occur in up to 45% of infections in children and 15% of infections in adults.[15] A causative agent is not isolated in approximately half of cases despite careful testing.[16] The term pneumonia is sometimes more broadly applied to inflammation of the lung (for example caused by autoimmune disease, chemical burns or drug reactions), however this is more accurately referred to as pneumonitis.[17][18]

Bacteria
Main article: Bacterial pneumonia

The bacterium Streptococcus pneumoniae, a common cause of pneumonia, imaged by an electron microscope Bacteria are the most common cause of community acquired pneumonia, with Streptococcus pneumoniae isolated in nearly 50% of cases.[19][7] Other commonly isolated bacteria include: Haemophilus influenzae in 20%, Chlamydophila pneumoniae in 13%, Mycoplasma pneumoniae in 3%,[7], Staphylococcus aureus, Moraxella catarrhalis, Legionella pneumophila and gramnegative bacilli.[16] Risk factors for infection depend on the organism involved.[16] Alcoholism is associated with Streptococcus pneumoniae, anaerobic organisms, and Mycobacterium tuberculosis, smoking is associated with Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Legionella pneumophila, exposure to bird with Chlamydia psittaci, farm animals with Coxiella burnetti, aspiration of stomach contents with anaerobes, and cystic fibrosis with Pseudomonas aeruginosa and Staphylococcus aureus.[16] Streptococcus pneumoniae is more common in the winter.[16]

Viruses
Main article: Viral pneumonia In adults viruses account for approximately a third of pneumonia cases.[15] Commonly implicated agents include: rhinoviruses,[15]coronaviruses,[15] influenza virus,[20] respiratory syncytial virus (RSV),[20] adenovirus,[20] and parainfluenza.[20] Herpes simplex virus is a rare cause of

pneumonia, except in newborns. People with weakened immune systems are at increased risk of pneumonia caused by cytomegalovirus (CMV).

Fungi
Main article: Fungal pneumonia Fungal pneumonia is uncommon,[16] but it may occur in individuals with weakened immune systems due to AIDS, immunosuppressive drugs, or other medical problems. The pathophysiology of pneumonia caused by fungi is similar to that of bacterial pneumonia. Fungal pneumonia is most often caused by Histoplasma capsulatum, blastomyces, Cryptococcus neoformans, Pneumocystis jiroveci, and Coccidioides immitis. Histoplasmosis is most common in the Mississippi River basin, and coccidioidomycosis is most common in the southwestern United States.[16]

Parasites
Main article: Parasitic pneumonia A variety of parasites can affect the lungs. These parasites typically enter the body through the skin or the mouth. Once inside the body, they travel to the lungs, usually through the blood. In parasitic pneumonia, as with other kinds of pneumonia, a combination of cellular destruction and immune response causes disruption of oxygen transportation. One type of white blood cell, the eosinophil, responds vigorously to parasite infection. Eosinophils in the lungs can lead to eosinophilic pneumonia, thus complicating the underlying parasitic pneumonia. The most common parasites causing pneumonia are Toxoplasma gondii, Strongyloides stercoralis, and Ascariasis.

Idiopathic
Main article: Idiopathic interstitial pneumonia Idiopathic interstitial pneumonia or noninfectious pneumonia[21] are a class of diffuse lung diseases. They include: diffuse alveolar damage, organizing pneumonia, nonspecific interstitial pneumonia, lymphocytic interstitial pneumonia, desquamative interstitial pneumonia, respiratory bronchiolitis interstitial lung disease, and usual interstitial pneumonia.[22]

Pathophysiology

Pneumonia fills the lung's alveoli with fluid, hindering oxygenation. The alveolus on the left is normal, while on the right it is full of fluid from pneumonia. Pneumonia frequently starts as a upper respiratory tract infection that moves into the lower respiratory tract.[23]

Viral
Viruses invade cells in order to reproduce. Typically, a virus reaches the lungs when airborne droplets are inhaled through the mouth or nose. Once in the lungs, the virus invades the cells lining the airways and alveoli. This invasion often leads to cell death, either from damage to the cell by the virus, or from a protective process called apoptosis in which the infected cell destroys itself before it can be used as a conduit for virus reproduction. When the immune system responds to the viral infection, even more lung damage occurs. White blood cells, mainly lymphocytes, activate certain chemical cytokines which allow fluid to leak into the alveoli. This combination of cell destruction and fluid-filled alveoli interrupts the normal transportation of oxygen into the bloodstream. As well as damaging the lungs, many viruses affect other organs and thus disrupt many body functions. Viruses can also make the body more susceptible to other bacterial infections; in this way bacterial pneumonia can arrise as a co-morbid condition.[20]

Bacterial
Bacteria typically enter the lung when airborne droplets are inhaled, but can also reach the lung through the bloodstream when there is an infection in another part of the body. Many bacteria live in parts of the upper respiratory tract, such as the nose, mouth and sinuses, and can easily be inhaled into the alveoli. Once inside, bacteria may invade the spaces between cells and between alveoli through connecting pores. This invasion triggers the immune system to send neutrophils, a type of defensive white blood cell, to the lungs. The neutrophils engulf and kill the offending organisms, and also release cytokines, causing a general activation of the immune system. This

leads to the fever, chills, and fatigue common in bacterial and fungal pneumonia. The neutrophils, bacteria, and fluid from surrounding blood vessels fill the alveoli and interrupt normal oxygen transportation.

Diagnosis
Crackles Crackles heard in the lungs of a person with pneumonia using a stethoscope.
Problems listening to this file? See media help.

Pneumonia is typically diagnosed based on a combination of physical signs and a chest X-ray.[24] Confirming the underlying cause can be difficult, however, with no definitive test able to distinguish between bacterial and not-bacterial origin.[15][24] The World Health Organization has defined pneumonia in children clinically based on a either a cough or difficulty breathing and a rapid respiratory rate, chest indrawing, or a decreased level of consciousness.[25] A rapid respiratory rate is defined as greater than 60 breaths per minute in children under 2 months old, 50 breaths per minute in children two months to one year old, or greater than 40 breaths per minute in children one to five years old.[25] In children, an increased respiratory rate and lower chest indrawing are more sensitive than hearing chest crackles with a stethoscope.[11] In adults investigations are generally not needed in mild cases[26] as if all vital signs and auscultation are normal the risk of pneumonia is very low.[27]In those requiring admission to a hospital, pulse oximetry, chest radiography, and blood tests including a complete blood count, serum electrolytes, C-reactive protein, and possibly liver function tests are recommended.[26] The diagnosis of influenza-like illness can be made based on presenting signs and symptoms however verification of an influenza infection requires testing.[28] Thus treatment is frequently based on the presence of influenza in the community or a rapid influenza test.[28]

Imaging

CT of the chest demonstrating right sided pneumonia (left side of the image). A chest radiograph is frequently used in diagnosis.[11] In people with mild disease imaging is only needed in those with potential complications, those who have not improved with treatment, or those in which the cause in uncertain.[11][26] If a person is sufficiently sick to require

hospitalization, a chest radiograph is recommended.[26] Findings do not always correlate with severity of disease and do not reliably distinguish between bacterial versus viral infection.[11] X-ray signs of bacterial community acquired pneumonia classically show lung consolidation of one lung segmental lobe.[7] However, radiographic findings may be variable, especially in other types of pneumonia.[7] Aspiration pneumonia may present with bilateral opacities primarily in the bases of the lungs and on the right side.[7] Radiographs of viral pneumonia cases may appear normal, hyper-inflated, have bilateral patchy areas, or present similar to bacterial pneumonia with lobar consolidation.[7] A CT scan can give additional information in indeterminate cases.[7]

Microbiology
For people managed in the community figuring out the causative agent is not cost effective, and typically does not alter management.[11] For those who do not respond to treatment, sputum culture should be considered, and culture for Mycobacterium tuberculosis should be carried out in those with a chronic productive cough.[26] Testing for other specific organisms may be recommended during outbreaks, for public health reasons.[26] In those who are hospitalized for severe disease both sputum and blood cultures are recommended.[26] Viral infections can be confirmed via detection of either the virus or its antigens with culture or polymerase chain reaction (PCR) among other techniques.[15] With routine microbiological testing a causative agent is determined in only 15% of cases.[10]

Differential diagnosis
Several diseases can present similar to pneumonia, including: chronic obstructive pulmonary disease (COPD), asthma, pulmonary edema, bronchiectasis, lung cancer and pulmonary emboli.[10] Unlike pneumonia, asthma and COPD typically present with wheezing, pulmonary edema presents with an abnormal electrocardiogram, cancer and bronchiectasis present with a cough of longer duration, and pulmonary emboli presents with acute onset sharp chest pain and shortness of breath.[10]

Prevention
Prevention includes vaccination, environmental measures, and appropriately treating other diseases.[11]

Vaccination
Vaccination is effective for preventing certain bacterial and viral pneumonias in both children and adults. Influenza vaccines are modestly effective against influenza A and B.[15][29] The Center for Disease Control and Prevention (CDC) recommends that everyone 6 months and older get yearly vaccination.[30] When an influenza outbreak is occurring, medications such as amantadine, rimantadine, zanamivir, and oseltamivir can help prevent influenza.[31][32]

Vaccinations against Haemophilus influenzae and Streptococcus pneumoniae have good evidence to support their use.[23] Vaccinating children against Streptococcus pneumoniae has also led to a decreased incidence of these infections in adults, because many adults acquire infections from children. A vaccine against Streptococcus pneumoniae is also available for adults, and has been found to decrease the risk of invasive pneumococcal disease.[33]

Environmental
Reducing indoor air pollution is recommended[11] as is smoking cessation.[26]

Other
Appropriately treating underlying illnesses (such as AIDS) can decrease a person's risk of pneumonia. There are several ways to prevent pneumonia in newborn infants. Testing pregnant women for Group B Streptococcus and Chlamydia trachomatis, and giving antibiotic treatment, if needed, reduces pneumonia in infants. Suctioning the mouth and throat of infants with meconium-stained amniotic fluid decreases the rate of aspiration pneumonia.

Management
Typically, oral antibiotics, rest, simple analgesics, and CURB-65 fluids are sufficient for complete resolution.[26] Symptom Points However, those with other medical conditions, the 1 elderly, or those with significant trouble breathing may Confusion Urea>7mmol/l 1 require more advanced care. If the symptoms worsen, the pneumonia does not improve with home treatment, Respiratory rate>30 1 or complications occur, hospitalization may be SBP<90mmHg, DBP<60mmHg 1 required.[26] Worldwide, approximately 713% of cases Age>=65 1 in children result in hospitalization[11] while in the developed world between 2242% of adults with community acquired pneumonia are admitted.[26] The CURB-65 score is useful for determining the need for admission in adults.[26] If the score is 0 or 1 people can typically be managed at home, if it is 2 a short hospital stay or close follow up is needed, if it is 35 hospitalization is recommended.[26] In children those with respiratory distress or oxygen saturation's of less than 90% should be hospitalized.[34] The utility of chest physiotherapy in pneumonia has not yet been determined.[35] Over the counter cough medicine has not been found to be effective.[36]

Bacterial
Antibiotics improve outcomes in those with bacterial pneumonia.[37] Initially antibiotic choice depends on the characteristics of the person affected, such as age, underlying health, and the location the infection was acquired. In the UK empiric treatment with amoxicillin is recommended first line for community-acquired pneumonia with doxycycline or clarithromycin

as alternatives.[26] In North America, where the "atypical" forms of community-acquired pneumonia are more common, macrolides (such as azithromycin), and doxycycline have displaced amoxicillin as first-line outpatient treatment in adults.[19][38] In children with mild or moderate symptoms amoxicillin is still the first line.[34] The use of fluoroquinolones in uncomplicated cases is discouraged due to concerns of side effects and resistance.[19] The duration of treatment has traditionally been seven to ten days, but there is increasing evidence that short courses (three to five days) are similarly effective.[39] Antibiotics recommended for hospital-acquired pneumonia include third- and fourth-generation cephalosporins, carbapenems, fluoroquinolones, aminoglycosides, and vancomycin.[40] These antibiotics are often given intravenously, and may be used in combination.

Viral
Neuraminidase inhibitors may be used to treat viral pneumonia caused by influenza viruses (influenza A and influenza B).[15] No specific antiviral medications are recommended for other types of community acquired viral pneumonias including SARS coronavirus, adenovirus, hantavirus, and parainfluenza virus.[15] Influenza A may be treated with rimantadine or amantadine, while influenza A or B may be treated with oseltamivir, zanamivir or peramivir.[15] These are of most benefit if they are started within 48 hours of the onset of symptoms.[15] Many strains of H5N1 influenza A, also known as avian influenza or "bird flu," have shown resistance to rimantadine and amantadine.[15] The use of antibiotics in viral pneumonia is recommended by some experts as it is impossible to rule out a complicating bacterial infection.[15] The British Thoracic Society recommends that antibiotics be withheld in those with mild disease.[15] The use of corticosteroids is controversial.[15]

Aspiration
Aspiration pneumonitis is generally treated conservatively with antibiotics only indicated for aspiration pneumonia.[41] The choice of antibiotic will depend on several factors, including the suspected causative organism and whether pneumonia was acquired in the community or developed in a hospital setting. Common options include clindamycin, a combination of a betalactam antibiotic and metronidazole, or an aminoglycoside.[42] Corticosteroids are commonly used in aspiration pneumonia, but there is no evidence to support their effectiveness.[42]

Prognosis
With treatment, most types of bacterial pneumonia can be cleared within two to four weeks[43] and mortality is very low.[15] Viral pneumonia may last longer, and mycoplasmal pneumonia may take four to six weeks to resolve completely.[43] The eventual outcome of an episode of pneumonia depends on how ill the person is when he or she was first diagnosed.[43] Before the advent of antibiotics mortality was typically 30% for hospitalized patients.[16] In the United States, about 5% of those diagnosed with pneumococcal pneumonia will die. In cases where the pneumonia progresses to blood infection, just over 20% will die.[44]

The death rate (or mortality) also depends on the underlying cause of the pneumonia. Pneumonia caused by Mycoplasma, for instance, is associated with lower mortality. However, about half of the people who develop methicillin-resistant Staphylococcus aureus (MRSA) pneumonia while on a ventilator will die.[45] In regions of the world without advanced health care systems, pneumonia is even more deadly. Limited access to clinics and hospitals, limited access to x-rays, limited antibiotic choices, and inability to diagnose and treat underlying conditions inevitably lead to higher rates of death from pneumonia. For these reasons, the majority of deaths in children under five due to pneumococcal disease occur in developing countries.[46] Adenovirus can cause severe necrotizing pneumonia in which all or part of a lung has increased translucency radiographically, which is called Swyer-James Syndrome.[47] Severe adenovirus pneumonia also may result in bronchiolitis obliterans, a subacute inflammatory process in which the small airways are replaced by scar tissue, resulting in a reduction in lung volume and lung compliance.[47] Sometimes pneumonia can lead to additional complications. Complications are more frequently associated with bacterial pneumonia than with viral pneumonia. The most important complications include respiratory and circulatory failure and pleural effusions, empyema or abscesses.

Clinical prediction rules

Clinical prediction rules have been developed to more objectively prognosticate outcomes in pneumonia. Although these rules are often used in deciding whether or not to hospitalize the person, they were derived simply to inform on prognosis; neither index was designed or tested as guide to determine whether the person would benefit by hospital admission.

Pneumonia severity index (or PORT Score)[48] online calculator CURB-65 score, which takes into account the severity of symptoms, any underlying diseases, and age[49] online calculator

Pleural effusion, empyema, and abscess

A pleural effusion as seen on chest x-ray. The A arrow indicates fluid layering in the right chest. The B arrow indicates the width of the right lung. The volume of the lung is reduced because of the collection of fluid around the lung.

In pneumonia, a collection of fluid (pleural effusion) often forms in the space that surrounds the lung (the pleural cavity). Occasionally, microorganisms will infect this fluid, causing what is called an empyema. To distinguish an empyema from the more common simple parapneumonic effusion, the fluid is collected with a needle (thoracentesis), and examined. If this shows evidence of empyema, complete drainage of the fluid may be necessary, often requiring a chest tube. In severe cases of empyema, surgery may be needed. If the infected fluid is not drained, the infection may persist, because antibiotics do not penetrate well into the pleural cavity. If the fluid is sterile, it need only be drained if it is causing symptoms or remains unresolved. Rarely, bacteria in the lung will form a pocket of infected fluid called a lung abscess. Lung abscesses can usually be seen with a chest x-ray or chest CT scan. Abscesses typically occur in aspiration pneumonia, and often contain several types of bacteria. Antibiotics are usually adequate to treat a lung abscess, but sometimes the abscess must be drained by a surgeon or radiologist.

Respiratory and circulatory failure

Because pneumonia affects the lungs, people with pneumonia often have difficulty breathing, sometimes to the point where mechanical assistance is required. Non-invasive breathing assistance may be helpful, such as with a bi-level positive airway pressure machine. In other cases, placement of an endotracheal tube (breathing tube) may be necessary, and a ventilator may be used to help the person breathe. Pneumonia can also cause respiratory failure by triggering acute respiratory distress syndrome (ARDS), which results from a combination of infection and inflammatory response. The lungs quickly fill with fluid and become very stiff. This stiffness, combined with severe difficulties extracting oxygen due to the alveolar fluid, creates a need for mechanical ventilation. Sepsis and septic shock are potential complications of pneumonia. Sepsis occurs when microorganisms enter the bloodstream and the immune system responds by secreting cytokines. Sepsis most often occurs with bacterial pneumonia; Streptococcus pneumoniae is the most common cause. Individuals with sepsis or septic shock need hospitalization in an intensive care unit. They often require intravenous fluids and medications to help keep their blood pressure up. Sepsis can cause liver, kidney, and heart damage, among other problems, and it is often fatal.

Epidemiology
Main article: Epidemiology of pneumonia

Age-standardized death from lower respiratory tract infections per 100,000 inhabitants in 2004.[50] no data 3500-4200 <100 4200-4900 100-700 4900-5600 700-1400 5600-6300 1400-2100 6300-7000 2100-2800 >7000 2800-3500 Pneumonia is a common illness affecting approximately 450 million people a year and occurring in all parts of the world.[15] It is a major cause of death among all age groups resulting in 4 million deaths (7% of the world's yearly total).[37][15] Rates are greatest in children less than five, and adults older than 75 years of age.[15] It occurs about five times more frequently in the developing world versus the developed world.[15] Viral pneumonia accounts for about 200 million cases.[15]

Children
In 2008 pneumonia occurred in approximately 156 million children (151 million in the developing world and 5 million in the developed world).[15] It resulted in 1.6 million deaths, or 2834% of all deaths in those under five years of age, of which 95% occurred in the developing world.[15][11] Countries with the greatest burden of disease include: India (43 million), China (21 million) and Pakistan (10 million).[51] It is the leading cause of death among children in low income countries.[37][15] Many of these deaths occur in the newborn period. The World Health Organization estimates that one in three newborn infant deaths are due to pneumonia.[52] Approximately half of these deaths are theoretically preventable, as they are caused by the bacteria for which an effective vaccine is available.[53]

History

WPA poster, 1936/1937 Pneumonia has been a common disease throughout human history.[54] The symptoms were described by Hippocrates (c. 460 BC 370 BC):[54] "Peripneumonia, and pleuritic affections, are to be thus observed: If the fever be acute, and if there be pains on either side, or in both, and if expiration be if cough be present, and the sputa expectorated be of a blond or livid color, or likewise thin, frothy, and florid, or having any other character different from the common... When pneumonia is at its height, the case is beyond remedy if he is not purged, and it is bad if he has dyspnoea, and urine that is thin and acrid, and if sweats come out about the neck and head, for such sweats are bad, as proceeding from the suffocation, rales, and the violence of the disease which is obtaining the upper hand."[55] However, Hippocrates referred to pneumonia as a disease "named by the ancients." He also reported the results of surgical drainage of empyemas. Maimonides (11351204 AD) observed "The basic symptoms which occur in pneumonia and which are never lacking are as follows: acute fever, sticking [pleuritic] pain in the side, short rapid breaths, serrated pulse and cough."[56] This clinical description is quite similar to those found in modern textbooks, and it reflected the extent of medical knowledge through the Middle Ages into the 19th century. Bacteria were first seen in the airways of individuals who died from pneumonia by Edwin Klebs in 1875.[57] Initial work identifying the two common bacterial causes Streptococcus pneumoniae and Klebsiella pneumoniae was performed by Carl Friedlnder[58] and Albert Frnkel[59] in 1882 and 1884, respectively. Friedlnder's initial work introduced the Gram stain, a fundamental laboratory test still used today to identify and categorize bacteria. Christian Gram's paper describing the procedure in 1884 helped differentiate the two different bacteria, and showed that pneumonia could be caused by more than one microorganism.[60]

Sir William Osler, known as "the father of modern medicine," appreciated the death and disability cause by pneumonia, describing it as the "captain of the men of death" in 1918, as it had overtaken tuberculosis as one of the leading causes of death in this time. This phrase was originally coined by John Bunyan in reference to "consumption" (tuberculosis).[61][62] Osler also described pneumonia as "the old man's friend" as death was often quick and painless when there was many slower more painful ways to die.[16] Several developments in the 1900s improved the outcome for those with pneumonia. With the advent of penicillin and other antibiotics, modern surgical techniques, and intensive care in the twentieth century, mortality from pneumonia, which had approached 30%, dropped precipitously in the developed world. Vaccination of infants against Haemophilus influenzae type B began in 1988 and led to a dramatic decline in cases shortly thereafter.[63] Vaccination against Streptococcus pneumoniae in adults began in 1977, and in children in 2000, resulting in a similar decline.[64]

Society and culture

See also: List of pneumonia victims Because of the combination of a very high burden of disease in developing countries and a relatively low awareness of the disease in industrialized countries, the global health community has declared November 12 to be World Pneumonia Day, a day for concerned citizens and policy makers to take action against the disease.

Hemothorax
From Wikipedia, the free encyclopedia

Hemothorax
Classification and external resources ICD-10 ICD-9 DiseasesDB eMedicine MeSH J94.2, S27.1 511.8, 860 19762 med/2915 ped/971 D006491

Hemothorax in an animal A hemothorax (or haemothorax) is a condition that results from blood accumulating in the pleural cavity.

Contents
[hide]

1 Cause and presentation 2 Prognosis 3 Signs and symptoms 4 Management 5 See also 6 References

[edit] Cause and presentation

Its cause is usually traumatic, from a blunt or penetrating injury to the thorax, resulting in a rupture of the serous membrane either lining the thorax or 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 3040% of a person's blood volume. Even minor injury to the chest wall can lead to significant hemothorax.[1]

[edit] 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.

[edit] Signs and symptoms

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

[edit] 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. Usually the lung will expand and the bleeding will stop after a chest tube is inserted. The blood in the chest can thicken as the clotting cascade is activated when the blood leaves the blood vessels and is activated by the pleural surface, injured lung or chest wall, or contact with the chest tube. As the blood thickens, it can clot in the pleural space (leading to a retained hemothorax) or within the chest tube, leading to chest tube clogging or occlusion. Chest tube clogging or occlusion can lead to worse outcomes as it prevents adequate drainage of the pleural space, contributing to the problem of retained hemothorax. In this case, patients can be hypoxic, short of breath, or in some cases, the retained hemothorax can become infected (empyema). Therefore adequately functioning chest tubes are essential in the setting of a hemothorax treated with a chest tube. To attempt to minimize the potential for clogging, the surgeons will often place more than one tube, or large diameter tubes. Maintaining an adequately functioning chest tube is an active process, usually for the nurses, that often requires tapping the tubes, milking the tubes, or stripping the tubes to minimize potential for clogging in the tube in the setting of a hemothorax. When these efforts fail a new chest tube must be placed, or the patient must be taken to the operating room by a surgeon to open the chest and remove the blood clot, and re insert adequately functioning chest tubes. Thrombolytic agents have been used to break up clot in tubes or when the clot becomes organized in the pleural space, however this is risky as it can lead to increased bleeding and the need for reoperation.[2] Therefore, ideally, the tubes maintain their function so that the blood cannot clot in the chest or the tube. In some cases bleeding continues and surgery is necessary to stop the source of bleeding. For example, if the cause is rupture of the aorta in high energy trauma, the intervention by a thoracic surgeon is mandatory.

[edit] Pleural

effusion

From Wikipedia, the free encyclopedia

Pleural effusion
Classification and external resources

A large left sided pleural effusion as seen on an upright chest X-ray ICD-10 ICD-9 MeSH J90-J91 511.9 D010996

Pleural effusion is excess fluid that accumulates between the pleura, the fluid-filled space that surrounds the lungs. Excessive amounts of such fluid can impair breathing by limiting the expansion of the lungs during respiration.

Contents
[hide]

1 Pathophysiology 2 Types of fluids 3 Diagnosis o 3.1 Imaging o 3.2 Thoracentesis o 3.3 Transudate vs. exudate: Light's criteria 4 Causes o 4.1 Transudative o 4.2 Exudative o 4.3 Other/ungrouped

5 Treatment 6 See also 7 References 8 External links

[edit] Pathophysiology
Pleural fluid is secreted by the parietal and visceral layer of the pleura.

[edit] Types of fluids

Four types of fluids can accumulate in the pleural space:

Serous fluid (hydrothorax) Blood (haemothorax) Chyle (chylothorax) Pus (pyothorax or empyema)

[edit] Diagnosis
Pleural effusion is usually diagnosed on the basis of medical history and physical exam, and confirmed by chest x-ray. Once accumulated fluid is more than 300 ml, there are usually detectable clinical signs in the patient, such as decreased movement of the chest on the affected side, stony dullness to percussion over the fluid, diminished breath sounds on the affected side, decreased vocal resonance and fremitus (though this is an inconsistent and unreliable sign), and pleural friction rub. Above the effusion, where the lung is compressed, there may be bronchial breathing and egophony. In large effusion there may be tracheal deviation away from the effusion. A systematic review (2009) published as part of the Rational Clinical Examination Series in the Journal of the American Medical Association (JAMA) showed that dullness to conventional percussion was most accurate for diagnosing pleural effusion (summary positive likelihood ratio, 8.7; 95% confidence interval, 2.233.8), while the absence of reduced tactile vocal fremitus made pleural effusion less likely (negative likelihood ratio, 0.21; 95% confidence interval, 0.120.37).[1]

[edit] Imaging
Normally the space between the two layers of the lung, the visceral pleura and the parietal pleura, cannot be seen. A pleural effusion infiltrates the space between these layers. Because the pleural effusion has a density similar to body fluid or water, it can be seen on radiographs. Since the effusion has greater density than the rest of the lung, it will gravitate towards the lower portions of the pleural cavity. The pleural effusion behaves according to basic fluid dynamics, conforming to the shape of the lung and chest cavity. If the pleural cavity contains both air and fluid, then the fluid will have a "fluid level" that is horizontal instead of conforming to the lung

space.[2] Chest radiographs acquired in the lateral decubitus position (with the patient lying on his side) are more sensitive and can pick up as little as 50 ml of fluid. At least 300 ml of fluid must be present before upright chest films can pick up signs of pleural effusion (e.g., blunted costophrenic angles).

Massive left-sided pleural effusion (whiteness) in a patient presenting with lung cancer.

CT scan of chest showing left sided pleural effusion. Effusion fluid often settles at the lowest space due to gravity; here at the back as the patient is lying under scanner.

Micrograph of a pleural fluid cytopathology specimen showing malignant mesothelioma, one cause of a pleural effusion.

[edit] Thoracentesis
Once a pleural effusion is diagnosed, the cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis. A needle is inserted through the back of the chest wall in the sixth, seventh, or eighth intercostal space on the midaxillary line, into the pleural space. The fluid may then be evaluated for the following: 1. Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pH, and glucose 2. Gram stain and culture to identify possible bacterial infections 3. Cell count and differential 4. Cytopathology to identify cancer cells, but may also identify some infective organisms 5. Other tests as suggested by the clinical situation lipids, fungal culture, viral culture, specific immunoglobulins

[edit] Transudate vs. exudate: Light's criteria

Transudate vs. exudate view talk edit Transudate Exudate Increased hydrostatic pressure, Main causes Inflammation Decreased colloid osmotic pressure Appearance Clear[3] Cloudy[3] Specific gravity < 1.012 > 1.020 Protein content < 2 g/dL > 2.9 g/dL[4] fluid protein < 0.5 > 0.5[5] serum protein Difference of albumin content > 1.2 g/dL < 1.2 g/dL[6] with blood albumin fluid LDH < 0.6 or < > 0.6[4] or > [5] upper limit for serum Cholesterol content < 45 mg/dL > 45 mg/dL[4]
See also: Rivalta test

Instruments for needle biopsy of the pleura

Definitions of the terms "transudate" and "exudate" are the source of much confusion. Briefly, transudate is produced through pressure filtration without capillary injury while exudate is "inflammatory fluid" leaking between cells. Transudative pleural effusions are defined as effusions that are caused by systemic factors that alter the pleural equilibrium, or Starling forces. The components of the Starling forces hydrostatic pressure, permeability, oncotic pressure (effective pressure due to the composition of the pleural fluid and blood)are altered in many diseases, e.g., left ventricular failure, renal failure, hepatic failure, and cirrhosis. Exudative pleural effusions, by contrast, are caused by alterations in local factors that influence the formation and absorption of pleural fluid (e.g., bacterial pneumonia, cancer, pulmonary embolism, and viral infection).[7] An accurate diagnosis of the cause of the effusion, transudate versus exudate, relies on a comparison of the chemistries in the pleural fluid to those in the blood, using Light's criteria. According to Light's criteria (Light, et al. 1972), a pleural effusion is likely exudative if at least one of the following exists:[8] 1. The ratio of pleural fluid protein to serum protein is greater than 0.5 2. The ratio of pleural fluid LDH and serum LDH is greater than 0.6 3. Pleural fluid LDH is greater than 0.6 [4] or [8] times the normal upper limit for serum. Different laboratories have different values for the upper limit of serum LDH, but examples include 200[9] and 300[9] IU/l.[10] Although Light's criteria are relatively accurate, twenty-five percent of patients with transudative pleural effusions are mistakenly identified by Light's criteria as having exudative pleural effusions. Therefore, if a patient identified by Light's criteria as having an exudative pleural effusion appears clinically to have a condition that usually produces transudative effusions, additional testing is needed. In such cases albumin levels in blood and pleural fluid are measured. If the difference between the albumin level in the blood and the pleural fluid is greater than 1.2 g/dL (12 g/L), this suggests that the patient has a transudative pleural effusion.[6] However, pleural fluid testing is not perfect, and the final decision about whether a fluid is a transudate or an exudate is based not on chemical analysis of the fluid, but on accurate diagnosis of the disease that produces the fluid. The traditional definitions of transudate as a pleural effusion due to systemic factors and an exudate as a pleural effusion due to local factors have been used since 1940 or earlier (Light et al., 1972). Previous to Light's landmark study, which was based on work by Chandrasekhar, investigators unsuccessfully attempted to use other criteria, such as specific gravity, pH, and protein content of the fluid, to differentiate between transudates and exudates. Light's criteria are highly statistically sensitive for exudates (although not very statistically specific). More recent studies have examined other characteristics of pleural fluid that may help to determine whether the process producing the effusion is local (exudate) or systemic (transudate). The chart at right illustrates some of the results of these more recent studies. However, it should be borne in mind that Light's criteria are still the most widely used criteria.

The Rational Clinical Examination Series review found that bilateral effusions, symmetric and asymmetric, are the most common distribution in heart failure (60% of effusions in heart failure will be bilateral). When there is asymmetry in heart failure-associated pleural effusions (either unilateral or one side larger than the other), the right side is usually more involved than the left.[1]

[edit] Causes
[edit] Transudative
The most common causes of transudative pleural effusions in the United States are left ventricular failure, and cirrhosis (causing hepatic hydrothorax),nephrotic syndrome leading to increased loss of albumin and resultant hypoalbuminemia and thus reducing colloid osmotic pressure is another less common cause. Pulmonary embolisms were once thought to be transudative but have been recently shown to be exudative[11]

[edit] Exudative

Pleural effusion Chest x-ray of a pleural effusion. The arrow A shows fluid layering in the right pleural cavity. The B arrow shows the normal width of the lung in the cavity Once identified as exudative, additional evaluation is needed to determine the cause of the excess fluid, and pleural fluid amylase, glucose, pH and cell counts are obtained.

Pleural fluid amylase is elevated in cases of esophageal rupture, pancreatic pleural effusion, or cancer. Glucose is decreased with cancer, bacterial infections, or rheumatoid pleuritis. Pleural fluid pH is low in empyema (<7.2) and may be low in cancer. If cancer is suspected, the pleural fluid is sent for cytology. If cytology is negative, and cancer is still suspected, either a thoracoscopy, or needle biopsy[12] of the pleura may be performed. The fluid is also sent for Gram staining and culture, and, if suspicious for tuberculosis, examination for TB markers (adenosine deaminase > 45 IU/L, interferon gamma > 140 pg/mL, or positive polymerase chain reaction (PCR) for tuberculous DNA).

The most common causes of exudative pleural effusions are bacterial pneumonia, cancer (with lung cancer, breast cancer, and lymphoma causing approximately 75% of all malignant pleural effusions), viral infection, and pulmonary embolism.

[edit] Other/ungrouped
Other causes of pleural effusion include tuberculosis (though pleural fluid smears are rarely positive for AFB, this is the most common cause of pleural effusion in some developing countries), autoimmune disease such as systemic lupus erythematosus, bleeding (often due to chest trauma), chylothorax (most commonly caused by trauma), and accidental infusion of fluids. Less common causes include esophageal rupture or pancreatic disease, intra-abdominal abscess, rheumatoid arthritis, asbestos pleural effusion, Meigs syndrome (ascites and pleural effusion due to a benign ovarian tumor), and ovarian hyperstimulation syndrome. Pleural effusions may also occur through medical/surgical interventions, including the use of medications (pleural fluid is usually eosinophilic), coronary artery bypass surgery, abdominal surgery, endoscopic variceal sclerotherapy, radiation therapy, liver or lung transplantation, and intra- or extravascular insertion of central lines.

[edit] Treatment

The free end of the Chest Drainage Device is usually attached to an underwater seal, below the level of the chest. This allows the air or fluid to escape from the pleural space, and prevents anything returning to the chest. Treatment depends on the underlying cause of the pleural effusion. Therapeutic aspiration may be sufficient; larger effusions may require insertion of an intercostal drain (either pigtail or surgical). When managing these chest tubes, it is important to make sure the chest tubes do not become occluded or clogged. A clogged chest tube in the setting of continued production of fluid will result in residual fluid left behind when the chest tube is removed. This fluid can lead to complications such as hypoxia due to lung collapse from the fluid, or fibrothorax, later, when the space scars down. Repeated effusions may require chemical (talc, bleomycin, tetracycline/doxycycline), or surgical pleurodesis, in which the two pleural surfaces are scarred to each other so that no fluid can accumulate between them. This is a surgical procedure that involves inserting a chest tube, then either mechanically abrading the pleura or inserting the chemicals to induce a scar. This requires the chest tube to stay in until the fluid drainage stops. This can take days to weeks and can require prolonged hospitalizations. If the chest tube becomes clogged, fluid will be left behind and the pleurodesis will fail.

Pleurodesis fails in as many as 30% of cases. An alternative is to place a Pleurex or Aspira Drainage Catheter. This is a 15Fr chest tube with a one-way valve. Each day the patient or care givers connect it to a simple vacuum tube and remove from 600 cc to 1000 cc of fluid. This can be repeated daily. When not in use, the tube is capped. This allows patients to be outside the hospital. For patients with malignant pleural effusions, it allows them to continue chemotherapy, if indicated. Generally the tube is in for about 30 days and then it is removed when the space undergoes a spontaneous pleurodesis.

Pulmonary contusion
From Wikipedia, the free encyclopedia

Pulmonary contusion
Classification and external resources

A CT scan showing a pulmonary contusion (red arrow) accompanied by a rib fracture (blue arrow) ICD-10 ICD-9 S27.3 861.21, 861.31

A pulmonary contusion (or lung contusion) is a contusion (bruise) of the lung, caused by chest trauma. As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue. The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels (hypoxia). Unlike pulmonary laceration, another type of lung injury, pulmonary contusion does not involve a cut or tear of the lung tissue. A pulmonary contusion is usually caused directly by blunt trauma but can also result from explosion injuries or a shock wave associated with penetrating trauma. With the use of explosives during World Wars I and II, pulmonary contusion resulting from blasts gained recognition. In the 1960s its occurrence in civilians began to receive wider recognition, in which cases it is usually caused by traffic accidents. The use of seat belts and airbags reduces the risk to vehicle occupants.

Diagnosis is made by studying the cause of the injury, physical examination and chest radiography. Typical signs and symptoms include direct effects of the physical trauma, such as chest pain and coughing up blood, as well as signs that the body is not receiving enough oxygen, such as cyanosis. The contusion frequently heals on its own with supportive care. Often nothing more than supplemental oxygen and close monitoring is needed; however, intensive care may be required. For example, if breathing is severely compromised, mechanical ventilation may be necessary. Fluid replacement may be required to ensure adequate blood volume, but fluids are given carefully since fluid overload can worsen pulmonary edema, which may be lethal. The severity ranges from mild to deadlysmall contusions may have little or no impact on the patient's healthyet pulmonary contusion is the most common type of potentially lethal chest trauma. It occurs in 3075% of severe chest injuries. With an estimated mortality rate of 14 40%, pulmonary contusion plays a key role in determining whether an individual will die or suffer serious ill effects as the result of trauma. Pulmonary contusion is usually accompanied by other injuries. Although associated injuries are often the cause of death, pulmonary contusion is thought to cause death directly in a quarter to half of cases. Children are at especially high risk for the injury because the relative flexibility of their bones prevents the chest wall from absorbing force from an impact, causing it to be transmitted instead to the lung. Pulmonary contusion is associated with complications including pneumonia and acute respiratory distress syndrome, and it can cause long-term respiratory disability.

Contents
[hide]

1 Classification 2 Signs and symptoms 3 Causes 4 Mechanism 5 Pathophysiology o 5.1 Bleeding and edema o 5.2 Consolidation and collapse o 5.3 Ventilation/perfusion mismatch 6 Diagnosis o 6.1 X-ray o 6.2 Computed tomography o 6.3 Ultrasound 7 Prevention 8 Treatment o 8.1 Ventilation o 8.2 Fluid therapy o 8.3 Supportive care 9 Prognosis o 9.1 Complications o 9.2 Associated injuries 10 Epidemiology

11 History 12 References 13 External links

[edit] Classification

The alveoli Pulmonary contusion and laceration are injuries to the lung tissue. Pulmonary laceration, in which lung tissue is torn or cut, differs from pulmonary contusion in that the former involves disruption of the macroscopic architecture of the lung,[1] while the latter does not.[2] When lacerations fill with blood, the result is pulmonary hematoma, a collection of blood within the lung tissue.[3] Contusion involves hemorrhage in the alveoli (tiny air-filled sacs responsible for absorbing oxygen), but a hematoma is a discrete clot of blood not interspersed with lung tissue.[4] A collapsed lung can result when the pleural cavity (the space outside the lung) accumulates blood (hemothorax) or air (pneumothorax) or both (hemopneumothorax). These conditions do not inherently involve damage to the lung tissue itself, but they may be associated with it. Injuries to the chest wall are also distinct from but may be associated with lung injuries. Chest wall injuries include rib fractures and flail chest, in which multiple ribs are broken so that a segment of the ribcage is detached from the rest of the chest wall and moves independently.

[edit] Signs and symptoms

Presentation may be subtle; people with mild contusion may have no symptoms at all.[5] However, pulmonary contusion is frequently associated with signs (objective indications) and symptoms (subjective states), including those indicative of the lung injury itself and of accompanying injuries. Because gas exchange is impaired, signs of low blood oxygen saturation, such as low concentrations of oxygen in arterial blood gas and cyanosis (bluish color of the skin and mucous membranes) are commonly associated.[6] Dyspnea (painful breathing or difficulty breathing) is commonly seen,[6] and tolerance for exercise may be lowered.[7] Rapid breathing and a rapid heart rate are other signs.[8][9] With more severe contusions, breath sounds heard through a stethoscope may be decreased, or rales (an abnormal crackling sound in the chest accompanying breathing) may be present.[6][10] People with severe contusions may have bronchorrhea (the production of watery sputum).[11] Wheezing and coughing are other signs.[12]

Coughing up blood or bloody sputum is present in up to half of cases.[12] Cardiac output (the volume of blood pumped by the heart) may be reduced,[11] and hypotension (low blood pressure) is frequently present.[6] The area of the chest wall near the contusion may be tender[13] or painful due to associated chest wall injury. Signs and symptoms take time to develop, and as many as half of cases are asymptomatic at the initial presentation.[5] The more severe the injury, the more quickly symptoms become apparent. In severe cases, symptoms may occur as quickly as three or four hours after the trauma.[11] Hypoxemia (low oxygen concentration in the arterial blood) typically becomes progressively worse over 2448 hours after injury.[14] In general, pulmonary contusion tends to worsen slowly over a few days,[4] but it may also cause rapid deterioration or death if untreated.[6]

[edit] Causes

Motor vehicle accidents are the most common cause of pulmonary contusion. Pulmonary contusion, which occurs in 2535% of all blunt chest trauma,[15] is usually caused by the rapid deceleration that results when the moving chest strikes a fixed object.[12] About 70% of cases result from motor vehicle collisions,[16] most often when the chest strikes the inside of the car.[6] Falls,[16] assaults,[17] and sports injuries are other causes.[18] Pulmonary contusion can also be caused by explosions; the organs most vulnerable to blast injuries are those that contain gas, such as the lungs.[19] Blast lung is severe pulmonary contusion, bleeding, or edema with damage to alveoli and blood vessels, or a combination of these.[20] This is the primary cause of death among people who initially survive an explosion.[21] In addition to blunt trauma, penetrating trauma can cause pulmonary contusion.[22] Contusion resulting from penetration by a rapidly moving projectile usually surrounds the path along which the projectile traveled through the tissue.[23] The pressure wave forces tissue out of the way, creating a temporary cavity; the tissue readily moves back into place, but it is hurt. Pulmonary contusions that accompany gun and knife wounds are not usually severe enough to have a major effect on outcome;[24] penetrating trauma causes less widespread lung damage than does blunt trauma.[16] An exception is shotgun wounds, which can seriously damage large areas of lung tissue through a blast injury mechanism.[24]

[edit] Mechanism

The physical processes behind pulmonary contusion are poorly understood. However, it is known that lung tissue can be crushed when the chest wall bends inward on impact.[25] Three other possible mechanisms have been suggested: the inertial effect, the spalling effect, and the implosion effect.

In the inertial effect, the lighter alveolar tissue is sheared from the heavier hilar structures, an effect similar to diffuse axonal injury in head injury.[5] It results from the fact that different tissues have different densities, and therefore different rates of acceleration or deceleration.[10] In the spalling effect, lung tissue bursts or is sheared where a shock wave meets the lung tissue, at interfaces between gas and liquid.[19] The alveolar walls form such a gas-liquid interface with the air in the alveoli.[5][26] The spalling effect occurs in areas with large differences in density; particles of the denser tissue are spalled (thrown) into the less dense particles.[27] The implosion effect occurs when a pressure wave passes through a tissue containing bubbles of gas: the bubbles first implode, then rebound and expand beyond their original volume.[28] The air bubbles cause many tiny explosions, resulting in tissue damage;[28] the overexpansion of gas bubbles stretches and tears alveoli.[29][30] This effect is thought to occur microscopically when the pressure in the airways increases sharply.[25]

Contusion usually occurs on the lung directly under the site of impact, but, as with traumatic brain injury, a contrecoup contusion may occur at the site opposite the impact as well.[23] A blow to the front of the chest may cause contusion on the back of the lungs because a shock wave travels through the chest and hits the curved back of the chest wall; this reflects the energy onto the back of the lungs, concentrating it. (A similar mechanism may occur at the front of the lungs when the back is struck.)[30] The amount of energy transferred to the lung is determined in a large part by the compliance (flexibility) of the chest wall.[23] Children's chests are more flexible because their ribs are more elastic and there is less ossification of their intercostal cartilage.[13] Therefore, their chest walls bend, absorbing less of the force and transmitting more of it to the underlying organs.[13][31] An adult's more bony chest wall absorbs more of the force itself rather than transmitting it.[31] Thus children commonly get pulmonary contusions without fractures overlying them, while elderly people are more likely to suffer fractures than contusions.[14][23] One study found that pulmonary contusions were accompanied by fractures 62% of the time in children and 80% of the time in adults.[30]

[edit] Pathophysiology

Normally, oxygen and carbon dioxide diffuse across the capillary and alveolar membranes and the interstitial space (top). Fluid impairs this diffusion, resulting in less oxygenated blood (bottom). Pulmonary contusion results in bleeding and fluid leakage into lung tissue, which can become stiffened and lose its normal elasticity. The water content of the lung increases over the first 72 hours after injury, potentially leading to frank pulmonary edema in more serious cases.[19] As a result of these and other pathological processes, pulmonary contusion progresses over time and can cause hypoxia (insufficient oxygen).

[edit] Bleeding and edema

In contusions, torn capillaries leak fluid into the tissues around them.[32] The membrane between alveoli and capillaries is torn; damage to this capillaryalveolar membrane and small blood vessels causes blood and fluids to leak into the alveoli and the interstitial space (the space

surrounding cells) of the lung.[11] With more severe trauma, there is a greater amount of edema, bleeding, and tearing of the alveoli.[16] Pulmonary contusion is characterized by microhemorrhages (tiny bleeds) that occur when the alveoli are traumatically separated from airway structures and blood vessels.[23] Blood initially collects in the interstitial space, and then edema occurs by an hour or two after injury.[29] An area of bleeding in the contused lung is commonly surrounded by an area of edema.[23] In normal gas exchange, carbon dioxide diffuses across the endothelium of the capillaries, the interstitial space, and across the alveolar epithelium; oxygen diffuses in the other direction. Fluid accumulation interferes with gas exchange,[33] and can cause the alveoli to fill with proteins and collapse due to edema and bleeding.[23] The larger the area of the injury, the more severe respiratory compromise will be.[16]

[edit] Consolidation and collapse

Pulmonary contusion can cause parts of the lung to consolidate, alveoli to collapse, and atelectasis (partial or total lung collapse) to occur.[34] Consolidation occurs when the parts of the lung that are normally filled with air fill with material from the pathological condition, such as blood.[35] Over a period of hours after the injury, the alveoli in the injured area thicken and may become consolidated.[23] A decrease in the amount of surfactant produced also contributes to the collapse and consolidation of alveoli;[15] inactivation of surfactant increases their surface tension.[30] Reduced production of surfactant can also occur in surrounding tissue that was not originally injured.[25] Inflammation of the lungs, which can result when components of blood enter the tissue due to contusion, can also cause parts of the lung to collapse. Macrophages, neutrophils, and other inflammatory cells and blood components can enter the lung tissue and release factors that lead to inflammation, increasing the likelihood of respiratory failure.[36] In response to inflammation, excess mucus is produced, potentially plugging parts of the lung and leading to their collapse.[23] Even when only one side of the chest is injured, inflammation may also affect the other lung.[36] Uninjured lung tissue may develop edema, thickening of the septa of the alveoli, and other changes.[37] If this inflammation is severe enough, it can lead to dysfunction of the lungs like that seen in acute respiratory distress syndrome.[38]

[edit] Ventilation/perfusion mismatch

Normally, the ratio of ventilation to perfusion is about one-to-one; the volume of air entering the alveoli (ventilation) is about equal to that of blood in the capillaries around them (perfusion).[39] This ratio is reduced in pulmonary contusion; fluid-filled alveoli cannot fill with air, oxygen does not fully saturate the hemoglobin, and the blood leaves the lung without being fully oxygenated.[40] Insufficient inflation of the lungs, which can result from inadequate mechanical ventilation or an associated injury such as flail chest, can also contribute to the ventilation/perfusion mismatch.[30] As the mismatch between ventilation and perfusion grows, blood oxygen saturation is reduced.[40] Pulmonary hypoxic vasoconstriction, in which blood vessels near the hypoxic alveoli constrict (narrow their diameter) in response to the lowered oxygen levels, can occur in pulmonary contusion.[26] The vascular resistance increases in the contused part of the lung, leading to a decrease in the amount of blood that flows into it,[37] directing blood to better-ventilated areas.[26] Although reducing blood flow to the unventilated

alveoli is a way to compensate for the fact that blood passing unventilated alveoli is not oxygenated,[26] the oxygenation of the blood remains lower than normal.[39] If it is severe enough, the hypoxemia resulting from fluid in the alveoli cannot be corrected just by giving supplemental oxygen; this problem is the cause of a large portion of the fatalities that result from trauma.[40]

[edit] Diagnosis
To diagnose pulmonary contusion, health professionals use clues from a physical examination, information about the event that caused the injury, and radiography.[16] Laboratory findings may also be used; for example, arterial blood gasses may show insufficient oxygen and excessive carbon dioxide even in someone receiving supplemental oxygen.[34] However, blood gas levels may show no abnormality early in the course of pulmonary contusion.[22]

[edit] X-ray

A chest X-ray showing right sided pulmonary contusion associated with rib fractures and subcutaneous emphysema Chest X-ray is the most common method used for diagnosis,[36] and may be used to confirm a diagnosis already made using clinical signs.[19] Consolidated areas appear white on an X-ray film.[41] Contusion is not typically restricted by the anatomical boundaries of the lobes or segments of the lung.[26][42][43] The X-ray appearance of pulmonary contusion is similar to that of aspiration,[31] and the presence of hemothorax or pneumothorax may obscure the contusion on a radiograph.[24] Signs of contusion that progress after 48 hours post-injury are likely to be actually due to aspiration, pneumonia, or ARDS.[10] Although chest radiography is an important part of the diagnosis, it is often not sensitive enough to detect the condition early after the injury.[34] In a third of cases, pulmonary contusion is not visible on the first chest radiograph performed.[7] It takes an average of six hours for the characteristic white regions to show up on a chest X-ray, and the contusion may not become apparent for 48 hours.[7][26][42] When a pulmonary contusion is apparent in an X-ray, it suggests that the trauma to the chest was severe and that a CT scan might reveal other injuries that were missed with X-ray.[2]

[edit] Computed tomography

A chest CT scan revealing pulmonary contusions, pneumothorax, and pseudocysts Computed tomography (CT scanning) is a more sensitive test for pulmonary contusion,[6][32] and it can identify abdominal, chest, or other injuries that accompany the contusion.[37] In one study, chest X-ray detected pulmonary contusions in 16.3% of people with serious blunt trauma, while CT detected them in 31.2% of the same people.[44] Unlike X-ray, CT scanning can detect the contusion almost immediately after the injury.[42] However, in both X-ray and CT a contusion may become more visible over the first 2448 hours after trauma as bleeding and edema into lung tissues progress.[45] CT scanning also helps determine the size of a contusion, which is useful in determining whether a patient needs mechanical ventilation; a larger volume of contused lung on CT scan is associated with an increased likelihood that ventilation will be needed.[42] CT scans also help differentiate between contusion and pulmonary hematoma, which may be difficult to tell apart otherwise.[46] However, pulmonary contusions that are visible on CT but not chest X-ray are usually not severe enough to affect outcome or treatment.[36]

[edit] Ultrasound

An ultrasound image showing early pulmonary contusion, at this moment not visible on radiography. Interstitial syndromes are expressed with the vertical white lines, the "B-lines".[47] Pulmonary ultrasound, performed at the bedside or on the accident scene, is being explored as a diagnosis for pulmonary contusion. Its use is still not widespread, being limited to facilities which are comfortable with its use for other applications, like pneumothorax, airway management, and hemothorax. Accuracy has been found to be comparable to CT scanning.[48]

[edit] Prevention

Prevention of pulmonary contusion is similar to that of other chest trauma. Airbags in combination with seat belts can protect vehicle occupants by preventing the chest from striking the interior of the vehicle during a collision, and by distributing forces involved in the crash more evenly across the body.[6] However, in rare cases, an airbag causes pulmonary contusion in a person who is not properly positioned when it deploys.[49] Child restraints such as carseats protect children in vehicle collisions from pulmonary contusion.[50] Equipment exists for use in some sports to prevent chest and lung injury; for example, in softball the catcher is equipped with a chest protector.[51] Athletes who do not wear such equipment, such as basketball players, can be trained to protect their chests from impacts.[51] Protective garments can also prevent pulmonary contusion in explosions.[52] Although traditional body armor made from rigid plates or other heavy materials protects from projectiles generated by a blast, it does not protect against pulmonary contusion, because it does not prevent the blast's shock wave from being transferred to the lung.[52] Special body armor has been designed for military personnel at high risk for blast injuries; these garments can prevent a shock wave from being propagated across the chest wall to the lung, and thus protect wearers from blast lung injuries.[52] These garments alternate layers of materials with high and low acoustic impedance (the product of a material's density and a wave's velocity through it) in order to "decouple" the blast wave, preventing its propagation into the tissues.[52]

[edit] Treatment
No treatment is known to speed the healing of a pulmonary contusion; the main care is supportive.[38] Attempts are made to discover injuries accompanying the contusion,[19] to prevent additional injury, and to provide supportive care while waiting for the contusion to heal.[38] Monitoring, including keeping track of fluid balance, respiratory function, and oxygen saturation using pulse oximetry is also required as the patient's condition may progressively worsen.[53] Monitoring for complications such as pneumonia and acute respiratory distress syndrome is of critical importance.[54] Treatment aims to prevent respiratory failure and to ensure adequate blood oxygenation.[15][22] Supplemental oxygen can be given and it may be warmed and humidified.[40] When the contusion does not respond to other treatments, extracorporeal membranous oxygenation may be used, pumping blood from the body into a machine that oxygenates it and removes carbon dioxide prior to pumping it back in.[55]

[edit] Ventilation

Mechanical ventilation may be required if pulmonary contusion causes inadequate oxygenation. Positive pressure ventilation, in which air is forced into the lungs, is needed when oxygenation is significantly impaired. Noninvasive positive pressure ventilation including continuous positive airway pressure (CPAP) and bi-level positive airway pressure (BiPAP), may be used to improve oxygenation and treat atelectasis.[38] In both, air is blown into the airways at a prescribed pressure via a mask fitted tightly to the face; in BiPAP the pressure changes between inhalation and exhalation, while in CPAP the pressure is the same during both.[38] Noninvasive ventilation has advantages over invasive methods because it does not carry the risk of infection that intubation does, and it allows normal coughing, swallowing, and speech.[38] However, the technique may cause complications; it may force air into the stomach or cause aspiration of stomach contents, especially when level of consciousness is decreased.[4] People with signs of inadequate respiration or oxygenation may need to be intubated[7] and mechanically ventilated.[12] Mechanical ventilation aims to reduce pulmonary edema and increase oxygenation.[26] Ventilation can reopen collapsed alveoli, but it is harmful for them to be repeatedly opened, and positive pressure ventilation can also damage the lung by overinflating it.[56] Intubation is normally reserved for when respiratory problems occur,[7] but most significant contusions do require intubation, and it may be done early in anticipation of this need.[4] People with pulmonary contusion who are especially likely to need ventilation include those with prior severe lung disease or kidney problems; the elderly; those with a lowered level of consciousness; those with low blood oxygen or high carbon dioxide levels; and those who are going to be operated on and need anesthesia.[40] Pulmonary contusion or its complications such as acute respiratory distress syndrome may cause lungs to lose compliance (stiffen), so higher pressures may be needed to give normal amounts of air[4] and oxygenate the blood adequately.[32] Positive end-expiratory pressure (PEEP), which delivers air at a given pressure at the end of the expiratory cycle, can reduce edema and keep alveoli from collapsing.[13] PEEP is considered necessary with mechanical ventilation; however, if the pressure is too great it can expand the size of the contusion[16] and injure the lung.[38] When the compliance of the injured lung differs significantly from that of the uninjured one, the lungs can be ventilated independently with two ventilators in order to deliver air at different pressures; this helps avoid injury from overinflation while providing adequate ventilation.[57]

[edit] Fluid therapy

The administration of fluid therapy in individuals with pulmonary contusion is controversial.[40] Excessive fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage from injured capillaries (pulmonary edema), which are more permeable than normal.[30][42] However, low blood volume (hypovolemia) resulting from insufficient fluid has an even worse impact, potentially causing hypovolemic shock; for people who have lost large amounts of blood, fluid resuscitation is necessary.[40] A lot of the evidence supporting the idea that fluids should be withheld from people with pulmonary contusion came from animal studies, not clinical trials with humans; human studies have had conflicting findings on whether fluid resuscitation worsens the condition.[19] For people who do require large amounts of intravenous fluid, a catheter may be placed in the pulmonary artery to measure the pressure within it.[6] Measuring pulmonary artery pressure allows the clinician to give enough fluids to prevent shock without exacerbating edema.[58] Diuretics, drugs that increase urine output to reduce excessive fluid in the system, can be used when fluid overload does occur.[59] Furosemide, a diuretic used in the treatment of pulmonary contusion, also relaxes the smooth muscle in the veins of the lungs, thereby decreasing pulmonary venous resistance and reducing the pressure in the pulmonary capillaries.[42]

[edit] Supportive care

Retaining secretions in the airways can worsen hypoxia[60] and lead to infections.[4] Thus, an important part of treatment is pulmonary toilet, the use of suction, deep breathing, coughing, and other methods to remove material such as mucus and blood from the airways.[7] Chest physical therapy makes use of techniques such as breathing exercises, stimulation of coughing, suctioning, percussion, movement, vibration, and drainage to rid the lungs of secretions, increase oxygenation, and expand collapsed parts of the lungs.[61] People with pulmonary contusion, especially those who do not respond well to other treatments, may be positioned with the uninjured lung lower than the injured one to improve oxygenation.[42] Inadequate pulmonary toilet can result in pneumonia.[39] People who do develop infections are given antibiotics.[16] No studies have yet shown a benefit of using antibiotics as a preventative measure before infection occurs, although some doctors do recommend prophylactic antibiotic use even without scientific evidence of its benefit.[13] However, this can cause the development of antibiotic resistant strains of bacteria, so giving antibiotics without a clear need is normally discouraged.[19] For people who are at especially high risk of developing infections, the sputum can be cultured to test for the presence of infection-causing bacteria; when they are present, antibiotics are used.[26] Pain control is another means to facilitate the elimination of secretions. A chest wall injury can make coughing painful, increasing the likelihood that secretions will accumulate in the airways.[62] Chest injuries also contribute to hypoventilation (inadequate breathing) because the chest wall movement involved in breathing adequately is painful.[62][63] Insufficient expansion of the chest may lead to atelectasis, further reducing oxygenation of the blood.[34] Analgesics (pain medications) can be given to reduce pain.[12] Injection of anesthetics into nerves in the chest wall, called nerve blockade, is another approach to pain management; this does not depress respiration the way some pain medications can.[30]

[edit] Prognosis

This CT scan, taken 22 days after pulmonary contusion with major chest trauma, shows that the contusion has completely resolved.[64] Pulmonary contusion usually resolves itself[22] without causing permanent complications;[1] however it may also have long-term ill effects on respiratory function.[37][65] Most contusions resolve in five to seven days after the injury.[1] Signs detectable by radiography are usually gone within 10 days after the injurywhen they are not, other conditions, such as pneumonia, are the likely cause.[26] Chronic lung disease correlates with the size of the contusion and can interfere with an individual's ability to return to work.[23] Fibrosis of the lungs can occur, resulting in dyspnea (shortness of breath), low blood oxygenation, and reduced functional residual capacity for as long as six years after the injury.[37] As late as four years post-injury, decreased functional residual capacity has been found in most pulmonary contusion patients studied.[42] During the six months after pulmonary contusion, up to 90% of people suffer difficulty breathing.[26][42] In some cases, dyspnea persists for an indefinite period.[7] Contusion can also permanently reduce the compliance of the lungs.[66]

[edit] Complications

A chest X-ray showing acute respiratory distress syndrome Pulmonary contusion can result in respiratory failureabout half of such cases occur within a few hours of the initial trauma.[42] Other severe complications, including infections and acute

respiratory distress syndrome (ARDS) occur in up to half of cases.[30] Elderly people and those who have heart, lung, or kidney disease prior to the injury are more likely to stay longer in hospital and have complications from the injury. Complications occur in 55% of people with heart or lung disease and 13% of those without.[36] Of people with pulmonary contusion alone, 17% develop ARDS, while 78% of people with at least two additional injuries develop the condition.[6] A larger contusion is associated with an increased risk. In one study, 82% of people with 20% or more of the lung volume affected developed ARDS, while only 22% of people with less than 20% did so.[7] Pneumonia, another potential complication, develops in as many as 20% of people with pulmonary contusion.[13] Contused lungs are less able to remove bacteria than uninjured lungs, predisposing them to infection.[67] Intubation and mechanical ventilation further increase the risk of developing pneumonia; the tube is passed through the nose or mouth into the airways, potentially tracking bacteria from the mouth or sinuses into them.[38] Also, intubation prevents coughing, which would clear bacteria-laden secretions from the airways, and secretions pool near the tube's cuff and allow bacteria to grow.[38] The sooner the endotracheal tube is removed, the lower the risk of pneumonia, but if it is removed too early and has to be put back in, the risk of pneumonia rises.[38] People who are at risk for pulmonary aspiration (e.g. those with lowered level of consciousness due to head injuries) are especially likely to get pneumonia.[38] As with ARDS, the chances of developing pneumonia increase with the size of the contusion.[7] Children and adults have been found to have similar rates of complication with pneumonia and ARDS.[30]

[edit] Associated injuries

Severe pulmonary contusion with pneumothorax and hemothorax following severe chest trauma[68] A large amount of force is required to cause pulmonary contusion; a person injured with such force is likely to have other types of injuries as well,[22] and pulmonary contusion can be used to gauge the severity of trauma.[24] Up to three quarters of cases are accompanied by other chest injuries,[38] the most common of these being hemothorax and pneumothorax.[36] Flail chest is usually associated with pulmonary contusion,[26][42] and the contusion, rather than the chest wall injury, is often the main cause of respiratory failure in people with these injuries.[69] Other indications of thoracic trauma may be associated, including fracture of the sternum and bruising of the chest wall.[63] Over half of fractures of the scapula are associated with pulmonary

contusion.[26] The contusion is frequently found underlying fracture sites.[34] When accompanied by a fracture, it is usually concentrated into a specific locationthe contusion is more diffuse when there is no fracture.[30][42] Pulmonary lacerations may result from the same blunt or penetrating forces that cause pulmonary contusion.[6] Lacerations can result in pulmonary hematomas; these are reported to develop in 411% of pulmonary contusions.[6]

[edit] Epidemiology
Pulmonary contusion is found in 3075% of severe cases of chest injury, making it the most common serious injury to occur in association with thoracic trauma.[6] Of people who have multiple injuries with an injury severity score of over 15, pulmonary contusion occurs in about 17%.[19] It is difficult to determine the death rate (mortality) because pulmonary contusion rarely occurs by itself.[16] Usually, deaths of people with pulmonary contusion result from other injuries, commonly traumatic brain injury.[23] It is controversial whether pulmonary contusion with flail chest is a major factor in mortality on its own or whether it merely contributes to mortality in people with multiple injuries.[70] The mortality rate of pulmonary contusion is estimated to range from 1440%, depending on the severity of the contusion itself and on associated injuries.[11] When the contusions are small, they do not normally increase the chance of death or poor outcome for people with blunt chest trauma; however, these chances increase with the size of the contusion.[36] One study found that 35% of people with multiple significant injuries including pulmonary contusion die.[16] In another study, 11% of people with pulmonary contusion alone died, while the number rose to 22% in those with additional injuries.[6] An accompanying flail chest increases the morbidity and mortality to more than twice that of pulmonary contusion alone.[42] Pulmonary contusion is thought to be the direct cause of death in a quarter to a half of people with polytrauma who die.[59]

A right-sided pulmonary contusion post blunt chest trauma with increased opacity just below the horizontal fissure Pulmonary contusion is the most common cause of death among vehicle occupants involved in accidents,[71] and it is thought to contribute significantly in about a quarter of deaths resulting from vehicle collisions.[24] As vehicle use has increased, so has the number of auto accidents, and with it the number of chest injuries.[38] However an increase in the number of airbags installed in

modern cars may be decreasing the incidence of pulmonary contusion.[6] Use of child restraint systems has brought the approximate incidence of pulmonary contusion in children in vehicle accidents from 22% to 10%.[50] Since their chest walls are more flexible, children are more vulnerable to pulmonary contusion than adults are,[22] and it is more common in children than in adults for that reason.[29] Children in forceful impacts suffer twice as many pulmonary contusions as adults with similar injury mechanisms, yet have proportionately fewer rib fractures.[13] Pulmonary contusion has been found in 53% of children with significant chest injuries (those requiring hospitalization).[72] The rates of certain types of injury mechanisms differ between children and adults; for example, children are more often hit by cars when they are pedestrians.[30] Differences in the bodies of children and adults also lead to different manifestations of pulmonary contusion and associated injuries; for example, children have less body mass, so the same force is more likely to lead to trauma to multiple body systems.[30] Some differences in children's physiology might be advantageous (for example they are less likely to have other medical conditions), and thus they have been predicted to have a better outcome.[73] However, despite these differences, children with pulmonary contusion have similar mortality rates to adults.[30]

[edit] History

Giovanni Battista Morgagni, credited with having first described lung trauma without chest wall trauma In 1761, the Italian anatomist Giovanni Battista Morgagni was first to describe a lung injury that was not accompanied by injury to the chest wall overlying it.[19] Nonetheless, it was the French military surgeon Guillaume Dupuytren who is thought to have coined the term pulmonary contusion in the 19th century.[59] It still was not until the early 20th century that pulmonary contusion and its clinical significance began to receive wide recognition.[70] With the use of explosives during World War I came many casualties with no external signs of chest injury but with significant bleeding in the lungs.[70] Studies of World War I injuries by D.R. Hooker

showed that pulmonary contusion was an important part of the concussive injury that results from explosions.[70] Pulmonary contusion received further attention during World War II, when the bombings of Britain caused blast injuries and associated respiratory problems in both soldiers and civilians.[19] Also during this time, studies with animals placed at varying distances from a blast showed that protective gear could prevent lung injuries.[65] These findings suggested that an impact to the outside of the chest wall was responsible for the internal lesions.[65] In 1945, Buford and Burbank described what they called "wet lung", in which the lungs accumulated fluid and were simultaneously less able to remove it.[19] They attributed the respiratory failure often seen in blunt chest trauma in part to excessive fluid resuscitation, and the question of whether and how much to administer fluids has remained controversial ever since.[19] During the Vietnam War, combat again provided the opportunity for study of pulmonary contusion; research during this conflict played an important role in the development of the modern understanding of its treatment.[19] The condition also began to be more widely recognized in a non-combat context in the 1960s, and symptoms and typical findings with imaging techniques such as X-ray were described.[19] Before the 1960s, it was believed that the respiratory insufficiency seen in flail chest was due to "paradoxical motion" of the flail segment of the chest wall (the flail segment moves in the opposite direction as the chest wall during respiration), so treatment was aimed at managing the chest wall injury, not the pulmonary contusion.[55] For example, positive pressure ventilation was used to stabilize the flail segment from within the chest.[38] It was first proposed in 1965 that this respiratory insufficiency is most often due to injury of the lung rather than to the chest wall,[19] and a group led by J.K. Trinkle confirmed this hypothesis in 1975.[37] Hence the modern treatment prioritizes the management of pulmonary contusion.[70] Animal studies performed in the late 1960s and 1970s shed light on the pathophysiological processes involved in pulmonary contusion.[65]

[edit]

Pneumothorax
From Wikipedia, the free encyclopedia

Pneumothorax
Classification and external resources

Right sided spontaneous pneumothorax (left in the image). An arrow indicating the edge of the collapsed lung. ICD-10 ICD-9 OMIM J93, P25.1, S27.0 512, 860 173600

DiseasesDB 10195 MedlinePlus 000087 eMedicine MeSH article/432979 article/424547 article/360796 article/808162 article/827551 article/1003552 D011030

Pneumothorax (plural pneumothoraces) is a collection of air or gas in the pleural cavity of the chest between the lung and the chest wall. It may occur spontaneously in people without chronic lung conditions ("primary") as well as in those with lung disease ("secondary"), and many pneumothoraces occur after physical trauma to the chest, blast injury, or as a complication of medical treatment.[1][2] The symptoms of a pneumothorax are determined by the size of the air leak and the speed by which it occurs; they may include chest pain in most cases and shortness of breath in many. The diagnosis can be made by physical examination in severe cases but usually requires a chest X-ray or computed tomography (CT scan) in milder forms. In a small proportion, the pneumothorax leads to severe oxygen shortage and low blood pressure, progressing to cardiac arrest unless treated; this situation is termed tension pneumothorax.[1][3] Small spontaneous pneumothoraces typically resolve by themselves and require no treatment, especially in those with no underlying lung disease. In larger pneumothoraces or when there are severe symptoms, the air may be aspirated with a syringe, or a one-way chest tube is inserted to allow the air to escape. Occasionally, surgical measures are required, especially if tube drainage is unsuccessful or someone has repeated episodes. Various treatments, usually involving

pleurodesis (sticking the lung to the chest wall), may be used if there is a significant risk of repeated episodes of pneumothorax.[1]

Contents
[hide]

1 Signs and symptoms o 1.1 Clinical subtypes o 1.2 Physical examination 2 Cause o 2.1 Spontaneous o 2.2 Traumatic 3 Mechanism 4 Diagnosis o 4.1 Chest X-ray o 4.2 Computed tomography o 4.3 Ultrasound 5 Treatment o 5.1 Conservative o 5.2 Aspiration o 5.3 Chest tube 6 Prevention 7 Epidemiology 8 History 9 References

[edit] Signs and symptoms

[edit] Clinical subtypes
Primary spontaneous pneumothorax (PSP), which tends to occur in young people without underlying lung problems, usually causes limited symptoms. Chest pain and sometimes mild breathlessness are the predominant symptoms.[1][2] Half of those with primary spontaneous pneumothorax wait several days to seek medical attention.[4] It is exceedingly uncommon for PSP to cause tension pneumothorax. The symptoms usually start at rest. Tall males, especially smokers, are characteristically at a higher risk of PSP.[1] It has been found that PSP occurs more commonly during changes in atmospheric pressure and during exposure to loud music, and this explains to an extent why episodes of pneumothorax may happen in clusters.[2] Secondary spontaneous pneumothorax (SSP) occurs by definition in those with underlying lung diseases. The symptoms tend to be more severe, as the unaffected lung is generally not capable of replacing the loss of function from the affected side. Hypoxemia (decreased blood oxygen levels) is usually present and may be observed as cyanosis (blue discoloration of the lips and

skin). Hypercapnia (accumulation of carbon dioxide in the blood) is sometimes encountered; this may cause confusion and coma. Sudden breathlessness in someone with lung problems such as chronic obstructive pulmonary disease and cystic fibrosis may therefore prompt investigations for a possible pneumothorax.[1] The size of the pneumothorax bears limited relationship to the symptoms experienced.[4] Traumatic pneumothorax occurs either because a hole in the chest wall, such as a stab wound or gunshot wound, allows air to enter the pleural space, or because of injury to the lung. It has been found to occur in half of all cases of injury to the chest, coming second after rib fracture in the complications after chest trauma. The pneumothorax can be small (occult) in half of these cases, but they may enlarge if the person requires mechanical ventilation and their presence is therefore still relevant.[2] It is also often encountered in those already receiving mechanical ventilation.[2][3] Tension pneumothorax is defined differently by different sources,[3] but is generally said to exist when there is severe hypoxia despite administration of oxygen, falling blood pressure or confusion. This is a medical emergency and may require immediate treatment without further investigations (see below).[3][4] Tension pneumothorax may also occur in those receiving mechanical ventilation, in which case it may be difficult to spot as the person is typically sedated; it is often noted because of sudden deterioration.[3]

[edit] Physical examination

There may be no abnormalities on physical examination, especially if the pneumothorax is small. The breath sounds as audible by stethoscope may be diminished on the affected side, as air in the pleural space dampens sound. Percussion of the chest may sound hyperresonant (higher pitched), and vocal resonance and tactile fremitus (both examining the conduction of voice by the lung) can be decreased.[2][4] Tension pneumothorax is characterized by rapid breathing, cyanosis, falling blood pressure (hypotension) and confusion. The affected side of the chest may be hyperexpanded and show decreased movement, with increased movement on the other side. In very severe cases, the respiratory rate falls sharply, with shock and coma. Recent studies have shown that the development of tension features may not always be as rapid as previously thought. Particular clinical signs may also be less useful in the recognition of tension pneumothorax, such as the deviation of the trachea (windpipe) to one side and the presence of raised jugular venous pressure (distended neck veins).[3]

[edit] Cause

A schematic drawing of a bulla and a bleb, two lung abnormalities that may rupture and lead to pneumothorax.

[edit] Spontaneous
Spontaneous pneumothoraces are divided into two types: primary, which occurs in the absence of known lung disease, and secondary, which occurs in someone with underlying lung disease. The exact cause of primary spontaneous pneumothorax is unknown, but established risk factors include male sex, smoking, and a family history of pneumothorax.[5] The various suspected underlying mechanisms are discussed below.[1][2] Secondary spontaneous pneumothorax occurs in the setting of a variety of lung diseases. The most common is chronic obstructive pulmonary disease which accounts for approximately 70% of cases.[5] Known lung diseases that may increase the risk for pneumothorax are:[1][2]

Diseases of the airways: chronic obstructive pulmonary disease (especially when emphysema and lung bullae are present), acute severe asthma, cystic fibrosis Lung infections: pneumocystis pneumonia (PCP), tuberculosis, necrotizing pneumonia Interstitial lung diseases: sarcoidosis, idiopathic pulmonary fibrosis, histiocytosis X, lymphangioleiomyomatosis (LAM) Connective tissue diseases: rheumatoid arthritis, ankylosing spondylitis, polymyositis and dermatomyositis, systemic sclerosis, Marfan's syndrome and Ehlers-Danlos syndrome Cancer: lung cancer, sarcomas involving the lung Catamenial (occurring in relation to the menstrual cycle): endometriosis in the chest

In children, additional causes include measles, echinococcosis, inhalation of a foreign body, and particular congenital malformations (congenital cystic adenomatoid malformation and congenital lobar emphysema).[6] A rare genetic disorder, Birt-Hogg-Dub syndrome, may cause spontaneous pneumothorax in families. It also causes skin lesions (fibrofolliculomas) and lung cysts, and carries an increased risk of kidney cancer. The lung cysts, which probably lead to increased risk of pneumothorax, tend to be in the lower lobes rather than the more common upper lobe cysts encountered in other conditions.[7] Birt-Hogg-Dub syndrome is caused by mutations in the FLCN gene (chromosome 17p11.2), which encodes a protein named folliculin.[6][7] FLCN mutations and lung lesions have also been identified in familial cases of pneumothorax where other features of Birt-Hogg-Dub syndrome are absent.[6]

[edit] Traumatic
A traumatic pneumothorax may result from both blunt trauma and penetrating injuries to the chest wall.[2] It may be observed in those exposed to an explosive blast, even if no direct injury to the chest has occurred.[8] The most common mechanism is a cut to the pleura by a fractured rib.[5] Medical procedures of the chest (iatrogenic), such as the taking of biopsy samples from lung tissue, inserting a central venous catheter into one of the chest veins, may lead to injury to the lung and resultant pneumothorax. The administration of positive pressure ventilation, either mechanical ventilation or non-invasive ventilation, may result in barotrauma (pressure-related injury) leading to a pneumothorax.[2]

[edit] Mechanism

CT scan of the chest showing a pneumothorax on the patient's left side (right side on the image). A chest tube is in place (small black mark on the right side of the image), the air-filled pleural cavity (black) and ribs (white) can be seen. The heart can be seen in the center. The thoracic cavity is the hollow space that contains the lungs. The lungs are physically connected at the hila, where the airways and blood vessels enter the lung. They remain inflated inside the thoracic cavity because the pressure inside the pleural space (the space between the chest wall and the lung) is almost consistently negative throughout the respiratory cycle, effectively sucking the lung to the chest wall. Both the lung and the chest wall are covered by a layer of cells known as the pleura (visceral and parietal pleura, respectively), and a small amount of serous fluid is typically present. The negative pressure normally does not allow air to enter the pleural space because there are no natural connections to air-containing space, and the pressure of gases in the bloodstream is too low for them to be released into the pleural space. Pneumothorax can therefore only develop if air is allowed to enter, either through damage in the chest wall, or damage to the lung itself, or occasionally because microorganisms in the space produce gas.[2] The chest wall defect is usually evident in cases of injury to the chest wall, such as bullet wounds ("open pneumothorax"). In secondary spontaneous pneumothorax, vulnerabilities in the lung tissue are caused by a variety of disease processes, such as bullae (large air-containing lesions) in emphysema. Areas of necrosis (tissue death) may precipitate pneumothorax episodes, although the exact mechanism is unclear.[1] Primary spontaneous pneumothorax has for many years been

thought to be caused by "blebs", small lesions just under the pleural surface, which were presumed to be more common in those classically at risk of pneumothorax (tall males) due to mechanical factors. Various lines of evidence suggest that this hypothesis may not be correct, such as the fact that pneumothorax may recur even after surgical treatment of blebs, and that blebs occur in 15% of healthy people. It has therefore been suggested that PSP is instead caused by areas of disruption (porosity) in the pleural layer, which are prone to rupture.[1][2] Smoking may lead to inflammation and obstruction of small airways, accounting for the markedly increased risk of PSP in smokers.[4] Once air has stopped entering the pleural cavity, it is gradually resorbed spontaneously. Estimated rates of resorption are between 1.25% and 2.2% the volume of the cavity per day. This would mean that even a completely collapsed lung would spontaneously reinflate over a period of about 6 weeks.[4] Tension pneumothorax occurs because the opening that allows air to enter the pleural space functions like a valve, and with every breath more air enters and cannot escape. Severe hypoxia follows, with a resultant drop in blood pressure and level of consciousness. A previously uttered theory that the collapsed lung compresses large blood vessels such as the aorta is probably incorrect.[3]

[edit] Diagnosis
The symptoms of pneumothorax can be subtle, especially in those with PSP, and confirmation with medical imaging is usually required.[4] In contrast, tension pneumothorax is ideally treated before imaging, especially if there is severe hypoxia, very low blood pressure, or an impaired level of consciousness; however, X-rays are sometimes required if there is doubt about the location of the pneumothorax.[3][5]

[edit] Chest X-ray

Chest X-ray of left-sided pneumothorax (visible on the right in this image). The left thoracic cavity is filled in part with free air. The mediastinum is shifted to the opposite side. Traditionally a plain radiograph of the chest, ideally with the X-ray beams being projected from the back (posteroanterior or PA), has been the most appropriate first investigation. Usually, these are performed in inspiration (holding one's breath); no added information is gathered by obtaining a chest X-ray in expiration (after exhaling).[2][4] If the PA X-ray does not show a

pneumothorax but there is a strong suspicion, lateral X-rays (with beams projecting from the side) may be performed, but this is not routine practice.[4][6] It is not unusual for the mediastinum (the structure between the lungs that contains the heart and several other organs) to be shifted away from the affected lung due to pressure. This is not equivalent to tension pneumothorax, which is determined mainly by symptoms, hypoxia and shock.[2] The size of the pneumothorax, i.e. the amount of space in the chest taken up by free air rather than air-containing lung, can be determined with a reasonable degree of accuracy by measuring the distance between the chest wall and the lung. This is relevant as smaller pneumothoraces may be treated differently. An air rim of 2 cm or more means that the pneumothorax occupies about 50% of the pleural cavity.[4] British professional guidelines have traditionally stated that the measurement should be performed at the level of the hilum (where blood vessels and airways enter the lung),[4] while American guidelines state that the measurement should happen at the apex (tip) of the lung.[9] The latter method may overestimate the size of a pneumothorax if it is located mainly at the apex, which is a common occurrence.[4] The various methods correlate poorly, but are the best immediately available ways of estimating pneumothorax size.[4][6] CT scanning (see below) would provide a more accurate determination of the size of the pneumothorax, but its routine use in this setting is not recommended.[9] Not all pneumothoraces are uniform; some only form a pocket of air in a particular place in the chest.[4] Small amounts of fluid (which may be blood - hemopneumothorax) may be noted on the chest X-ray.[2] In some cases, the only significant abnormality may be the "deep sulcus sign", in which the usually small space between the chest wall and the diaphragm appears enlarged due to the presence of air.[3]

[edit] Computed tomography

Computed tomography (CT or CAT scan) can be useful in particular situations. In some lung diseases, especially emphysema, it is possible for abnormal lung areas such as bullae (large airfilled sacs) to have the same appearance as a pneumothorax, and it may not be safe to apply any treatment before the distinction is made and before the exact location and size of the pneumothorax is determined.[4] In trauma, where it may not be possible to perform an upright film, chest radiography may miss up to a third of pneumothoraces, while CT remains very sensitive.[5] A further use of CT is in the identification of underlying lung lesions. In presumed primary pneumothorax, it may help identify blebs or cystic lesions (in anticipation of treatment, see below), and in secondary pneumothorax it can identify most of the causes listed above.[4][6]

[edit] Ultrasound
Ultrasound is used commonly in the evaluation of people who have sustained physical trauma, for example with the FAST protocol.[10] Ultrasound may be more sensitive than chest X-rays in the identification of pneumothorax after blunt trauma to the chest.[11]

[edit] Treatment

Schematic drawing of a person with a chest tube in the left thoracic cavity. It is connected to a water seal. The treatment of pneumothorax depends on a number of factors, and may vary from discharge with early follow-up to immediate needle decompression or insertion of a chest tube. Treatment is determined by the severity of symptoms and indicators of acute illness, the presence of underlying lung disease, the estimated size of the pneumothorax on X-ray, and in some instances also on the personal preference of the person involved. In spontaneous pneumothorax, air travel is discouraged until it has completely resolved.[4] In traumatic pneumothorax, chest tubes are usually inserted (unless iatrogenic, see below). It is not yet clear if there is a subgroup of patients with small pneumothoraces who do not require tube treatment and could be managed conservatively. If mechanical ventilation is required, the insertion of a chest tube is mandatory as it would increase the risk of tension pneumothorax.[2][12] Tension pneumothorax is usually treated with urgent needle decompression. This may need to happen before transport to hospital, and can be performed by an emergency medical technician or other trained professional. The needle or cannula is left in place until a chest tube can be

inserted.[3][13] Any open chest wound is covered, as it carries a high risk of leading to tension pneumothorax, ideally with a dressing called the Asherman seal, which appears to be more effective than standard "three-sided" dressing. The Asherman seal is a specially designed device that adheres to the chest wall and allows air to escape but not to enter the chest through a valvelike mechanism.[13]

[edit] Conservative
Small spontaneous pneumothoraces do not always require treatment, as they are unlikely to proceed to respiratory failure or tension pneumothorax and generally resolve spontaneously. This approach is most appropriate if the estimated size of the pneumothorax is small (e.g. <50%), there is no breathlessness, and there is no underlying lung disease.[6][9] It may be appropriate to treat a larger PSP conservatively if the symptoms are limited.[4] Admission to hospital is often not required, as long as clear instructions are given to return to hospital if there are worsening symptoms. Further investigations may be performed as an outpatient, at which time X-rays are repeated to confirm improvement, and advice may be given with regards to preventing recurrence such as surgery (see below).[4] Secondary pneumothoraces are only treated conservatively if the size is very small (1 cm or less air rim) and there are limited symptoms. Admission to hospital is usually recommended. Oxygen given at a high flow rate may accelerate resorption.[4]

[edit] Aspiration
In a large primary spontaneous pneumothorax (>50%) or PSP associated with breathlessness, some professional guidelines recommend that reducing the size by aspiration is equally effective as insertion of a chest tube. This involves the administration of local anesthetic and inserting a needle connected to a three-way tap; up to 2.5 liters of air (in adults) are removed. If there has been significant reduction in the size of the pneumothorax on a further X-ray, the remainder of the treatment can be conservative. This approach is effective in over 50% of cases.[1][4][6] Firstline aspiration in PSP reduces the number of people requiring admission to hospital significantly as opposed to tube drainage, without increasing the risk of complications.[14] Aspiration may also be considered in secondary pneumothorax of moderate size (air rim 12 cm) without breathlessness, with the difference that ongoing observation in hospital is required even after a successful procedure.[4] American professional guidelines state that all large pneumothoraces, even those due to PSP, should be treated with a chest tube.[9] Moderately-sized traumatic pneumothorax due to medical procedures (iatrogenic) may initially be treated with aspiration.[2]

[edit] Chest tube

A chest tube (or intercostal drain) is the most definitive initial treatment of a pneumothorax. This is typically inserted in an area under the axilla (armpit) called the "safe triangle", where damage to internal organs can be avoided; this is delineated by a horizontal line at the level of the nipple and two muscles of the chest wall (latissimus dorsi and pectoralis major). Local anesthetic is applied. Two types of tubes may be used. In spontaneous pneumothorax, small-bore (smaller

than 14 FG, 4.7 mm diameter) tubes may be inserted by the Seldinger technique, and larger tubes do not have an advantage.[4] In traumatic pneumothorax, larger tubes (28 FG, 9.3 mm) are used.[13] Chest tubes are required in PSP that has not responded to needle aspiration, in any SSP that is large (>50%), and in cases of tension pneumothorax. They are connected to a one-way valve system that allows air to escape but not to reenter the chest. This may include a bottle with water that functions like a water seal, or a Heimlich valve. They are not normally connected to a negative pressure circuit, as this would result in rapid reexpansion of the lung and a risk of pulmonary edema ("reexpansion pulmonary edema"). The tube is left in place until no air is seen to escape from it for a period of time, and X-rays confirm reexpansion of the lung.[4][6][9] If after 24 days there is still evidence of air leak, various options are available. Negative pressure suction (at low pressures of 10 to 20 cmH2O) at a high flow rate may be attempted, especially in PSP; it is thought that this may accelerate the healing of the leak. In SSP, assistance from a thoracic surgeon may be required earlier.[4] Surgical options are similar to those used to prevent further episodes, and are discussed below (thoracotomy and VATS).

[edit] Prevention
Both medical and surgical treatments exist to reduce the risk of recurrence of a pneumothorax.[15] The main aim is to achieve pleurodesis, the adherence between the lung and the chest wall. The evidence on the most effective treatment is still conflicting in some areas, and there is variation between treatments available in Europe and the USA.[1] Not all episodes of pneumothorax require such interventions; the decision depends largely on the suspected risk of recurrence. They however are often recommended after a second pneumothorax.[15] An exception applies in those who engage in diving; diving is considered unsafe unless permanent treatment has been applied; professional guidelines suggest that pleurectomy is performed on both lungs (see below) and that lung function tests and CT scan must be normal before diving is resumed.[4][9] The best results, with a recurrence rate less than 1%, are achieved with a thoracotomy (surgical opening of the chest) with identification of any clear air leak and stapling of blebs, followed by pleurectomy (stripping of the pleural lining) of the outer pleural layer and pleural abrasion (scraping of the pleura) of the inner layer. During the healing process, the lung adheres to the chest wall, effectively obliterating the pleural space. Thoracotomy is always performed under a general anesthetic.[1][4] A less invasive approach is thoracoscopy, usually in the form of a procedure called videoassisted thoracoscopic surgery. This also involves a general anesthetic but the lung is approached through a number of small incisions between the ribs. The results from VATS-based pleural abrasion are slightly worse than those achieved by thoracotomy, but with less unsightly skin Scars. VATS may be also be used to achieve chemical pleurodesis; this involves the instillation of talc, which activates a scarring reaction that may also stick the lung to the chest wall.[1][4] Not everyone may be prepared to undergo surgery. If a chest tube is already in place, various agents may be instilled through the tube to achieve pleurodesis, specifically talc and the

antibiotic tetracycline. The results from this tend to be worse than from surgical approaches.[1][4] Talc pleurodesis has few long term consequences in young people.[1]

[edit] Epidemiology
Spontaneous pneumothorax is more common in males than in females. The annual incidence of PSP is 1828 per 100,000 in males and 1.26.0 in females. Secondary spontaneous pneumothorax is less common, with 6.3 for males and 2.0 for females. Risk of recurrence depends on underlying lung disease. Once a second episode has occurred, there is a high likelihood of subsequent further episodes.[1] Smokers have an increased risk of contracting a first spontaneous pneumothorax of approximately ninefold among women and 22-fold among men compared to non-smokers.[16] The incidence in children has not been well studied, but it is probably less than that of adults and often reflects underlying lung disease.[6] Death from pneumothorax is very uncommon (except for tension pneumothorax). British statistics have revealed an annual mortality of 1.26 per million per year in men and 0.62 in women.[4] Mortality is higher in older people and those with secondary pneumothorax.[1]

[edit] History
Jean Marc Gaspard Itard, a student of Ren Laennec, first recognised pneumothorax in 1803, and Laennec himself described the full clinical picture in 1819.[17] While Itard and Laennec recognized that some cases were not due to tuberculosis (then the most common cause), the concept of primary spontaneous pneumothorax was reintroduced by the Danish physician Hans Kjrgaard in 1932.[4][18] Prior to the advent of anti-tuberculous medications, iatrogenic pneumothoraces were intentionally given to tuberculosis patients in an effort to collapse a lobe, or entire lung around a cavitating lesion. This was known as "resting the lung". It was introduced by the Italian surgeon Carlo Forlanini in 1888 and publicized by the American surgeon John Benjamin Murphy in the early 20th century after discovering the same procedure independently. Murphy used the then recently discovered X-ray technology to create pneumothoraces of the correct size.[1

Pneumothorax
From Wikipedia, the free encyclopedia (Redirected from Tension pneumothorax)

Pneumothorax
Classification and external resources

Right sided spontaneous pneumothorax (left in the image). An arrow indicating the edge of the collapsed lung. ICD-10 ICD-9 OMIM J93, P25.1, S27.0 512, 860 173600

DiseasesDB 10195 MedlinePlus 000087 eMedicine MeSH article/432979 article/424547 article/360796 article/808162 article/827551 article/1003552 D011030

Pneumothorax (plural pneumothoraces) is a collection of air or gas in the pleural cavity of the chest between the lung and the chest wall. It may occur spontaneously in people without chronic lung conditions ("primary") as well as in those with lung disease ("secondary"), and many pneumothoraces occur after physical trauma to the chest, blast injury, or as a complication of medical treatment.[1][2] The symptoms of a pneumothorax are determined by the size of the air leak and the speed by which it occurs; they may include chest pain in most cases and shortness of breath in many. The diagnosis can be made by physical examination in severe cases but usually requires a chest X-ray or computed tomography (CT scan) in milder forms. In a small proportion, the pneumothorax leads to severe oxygen shortage and low blood pressure, progressing to cardiac arrest unless treated; this situation is termed tension pneumothorax.[1][3] Small spontaneous pneumothoraces typically resolve by themselves and require no treatment, especially in those with no underlying lung disease. In larger pneumothoraces or when there are severe symptoms, the air may be aspirated with a syringe, or a one-way chest tube is inserted to allow the air to escape. Occasionally, surgical measures are required, especially if tube drainage is unsuccessful or someone has repeated episodes. Various treatments, usually involving

pleurodesis (sticking the lung to the chest wall), may be used if there is a significant risk of repeated episodes of pneumothorax.[1]

Contents
[hide]

1 Signs and symptoms o 1.1 Clinical subtypes o 1.2 Physical examination 2 Cause o 2.1 Spontaneous o 2.2 Traumatic 3 Mechanism 4 Diagnosis o 4.1 Chest X-ray o 4.2 Computed tomography o 4.3 Ultrasound 5 Treatment o 5.1 Conservative o 5.2 Aspiration o 5.3 Chest tube 6 Prevention 7 Epidemiology 8 History 9 References

[edit] Signs and symptoms

[edit] Clinical subtypes
Primary spontaneous pneumothorax (PSP), which tends to occur in young people without underlying lung problems, usually causes limited symptoms. Chest pain and sometimes mild breathlessness are the predominant symptoms.[1][2] Half of those with primary spontaneous pneumothorax wait several days to seek medical attention.[4] It is exceedingly uncommon for PSP to cause tension pneumothorax. The symptoms usually start at rest. Tall males, especially smokers, are characteristically at a higher risk of PSP.[1] It has been found that PSP occurs more commonly during changes in atmospheric pressure and during exposure to loud music, and this explains to an extent why episodes of pneumothorax may happen in clusters.[2] Secondary spontaneous pneumothorax (SSP) occurs by definition in those with underlying lung diseases. The symptoms tend to be more severe, as the unaffected lung is generally not capable of replacing the loss of function from the affected side. Hypoxemia (decreased blood oxygen levels) is usually present and may be observed as cyanosis (blue discoloration of the lips and

skin). Hypercapnia (accumulation of carbon dioxide in the blood) is sometimes encountered; this may cause confusion and coma. Sudden breathlessness in someone with lung problems such as chronic obstructive pulmonary disease and cystic fibrosis may therefore prompt investigations for a possible pneumothorax.[1] The size of the pneumothorax bears limited relationship to the symptoms experienced.[4] Traumatic pneumothorax occurs either because a hole in the chest wall, such as a stab wound or gunshot wound, allows air to enter the pleural space, or because of injury to the lung. It has been found to occur in half of all cases of injury to the chest, coming second after rib fracture in the complications after chest trauma. The pneumothorax can be small (occult) in half of these cases, but they may enlarge if the person requires mechanical ventilation and their presence is therefore still relevant.[2] It is also often encountered in those already receiving mechanical ventilation.[2][3] Tension pneumothorax is defined differently by different sources,[3] but is generally said to exist when there is severe hypoxia despite administration of oxygen, falling blood pressure or confusion. This is a medical emergency and may require immediate treatment without further investigations (see below).[3][4] Tension pneumothorax may also occur in those receiving mechanical ventilation, in which case it may be difficult to spot as the person is typically sedated; it is often noted because of sudden deterioration.[3]

[edit] Physical examination

There may be no abnormalities on physical examination, especially if the pneumothorax is small. The breath sounds as audible by stethoscope may be diminished on the affected side, as air in the pleural space dampens sound. Percussion of the chest may sound hyperresonant (higher pitched), and vocal resonance and tactile fremitus (both examining the conduction of voice by the lung) can be decreased.[2][4] Tension pneumothorax is characterized by rapid breathing, cyanosis, falling blood pressure (hypotension) and confusion. The affected side of the chest may be hyperexpanded and show decreased movement, with increased movement on the other side. In very severe cases, the respiratory rate falls sharply, with shock and coma. Recent studies have shown that the development of tension features may not always be as rapid as previously thought. Particular clinical signs may also be less useful in the recognition of tension pneumothorax, such as the deviation of the trachea (windpipe) to one side and the presence of raised jugular venous pressure (distended neck veins).[3]

[edit] Cause

A schematic drawing of a bulla and a bleb, two lung abnormalities that may rupture and lead to pneumothorax.

[edit] Spontaneous
Spontaneous pneumothoraces are divided into two types: primary, which occurs in the absence of known lung disease, and secondary, which occurs in someone with underlying lung disease. The exact cause of primary spontaneous pneumothorax is unknown, but established risk factors include male sex, smoking, and a family history of pneumothorax.[5] The various suspected underlying mechanisms are discussed below.[1][2] Secondary spontaneous pneumothorax occurs in the setting of a variety of lung diseases. The most common is chronic obstructive pulmonary disease which accounts for approximately 70% of cases.[5] Known lung diseases that may increase the risk for pneumothorax are:[1][2]

Diseases of the airways: chronic obstructive pulmonary disease (especially when emphysema and lung bullae are present), acute severe asthma, cystic fibrosis Lung infections: pneumocystis pneumonia (PCP), tuberculosis, necrotizing pneumonia Interstitial lung diseases: sarcoidosis, idiopathic pulmonary fibrosis, histiocytosis X, lymphangioleiomyomatosis (LAM) Connective tissue diseases: rheumatoid arthritis, ankylosing spondylitis, polymyositis and dermatomyositis, systemic sclerosis, Marfan's syndrome and Ehlers-Danlos syndrome Cancer: lung cancer, sarcomas involving the lung Catamenial (occurring in relation to the menstrual cycle): endometriosis in the chest

In children, additional causes include measles, echinococcosis, inhalation of a foreign body, and particular congenital malformations (congenital cystic adenomatoid malformation and congenital lobar emphysema).[6] A rare genetic disorder, Birt-Hogg-Dub syndrome, may cause spontaneous pneumothorax in families. It also causes skin lesions (fibrofolliculomas) and lung cysts, and carries an increased risk of kidney cancer. The lung cysts, which probably lead to increased risk of pneumothorax, tend to be in the lower lobes rather than the more common upper lobe cysts encountered in other conditions.[7] Birt-Hogg-Dub syndrome is caused by mutations in the FLCN gene (chromosome 17p11.2), which encodes a protein named folliculin.[6][7] FLCN mutations and lung lesions have also been identified in familial cases of pneumothorax where other features of Birt-Hogg-Dub syndrome are absent.[6]

[edit] Traumatic
A traumatic pneumothorax may result from both blunt trauma and penetrating injuries to the chest wall.[2] It may be observed in those exposed to an explosive blast, even if no direct injury to the chest has occurred.[8] The most common mechanism is a cut to the pleura by a fractured rib.[5] Medical procedures of the chest (iatrogenic), such as the taking of biopsy samples from lung tissue, inserting a central venous catheter into one of the chest veins, may lead to injury to the lung and resultant pneumothorax. The administration of positive pressure ventilation, either mechanical ventilation or non-invasive ventilation, may result in barotrauma (pressure-related injury) leading to a pneumothorax.[2]

[edit] Mechanism

CT scan of the chest showing a pneumothorax on the patient's left side (right side on the image). A chest tube is in place (small black mark on the right side of the image), the air-filled pleural cavity (black) and ribs (white) can be seen. The heart can be seen in the center. The thoracic cavity is the hollow space that contains the lungs. The lungs are physically connected at the hila, where the airways and blood vessels enter the lung. They remain inflated inside the thoracic cavity because the pressure inside the pleural space (the space between the chest wall and the lung) is almost consistently negative throughout the respiratory cycle, effectively sucking the lung to the chest wall. Both the lung and the chest wall are covered by a layer of cells known as the pleura (visceral and parietal pleura, respectively), and a small amount of serous fluid is typically present. The negative pressure normally does not allow air to enter the pleural space because there are no natural connections to air-containing space, and the pressure of gases in the bloodstream is too low for them to be released into the pleural space. Pneumothorax can therefore only develop if air is allowed to enter, either through damage in the chest wall, or damage to the lung itself, or occasionally because microorganisms in the space produce gas.[2] The chest wall defect is usually evident in cases of injury to the chest wall, such as bullet wounds ("open pneumothorax"). In secondary spontaneous pneumothorax, vulnerabilities in the lung tissue are caused by a variety of disease processes, such as bullae (large air-containing lesions) in emphysema. Areas of necrosis (tissue death) may precipitate pneumothorax episodes, although the exact mechanism is unclear.[1] Primary spontaneous pneumothorax has for many years been

thought to be caused by "blebs", small lesions just under the pleural surface, which were presumed to be more common in those classically at risk of pneumothorax (tall males) due to mechanical factors. Various lines of evidence suggest that this hypothesis may not be correct, such as the fact that pneumothorax may recur even after surgical treatment of blebs, and that blebs occur in 15% of healthy people. It has therefore been suggested that PSP is instead caused by areas of disruption (porosity) in the pleural layer, which are prone to rupture.[1][2] Smoking may lead to inflammation and obstruction of small airways, accounting for the markedly increased risk of PSP in smokers.[4] Once air has stopped entering the pleural cavity, it is gradually resorbed spontaneously. Estimated rates of resorption are between 1.25% and 2.2% the volume of the cavity per day. This would mean that even a completely collapsed lung would spontaneously reinflate over a period of about 6 weeks.[4] Tension pneumothorax occurs because the opening that allows air to enter the pleural space functions like a valve, and with every breath more air enters and cannot escape. Severe hypoxia follows, with a resultant drop in blood pressure and level of consciousness. A previously uttered theory that the collapsed lung compresses large blood vessels such as the aorta is probably incorrect.[3]

[edit] Diagnosis
The symptoms of pneumothorax can be subtle, especially in those with PSP, and confirmation with medical imaging is usually required.[4] In contrast, tension pneumothorax is ideally treated before imaging, especially if there is severe hypoxia, very low blood pressure, or an impaired level of consciousness; however, X-rays are sometimes required if there is doubt about the location of the pneumothorax.[3][5]

[edit] Chest X-ray

Chest X-ray of left-sided pneumothorax (visible on the right in this image). The left thoracic cavity is filled in part with free air. The mediastinum is shifted to the opposite side. Traditionally a plain radiograph of the chest, ideally with the X-ray beams being projected from the back (posteroanterior or PA), has been the most appropriate first investigation. Usually, these are performed in inspiration (holding one's breath); no added information is gathered by obtaining a chest X-ray in expiration (after exhaling).[2][4] If the PA X-ray does not show a

pneumothorax but there is a strong suspicion, lateral X-rays (with beams projecting from the side) may be performed, but this is not routine practice.[4][6] It is not unusual for the mediastinum (the structure between the lungs that contains the heart and several other organs) to be shifted away from the affected lung due to pressure. This is not equivalent to tension pneumothorax, which is determined mainly by symptoms, hypoxia and shock.[2] The size of the pneumothorax, i.e. the amount of space in the chest taken up by free air rather than air-containing lung, can be determined with a reasonable degree of accuracy by measuring the distance between the chest wall and the lung. This is relevant as smaller pneumothoraces may be treated differently. An air rim of 2 cm or more means that the pneumothorax occupies about 50% of the pleural cavity.[4] British professional guidelines have traditionally stated that the measurement should be performed at the level of the hilum (where blood vessels and airways enter the lung),[4] while American guidelines state that the measurement should happen at the apex (tip) of the lung.[9] The latter method may overestimate the size of a pneumothorax if it is located mainly at the apex, which is a common occurrence.[4] The various methods correlate poorly, but are the best immediately available ways of estimating pneumothorax size.[4][6] CT scanning (see below) would provide a more accurate determination of the size of the pneumothorax, but its routine use in this setting is not recommended.[9] Not all pneumothoraces are uniform; some only form a pocket of air in a particular place in the chest.[4] Small amounts of fluid (which may be blood - hemopneumothorax) may be noted on the chest X-ray.[2] In some cases, the only significant abnormality may be the "deep sulcus sign", in which the usually small space between the chest wall and the diaphragm appears enlarged due to the presence of air.[3]

[edit] Computed tomography

Computed tomography (CT or CAT scan) can be useful in particular situations. In some lung diseases, especially emphysema, it is possible for abnormal lung areas such as bullae (large airfilled sacs) to have the same appearance as a pneumothorax, and it may not be safe to apply any treatment before the distinction is made and before the exact location and size of the pneumothorax is determined.[4] In trauma, where it may not be possible to perform an upright film, chest radiography may miss up to a third of pneumothoraces, while CT remains very sensitive.[5] A further use of CT is in the identification of underlying lung lesions. In presumed primary pneumothorax, it may help identify blebs or cystic lesions (in anticipation of treatment, see below), and in secondary pneumothorax it can identify most of the causes listed above.[4][6]

[edit] Ultrasound
Ultrasound is used commonly in the evaluation of people who have sustained physical trauma, for example with the FAST protocol.[10] Ultrasound may be more sensitive than chest X-rays in the identification of pneumothorax after blunt trauma to the chest.[11]

[edit] Treatment

Schematic drawing of a person with a chest tube in the left thoracic cavity. It is connected to a water seal. The treatment of pneumothorax depends on a number of factors, and may vary from discharge with early follow-up to immediate needle decompression or insertion of a chest tube. Treatment is determined by the severity of symptoms and indicators of acute illness, the presence of underlying lung disease, the estimated size of the pneumothorax on X-ray, and in some instances also on the personal preference of the person involved. In spontaneous pneumothorax, air travel is discouraged until it has completely resolved.[4] In traumatic pneumothorax, chest tubes are usually inserted (unless iatrogenic, see below). It is not yet clear if there is a subgroup of patients with small pneumothoraces who do not require tube treatment and could be managed conservatively. If mechanical ventilation is required, the insertion of a chest tube is mandatory as it would increase the risk of tension pneumothorax.[2][12] Tension pneumothorax is usually treated with urgent needle decompression. This may need to happen before transport to hospital, and can be performed by an emergency medical technician or other trained professional. The needle or cannula is left in place until a chest tube can be

inserted.[3][13] Any open chest wound is covered, as it carries a high risk of leading to tension pneumothorax, ideally with a dressing called the Asherman seal, which appears to be more effective than standard "three-sided" dressing. The Asherman seal is a specially designed device that adheres to the chest wall and allows air to escape but not to enter the chest through a valvelike mechanism.[13]

[edit] Conservative
Small spontaneous pneumothoraces do not always require treatment, as they are unlikely to proceed to respiratory failure or tension pneumothorax and generally resolve spontaneously. This approach is most appropriate if the estimated size of the pneumothorax is small (e.g. <50%), there is no breathlessness, and there is no underlying lung disease.[6][9] It may be appropriate to treat a larger PSP conservatively if the symptoms are limited.[4] Admission to hospital is often not required, as long as clear instructions are given to return to hospital if there are worsening symptoms. Further investigations may be performed as an outpatient, at which time X-rays are repeated to confirm improvement, and advice may be given with regards to preventing recurrence such as surgery (see below).[4] Secondary pneumothoraces are only treated conservatively if the size is very small (1 cm or less air rim) and there are limited symptoms. Admission to hospital is usually recommended. Oxygen given at a high flow rate may accelerate resorption.[4]

[edit] Aspiration
In a large primary spontaneous pneumothorax (>50%) or PSP associated with breathlessness, some professional guidelines recommend that reducing the size by aspiration is equally effective as insertion of a chest tube. This involves the administration of local anesthetic and inserting a needle connected to a three-way tap; up to 2.5 liters of air (in adults) are removed. If there has been significant reduction in the size of the pneumothorax on a further X-ray, the remainder of the treatment can be conservative. This approach is effective in over 50% of cases.[1][4][6] Firstline aspiration in PSP reduces the number of people requiring admission to hospital significantly as opposed to tube drainage, without increasing the risk of complications.[14] Aspiration may also be considered in secondary pneumothorax of moderate size (air rim 12 cm) without breathlessness, with the difference that ongoing observation in hospital is required even after a successful procedure.[4] American professional guidelines state that all large pneumothoraces, even those due to PSP, should be treated with a chest tube.[9] Moderately-sized traumatic pneumothorax due to medical procedures (iatrogenic) may initially be treated with aspiration.[2]

[edit] Chest tube

A chest tube (or intercostal drain) is the most definitive initial treatment of a pneumothorax. This is typically inserted in an area under the axilla (armpit) called the "safe triangle", where damage to internal organs can be avoided; this is delineated by a horizontal line at the level of the nipple and two muscles of the chest wall (latissimus dorsi and pectoralis major). Local anesthetic is applied. Two types of tubes may be used. In spontaneous pneumothorax, small-bore (smaller

than 14 FG, 4.7 mm diameter) tubes may be inserted by the Seldinger technique, and larger tubes do not have an advantage.[4] In traumatic pneumothorax, larger tubes (28 FG, 9.3 mm) are used.[13] Chest tubes are required in PSP that has not responded to needle aspiration, in any SSP that is large (>50%), and in cases of tension pneumothorax. They are connected to a one-way valve system that allows air to escape but not to reenter the chest. This may include a bottle with water that functions like a water seal, or a Heimlich valve. They are not normally connected to a negative pressure circuit, as this would result in rapid reexpansion of the lung and a risk of pulmonary edema ("reexpansion pulmonary edema"). The tube is left in place until no air is seen to escape from it for a period of time, and X-rays confirm reexpansion of the lung.[4][6][9] If after 24 days there is still evidence of air leak, various options are available. Negative pressure suction (at low pressures of 10 to 20 cmH2O) at a high flow rate may be attempted, especially in PSP; it is thought that this may accelerate the healing of the leak. In SSP, assistance from a thoracic surgeon may be required earlier.[4] Surgical options are similar to those used to prevent further episodes, and are discussed below (thoracotomy and VATS).

[edit] Prevention
Both medical and surgical treatments exist to reduce the risk of recurrence of a pneumothorax.[15] The main aim is to achieve pleurodesis, the adherence between the lung and the chest wall. The evidence on the most effective treatment is still conflicting in some areas, and there is variation between treatments available in Europe and the USA.[1] Not all episodes of pneumothorax require such interventions; the decision depends largely on the suspected risk of recurrence. They however are often recommended after a second pneumothorax.[15] An exception applies in those who engage in diving; diving is considered unsafe unless permanent treatment has been applied; professional guidelines suggest that pleurectomy is performed on both lungs (see below) and that lung function tests and CT scan must be normal before diving is resumed.[4][9] The best results, with a recurrence rate less than 1%, are achieved with a thoracotomy (surgical opening of the chest) with identification of any clear air leak and stapling of blebs, followed by pleurectomy (stripping of the pleural lining) of the outer pleural layer and pleural abrasion (scraping of the pleura) of the inner layer. During the healing process, the lung adheres to the chest wall, effectively obliterating the pleural space. Thoracotomy is always performed under a general anesthetic.[1][4] A less invasive approach is thoracoscopy, usually in the form of a procedure called videoassisted thoracoscopic surgery. This also involves a general anesthetic but the lung is approached through a number of small incisions between the ribs. The results from VATS-based pleural abrasion are slightly worse than those achieved by thoracotomy, but with less unsightly skin Scars. VATS may be also be used to achieve chemical pleurodesis; this involves the instillation of talc, which activates a scarring reaction that may also stick the lung to the chest wall.[1][4] Not everyone may be prepared to undergo surgery. If a chest tube is already in place, various agents may be instilled through the tube to achieve pleurodesis, specifically talc and the

antibiotic tetracycline. The results from this tend to be worse than from surgical approaches.[1][4] Talc pleurodesis has few long term consequences in young people.[1]

[edit] Epidemiology
Spontaneous pneumothorax is more common in males than in females. The annual incidence of PSP is 1828 per 100,000 in males and 1.26.0 in females. Secondary spontaneous pneumothorax is less common, with 6.3 for males and 2.0 for females. Risk of recurrence depends on underlying lung disease. Once a second episode has occurred, there is a high likelihood of subsequent further episodes.[1] Smokers have an increased risk of contracting a first spontaneous pneumothorax of approximately ninefold among women and 22-fold among men compared to non-smokers.[16] The incidence in children has not been well studied, but it is probably less than that of adults and often reflects underlying lung disease.[6] Death from pneumothorax is very uncommon (except for tension pneumothorax). British statistics have revealed an annual mortality of 1.26 per million per year in men and 0.62 in women.[4] Mortality is higher in older people and those with secondary pneumothorax.[1]

[edit] History
Jean Marc Gaspard Itard, a student of Ren Laennec, first recognised pneumothorax in 1803, and Laennec himself described the full clinical picture in 1819.[17] While Itard and Laennec recognized that some cases were not due to tuberculosis (then the most common cause), the concept of primary spontaneous pneumothorax was reintroduced by the Danish physician Hans Kjrgaard in 1932.[4][18] Prior to the advent of anti-tuberculous medications, iatrogenic pneumothoraces were intentionally given to tuberculosis patients in an effort to collapse a lobe, or entire lung around a cavitating lesion. This was known as "resting the lung". It was introduced by the Italian surgeon Carlo Forlanini in 1888 and publicized by the American surgeon John Benjamin Murphy in the early 20th century after discovering the same procedure independently. Murphy used the then recently discovered X-ray technology to create pneumothoraces of the correct size.[19]

[edit] Hiatus

hernia

From Wikipedia, the free encyclopedia

Ventricular hernia
Classification and external resources

ICD-10 ICD-9 OMIM DiseasesDB MedlinePlus eMedicine MeSH

K44, Q40.1 553.3, 750.6 142400 29116 001137 med/1012 radio/337 D006551

A hiatus hernia or hiatal hernia is the protrusion (or herniation) of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm.

Contents
[hide]

1 Classification 2 Signs and symptoms 3 Risk factors 4 Diagnosis 5 Treatment 6 Prognosis 7 Epidemiology 8 Notes and references 9 External links

[edit] Classification

Schematic diagram of different types of hiatus hernia. Green is the esophagus, red is the stomach, purple is the diaphragm, blue is the HIS-angle. A is the normal anatomy, B is a prestage, C is a sliding hiatal hernia, and D is a paraesophageal type. There are two major kinds of hiatus hernia: [1]

The most common (95%) is the sliding hiatus hernia, where the gastroesophageal junction moves above the diaphragm together with some of the stomach. The second kind is rolling (or paraesophageal) hiatus hernia, when a part of the stomach herniates through the esophageal hiatus and lies beside the esophagus, without movement of the gastroesophageal junction. It accounts for the remaining 5% of hiatus hernias. [2]

A third kind is also sometimes described, and is a combination of the first and second kinds.[citation needed]

[edit] Signs and symptoms

Hiatal hernia has often been called the "great mimic" because its symptoms can resemble many disorders. For example, a person with this problem can experience dull pains in the chest, shortness of breath (caused by the hernia's effect on the diaphragm), and heart palpitations (due to irritation of the vagus nerve). In most cases however, a hiatal hernia does not cause any symptoms. The pain and discomfort that a patient experiences is due to the reflux of gastric acid, air or bile. While there are several causes of acid reflux, it does happen more frequently in the presence of hiatal hernia.

[edit] Risk factors

The following are risk factors that can result in a hiatus hernia.

Increased pressure within the abdomen caused by: o Heavy lifting or bending over o Frequent or hard coughing o Hard sneezing o Pregnancy and delivery o Violent vomiting o Straining with constipation o Obesity (extra weight pushes down on the abdomen increasing the pressure) [3] o Use of the sitting position for defecation (See epidemiology below) Heredity Smoking[citation needed] Drug use, such as cocaine[citation needed] Stress Diaphragm weakness[citation needed]

[edit] Diagnosis

A large hiatus hernia on X-ray marked by open arrows in contrast to the heart borders marked by closed arrows

Upper GI endoscopy depicting hiatus hernia

A hiatus hernia as seen on CT The diagnosis of a hiatus hernia is typically made through an upper GI series, endoscopy or high resolution manometry.

[edit] Treatment
In most cases, sufferers experience no discomfort and no treatment is required. However, when the hiatal hernia is large, or is of the paraesophageal type, it is likely to cause esophageal stricture and discomfort. Symptomatic patients should elevate the head of their beds and avoid lying down directly after meals until treatment is rendered. If the condition has been brought on by stress, stress reduction techniques may be prescribed, or if overweight, weight loss may be indicated. Medications that reduce the lower esophageal sphincter (or LES) pressure should be avoided. Antisecretory drugs like proton pump inhibitors and H2 receptor blockers can be used to reduce acid secretion. Where hernia symptoms are severe and chronic acid reflux is involved, surgery is sometimes recommended, as chronic reflux can severely injure the esophagus and even lead to esophageal cancer. The surgical procedure used is called Nissen fundoplication. In fundoplication, the gastric fundus (upper part) of the stomach is wrapped, or plicated, around the inferior part of the esophagus, preventing herniation of the stomach through the hiatus in the diaphragm and the reflux of gastric acid. The procedure is now commonly performed laparoscopically. With proper patient selection, laparoscopic fundoplication has low complication rates and a quick recovery.[4] Complications include gas bloat syndrome, dysphagia (trouble swallowing), dumping syndrome, excessive scarring, and rarely, achalasia. The procedure sometimes fails over time, requiring a second surgery to make repairs.

[edit] Prognosis
A hiatus hernia per se does not cause any symptoms. The condition promotes reflux of gastric contents (via its direct and indirect actions on the anti-reflux mechanism) and thus is associated

with gastroesophageal reflux disease (GERD). In this way a hiatus hernia is associated with all the potential consequences of GERD heartburn, esophagitis, Barrett's esophagus, esophageal cancer and dental erosion. However the risk attributable to the hiatus hernia is difficult to quantify, and at most is low.[citation needed] Besides discomfort from GERD and dysphagia, hiatal hernias can have severe consequences if not treated. While sliding hernias are primarily associated with gastroesophageal acid reflux, rolling hernias can strangulate a portion of the stomach above the diaphragm. This strangulation can result in esophageal or GI tract obstruction and the tissue can even become ischemic and necrose. Another severe complication, although very rare, is a large herniation that can restrict the inflation of a lung, causing pain and breathing problems. Most cases are asymptomatic.

[edit] Epidemiology
Incidence of hiatal hernias increases with age; approximately 60% of individuals aged 50 or older have a hiatal hernia.[5] Of these, 9% are symptomatic, depending on the competence of the lower esophageal sphincter (LES). 95% of these are "sliding" hiatus hernias, in which the LES protrudes above the diaphragm along with the stomach, and only 5% are the "rolling" type (paraesophageal), in which the LES remains stationary but the stomach protrudes above the diaphragm. People of all ages can get this condition, but it is more common in older people. According to Dr. Denis Burkitt, "Hiatus hernia has its maximum prevalence in economically developed communities in North America and Western Europe ... In contrast the disease is rare in situations typified by rural African communities."[3] Burkitt attributes the disease to insufficient dietary fiber and the use of the unnatural sitting position for defecation. Both factors create the need for straining at stool, increasing intraabdominal pressure and pushing the stomach through the esophageal hiatus in the diaphragm.[6]

[edit]

Hemopneumothorax
From Wikipedia, the free encyclopedia This article does not cite any references or sources. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (August 2008)

Hemopneumothorax
Classification and external resources

ICD-10 ICD-9 MeSH

J94.2, S27.2 511.8, 860 D006468

Hemopneumothorax, or haemopneumothorax, is a medical term describing the combination of two conditions: pneumothorax, or air in the chest cavity, and hemothorax (also called hmothorax), or blood in the chest cavity. A haemothorax, pneumothorax or both can occur if the chest wall is punctured. To understand the ramifications of this it is important to have an understanding of the role of the pleural space. The pleural space is located anatomically between the visceral membrane, which is firmly attached to the lungs, and the parietal membrane which is firmly attached to the chest wall (aka ribcage and intercostal muscles, muscles between the ribs). The pleural space contains pleural fluid. This fluid holds the two membranes together by surface tension, much as a drop of water between two sheets of glass prevents them from separating. Because of this, when the intercostal muscles move the ribcage outward, the lungs are pulled out as well, dropping the pressure in the lungs and pulling air into the bronchi, when we 'breathe in'. The pleural space is maintained in a constant state of negative pressure (in comparison to atmospheric pressure). If the chest wall, and thus the pleural space, is punctured, blood, air or both can enter the pleural space. Air/blood rushes into the space in order to equalise the pressure with that of the atmosphere. As a result the fluid is disrupted and the two membranes no longer adhere to each other. When the rib cage moves out, it no longer pulls the lungs with it. Thus the lungs cannot expand, the pressure in the lungs never drops and no air is pulled into the bronchi. Respiration is not possible. The affected lung, which has a great deal of elastic tissue, shrivels in what is referred to as a collapsed lung.

[edit] Treatment
Treatment for this condition is the same as for hemothorax and pneumothorax independently: by tube thoracostomy, the insertion of a chest drain through an incision made between the ribs, into the intercostal space. A chest tube must be inserted to drain blood and air from the pleural space so it can return to a state of negative pressure and function normally. Commonly, surgery is needed to close off whatever injuries caused the blood and air to enter the cavity (e.g. stabbing, broken ribs).

Catamenial pneumothorax
From Wikipedia, the free encyclopedia

Catamenial pneumothorax is a condition of collapsed lung (pneumothorax) occurring in conjunction with menstrual periods (catamenial refers to menstruation), believed to be caused primarily by endometriosis of the pleura (the membrane surrounding the lung).[1]

Contents
[hide]

1 Classification 2 Symptoms and signs 3 Pathophysiology 4 Diagnosis 5 Treatment 6 Epidemiology 7 References 8 External links

[edit] Classification
Catamenial pneumothorax is the most common form of thoracic endometriosis syndrome, which also includes catamenial hemothorax, catamenial hemoptysis, catamenial hemopneumothorax and endometriosis lung nodules, as well as some exceptional presentations.

[edit] Symptoms and signs

Onset of lung collapse is less than 72 hours after menstruation. Typically, it occurs in women aged 3040 years, but has been diagnosed in young girls as early as 10 years of age and post menopausal women (exclusively in women of menstrual age) most with a history of pelvic endometriosis.

[edit] Pathophysiology
Endometrial tissue attaches within the thoracic cavity, forming chocolate-like cysts. Generally the parietal pleura is involved, but the lung itself, the visceral layer, the diaphragm, and more rarely the tracheobronchial tree may also be afflicted.[2] How this endometrial tissue reaches the thorax remains enigmatic. Defects in the diaphragm, which are found often in affected individuals, could provide an entry path,[3] as could microembolization through pelvic veins.[4] The cysts can release blood; the endometrial cyst "menstruates" in the lung. Air can move in by an unknown mechanism. The blood and air cause the lung to collapse (i.e. catamenial hemopneumothorax).[5]

[edit] Diagnosis
Diagnosis can be hinted by high recurrence rates of lung collapse in a woman of reproductive age with endometriosis. CA-125 is elevated. Nowadays, video-assisted thoracoscopy is used for confirmation.

[edit] Treatment
Pneumothorax can be a medical emergency, as it can become associated with severe pain and decreased lung function. A chest tube should be inserted after clinical assessment. This releases the air and menstrual blood, and the lung can re-expand. Surgery, hormonal treatments and combined approaches have all been proposed, with variable results in terms of short and long term outcome.[6] Surgical removal of the endometrial tissue should be endeavoured during menstruation for optimal visualisation of the cyst.[7] Pleurodesis may also be helpful. Menstruation and accompanying lung collapse can be suppressed with hormone therapy,[8] like with Lupron Depot, danazol or extended cycle combined oral contraceptive pills.

[edit] Epidemiology
Some sources claim this entity represents 3-6% of pneumothorax in women.[8] In regard of the low incidence of primary spontaneous pneumothorax (i.e. not due to surgical trauma etc.) in women (about 1/100'000/year),[8] this is a very rare condition. Hence, many basic textbooks don't mention it, and many doctors have never heard of it. However, catamenial pneumothorax is probably under-recognised.[3]

Shock (circulatory)
From Wikipedia, the free encyclopedia "Acute shock" redirects here. For the psychological condition, see Acute stress reaction. Shock ICD-10 ICD-9 DiseasesDB MedlinePlus many incl. R57 785 12013 000039

eMedicine

emerg/531 med/285 emerg/533

Circulatory shock, commonly known simply as shock, is a life-threatening medical condition that occurs due to inadequate substrate for aerobic cellular respiration.[1] In the early stages this is generally an inadequate tissue levels of oxygen.[2] The typical signs of shock are low blood pressure, a rapid heartbeat and signs of poor end-organ perfusion or "decompensation" (such as low urine output, confusion or loss of consciousness). There are times that a person's blood pressure may remain stable, but may still be in circulatory shock, so it is not always a symptom.[3] A circulatory shock should not be confused with the emotional state of shock, as the two are not related. Medical shock is a life-threatening medical emergency and one of the most common causes of death for critically ill people. Shock can have a variety of effects, all with similar outcomes, but all relate to a problem with the body's circulatory system. For example, shock may lead to hypoxemia (a lack of oxygen in arterial blood) or cardiac arrest (the heart stopping).[4] One of the key dangers of shock is that it progresses by a positive feedback mechanism. Once shock begins, it tends to make itself worse. This is why immediate treatment of shock is critical.[3]

Contents
[hide]

1 Signs and symptoms o 1.1 Hypovolaemic o 1.2 Cardiogenic o 1.3 Distributive 2 Pathophysiology o 2.1 Initial o 2.2 Compensatory o 2.3 Progressive o 2.4 Refractory o 2.5 Septic shock 3 Diagnosis 4 Differential diagnosis o 4.1 Hypovolemic o 4.2 Cardiogenic o 4.3 Obstructive o 4.4 Distributive o 4.5 Endocrine 5 Management o 5.1 Fluids o 5.2 Medications

o 5.3 Treatment goals 6 Prognosis 7 History 8 References

[edit] Signs and symptoms

The presentation of shock is variable with some people having only minimal symptoms such as confusion and weakness.[2] While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion these may not always be present.[2] While a fast heart rate is common, those on B-blockers, those who are athletic and in 30% of cases those with shock due to intra abdominal bleeding may have a normal or slow heart rate.[5] Specific subtypes of shock may have additional symptoms.

[edit] Hypovolaemic
Hemorrhage classes[6] Class I II III IV Blood loss <15 %(0.75 l) 15-30 %(0.75-1.5 l) Response min. fast heart rate, normal blood pressure fast heart rate, min. low blood pressure Treatment minimal intravenous fluids

30-40 %(1.5-2 l) very fast heart rate, low blood pressure, confusion fluids and packed RBCs >40 %(>2 l) critical blood pressure and heart rate aggressive interventions

Direct loss of effective circulating blood volume leading to:

A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction Rapid and shallow respirations due to sympathetic nervous system stimulation and acidosis Hypothermia due to decreased perfusion and evaporation of sweat Thirst and dry mouth, due to fluid depletion Cold and mottled skin (cutis marmorata), especially extremities, due to insufficient perfusion of the skin

The severity of hemorrhagic shock can be graded on a 1-4 scale on the physical signs. This approximates to the effective loss of blood volume.

[edit] Cardiogenic

Distended jugular veins due to increased jugular venous pressure Weak or absent pulse Arrhythmia, often tachycardic Pulsus paradoxus in case of tamponade

[edit] Distributive
Systemic inflammatory response syndrome[7] Finding Temperature Heart rate Respiratory rate WBC Value <36 C (97 F) or >38 C (100 F) >90/min >20/min or PaCO2<32 mmHg (4.3 kPa) <4x109/L (<4000/mm), >12x109/L (>12,000/mm), or 10% bands

Distributive shock includes infectious, anaphylactic, and neurogenic causes. The SIRS features typically occur in early septic shock.[2]
[edit] Septic shock

Fever may occur in sepsis Warm and sweaty skin due to vasodilation

[edit] Anaphylaxisis

Hives may present on the skin Localised oedema, especially around the face Weak and rapid pulse Breathlessness and cough due to narrowing of airways and swelling of the throat

[edit] Pathophysiology

Effects of inadequate perfusion on cell function.

There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next.[8] At a cellular level shock is oxygen demand greater than oxygen supply.[2]

[edit] Initial
During this stage, the hypoperfusional state causes hypoxia. Due to the lack of oxygen, the cell membranes become damaged[why?], they become leaky to extra-cellular fluid, and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent.[citation needed]

[edit] Compensatory
This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline. Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. This is known as Cushing reflex and its triad is the subjective identifying characteristic of this stage. Renin-angiotensin axis is activated and arginine vasopressin (Anti-diuretic

hormone; ADH) is released to conserve fluid via the kidneys. These hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin-angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock.[citation needed]

[edit] Progressive
Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries.[9] Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.[9] If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.[9][3]

[edit] Refractory
At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently. One of the primary reasons that shock is irreversible at this point is that much cellular ATP has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid. Because cells can only produce adenosine at a rate of about 2% of the cell's total need per hour, even restoring oxygen is futile at this point because there is no adenosine to phosphorylate into ATP.[3]

[edit] Septic shock

Systemic leukocyte adhesion to endothelial tissue[9] Reduced contractility of the heart[9] Activation of the coagulation pathways, resulting in disseminated intravascular coagulation[9] Increased levels of neutrophils[9]

[edit] Diagnosis
The first changes seen in shock is an increased cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and are easier to acquire. If shock progresses anaerobic metabolism will begin to occur with an increased blood lactic acid as the result. While many laboratory tests are typically

performed there is no test that either makes or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be useful to determine volume state.[2][5]

[edit] Differential diagnosis

Shock is a common end point of many medical conditions.[1] It has been divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic and obstructive.[10] A few additional classifications are occasionally used including: endocrinologic shock.[1]

[edit] Hypovolemic
This is the most common type of shock and is caused by insufficient circulating volume.[2] Its primary cause is hemorrhage or loss of fluid from the circulation. Vomiting and diarrhea are the most common cause in children.[1] With other causes including burns, environmental exposure and excess urine loss due to diabetic ketoacidosis and diabetes insipidus.[1]

[edit] Cardiogenic
This type of shock is caused by the failure of the heart to pump effectively.[2] This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart failure (CHF), contusio cordis, or cardiac valveproblems.[1]

[edit] Obstructive
Obstructive shock is due to obstruction of blood flow outside of the heart.[2] Several conditions can result in this form of shock.

Cardiac tamponade[1] in which fluid in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation. Tension pneumothorax[1] Through increased intrathoracic pressure, bloodflow to the heart is prevented (venous return). Pulmonary embolism is the result of a thromboembolic incident in the bloodvessels of the lungs and hinders the return of blood to the heart. Aortic stenosis hinders circulation by obstructing the ventricular outflow tract

[edit] Distributive
Distributive shock is due to impaired utilization of oxygen and thus production of energy by the cell.[2] Examples of this form of shock are:

Septic shock is the most common cause of distributive shock.[1] Caused by an overwhelming systemic infection resulting in vasodilation leading to hypotension. Septic shock can be caused by Gram negativebacteria such as (among others) Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces adverse biochemical, immunological

and occasionally neurological effects which are harmful to the body, and other Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins. Septic shock also includes some elements of cardiogenic shock. In 1992, the ACCP/SCCM Consensus Conference Committee defined septic shock: ". . .sepsis-induced hypotension (systolic blood pressure <90 mm Hg or a reduction of 40 mm Hg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified." Anaphylactic shock Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability. High spinal injuries may cause neurogenic shock.[11] The classic symptoms include a slow heartrate due to loss of cardiac sympathetic tone and warm skin due to dilation of the peripheral blood vessels.[12] (This term can be confused with spinal shock which is a recoverable loss of function of the spinal cord after injury and does not refer to the haemodynamic instability per se.)

[edit] Endocrine
Based on endocrine disturbances such as:

Hypothyroidism (Can be considered a form of Cardiogenic shock) in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency. Thyrotoxicosis (Cardiogenic shock) o may induce a reversible cardiomyopathy. Acute adrenal insufficiency (Distributive shock) is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition. Relative adrenal insufficiency (Distributive shock) in critically ill patients where present hormone levels are insufficient to meet the higher demands

[edit] Management
The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas.[1] Management may include securing the airway via intubation to decrease the work of breathing, oxygen supplementation, intravenous fluids and a passive leg raise (not Trendelenburg position), and blood transfusions.[2] It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.[2]

[edit] Fluids
Aggressive intravenous fluids are recommended in shock (e.g. 1-2 liter normal saline bolus over 10 minutes or 20ml/kg in a child) which is usually instituted as the person is being further

evaluated.[13] Which intravenous fluid is superior, colloids or crystalloids, remains undetermined.[2] Thus as crystalloids are less expensive they are recommended.[14] If the person remains in shock after initial resuscitation packed red blood cells should be administer to keep the hemoglobin greater than 100 gms/l.[2]

[edit] Medications
Vasopressors may be used if blood pressure does not improve with fluids. There is no evidence of superiority of one vasopressor over another.[15] Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma[16] but may be of use in neurogenic shock.[12] Activated protein C (Xigris) while once aggressively promoted for the management of septic shock has not been found to improve survival and is associated with a number of complication, thus is no longer recommended.[17] The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes.[18] If used at all it should only be considered if the pH is less than 7.0.[18]

[edit] Treatment goals

The goal of treatment is to achieve a urine output of greater than 0.5 cc/kg/hr, a central venous pressure of 8-12 mmHg and a mean arterial pressure of 65-95 mmHg.[2]

[edit] Prognosis
The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse.[19] Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction of the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood is reinfused. In pigs and humans 1) this is not seen and cessation of bleeding and restoration of blood volume is usually very effective; however 2) prolonged hypovolemia and hypotension does carry a risk of respiratory and then cardiac arrest. Perfusion of the brain may be the greatest danger during shock. Therefore urgent treatment (cessation of bleeding, rapid restoration of circulating blood volume and ready respiratory support) is essential for a good prognosis in hypovolemic shock.