Pneumonia Code J13

Pneumonia

From Wikipedia, the free encyclopedia
For other uses, see Pneumonia (disambiguation).
Pneumonia
A black and white X-ray picture showing a triangular white area on the left side. A circle highlights the area.

A chest X-ray showing a very prominent wedge-shape area of airspace consolidation in the right lung characteristic of bacterial pneumonia.
Classification and external resources
Pronunciation /njuːˈm.ni.ə/
Synonyms pneumonitis, bronchopneumonia[1]
Specialty Infectious disease,pulmonology
ICD10 J12, J13, J14, J15,J16, J17, J18, P23
ICD9-CM 480486, 770.0
DiseasesDB 10166
MedlinePlus 000145
eMedicine topic list
Patient UK Pneumonia
MeSH D011014

Pneumonia is an inflammatory condition of the lung affecting primarily the microscopic air sacs known as alveoli.[2][3] Typical signs and symptoms include a cough with phlegm, chest pain, fever, and trouble breathing.[4]Symptoms can vary from mild to severe.[5] People who are old or very young may not have typical symptoms.[6] Usually people begin improving within three days of starting treatment; however, they may feel tired for more than a month afterwards.[5]

Pneumonia is usually caused by infection with viruses or bacteria and less commonly by other microorganisms, certain medications and conditions such as autoimmune diseases.[2][7] Risk factors include other lung diseases such as cystic fibrosis, COPD, and asthma, diabetes, heart failure, a history of smoking, a poor ability to cough such as following a stroke, or a weak immune system.[8] Diagnosis is often based on the symptoms and physical examination. Chest X-ray, blood tests, and culture of the sputum may help confirm the diagnosis.[9] The disease may be classified by where it was acquired with community, hospital, or health care associated pneumonia.[10]

Vaccines to prevent certain types of pneumonia are available. Other methods of prevention include handwashing and not smoking.[11] Treatment depends on the underlying cause.[5] Pneumonia believed to be due to bacteria is treated with antibiotics.[12] If the pneumonia is severe, the affected person is generally hospitalized.[5] Oxygen therapy may be used if oxygen levels are low.[12]

Pneumonia affects approximately 450 million people globally (7% of the population) and results in about 4 million deaths per year.[13][14] Pneumonia was regarded by William Osler in the 19th century as “the captain of the men of death”.[15] With the introduction of antibiotics and vaccines in the 20th century survival improved.[13] Nevertheless, in developing countries, and among the very old, the very young, and the chronically ill, pneumonia remains a leading cause of death.[13][16] Pneumonia often shortens suffering among those already close to death and has thus been called “the old man’s friend”.[17]

File:Pneumonia.webm

A video explanation of pneumonia

Signs and symptoms

Symptoms frequency[18]
Symptom Frequency
Cough
79–91%
Fatigue
90%
Fever
71–75%
Shortness of breath
67–75%
Sputum
60–65%
Chest pain
39–49%
A diagram of the human body outlining the key symptoms of pneumonia

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, and an increased rate of breathing.[19] In the elderly, confusion may be the most prominent sign.[19]

The typical signs and symptoms in children under five are fever, cough, and fast or difficult breathing.[20] Fever is not very specific, as it occurs in many other common illnesses, may be absent in those with severe disease, malnutrition or in the elderly. In addition, a cough is frequently absent in children less than 2 months old.[20] More severe signs and symptoms in children may include blue-tinged skin, unwillingness to drink, convulsions, ongoing vomiting, extremes of temperature, or a decreased level of consciousness.[20][21]

Bacterial and viral cases of pneumonia usually present with similar symptoms.[22] Some causes are associated with classic, but non-specific, clinical characteristics. Pneumonia caused by Legionella may occur with abdominal pain, diarrhea, or confusion,[23] while pneumonia caused by Streptococcus pneumoniae is associated with rusty colored sputum,[24]and pneumonia caused by Klebsiella may have bloody sputum often described as “currant jelly”.[18] Bloody sputum (known as hemoptysis) may also occur with tuberculosis, Gram-negative pneumonia, and lung abscesses as well as more commonly with acute bronchitis.[21] Mycoplasma pneumonia may occur in association with swelling of the lymph nodes in the neck, joint pain, or a middle ear infection.[21] Viral pneumonia presents more commonly with wheezing than does bacterial pneumonia.[22] Pneumonia was historically divided into “typical” and “atypical” based on the belief that the presentation predicted the underlying cause.[25] However, evidence has not supported this distinction, thus it is no longer emphasized.[25]

Cause

Three one round objects in a black background

The bacterium Streptococcus pneumoniae, a common cause of pneumonia, imaged by an electron microscope

Pneumonia is due to infections caused primarily by bacteria or viruses and less commonly by fungi and parasites. Although there are more than 100 strains of infectious agents identified, only a few are responsible for the majority of the cases. Mixed infections with both viruses and bacteria may occur in up to 45% of infections in children and 15% of infections in adults.[13] A causative agent may not be isolated in approximately half of cases despite careful testing.[17]

The term pneumonia is sometimes more broadly applied to any condition resulting in inflammation of the lungs (caused for example by autoimmune diseases, chemical burns or drug reactions); however, this inflammation is more accurately referred to as pneumonitis.[26][27]

Conditions and risk factors that predispose to pneumonia include smoking, immunodeficiency, alcoholism, chronic obstructive pulmonary disease, asthma, chronic kidney disease, and liver disease.[21][28] The use of acid-suppressing medications—such as proton-pump inhibitors or H2 blockers—is associated with an increased risk of pneumonia.[29] The risk is also increased in old age.[21]

Bacteria

Main article: Bacterial pneumonia

Cavitating pneumonia as seen on CT. Pneumonia due to MRSA

Bacteria are the most common cause of community-acquired pneumonia (CAP), with Streptococcus pneumoniae isolated in nearly 50% of cases.[30][31] Other commonly isolated bacteria include Haemophilus influenzae in 20%,Chlamydophila pneumoniae in 13%, and Mycoplasma pneumoniae in 3% of cases;[30] Staphylococcus aureus; Moraxella catarrhalis; Legionella pneumophila and Gram-negative bacilli.[17] A number of drug-resistant versions of the above infections are becoming more common, including drug-resistant Streptococcus pneumoniae (DRSP) and methicillin-resistant Staphylococcus aureus (MRSA).[21]

The spreading of organisms is facilitated when risk factors are present.[17] Alcoholism is associated with Streptococcus pneumoniae, anaerobic organisms, and Mycobacterium tuberculosis; smoking facilitates the effects ofStreptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Legionella pneumophila. Exposure to birds is associated with Chlamydia psittaci; farm animals with Coxiella burnetti; aspiration of stomach contents with anaerobic organisms; and cystic fibrosis with Pseudomonas aeruginosa and Staphylococcus aureus.[17] Streptococcus pneumoniae is more common in the winter,[17] and should be suspected in persons aspirating a large amount anaerobic organisms.[21]

Viruses

Main article: Viral pneumonia

In adults, viruses account for approximately a third[13] and in children for about 15% of pneumonia cases.[32] Commonly implicated agents include rhinoviruses, coronaviruses, influenza virus, respiratory syncytial virus (RSV),adenovirus, and parainfluenza.[13][33] Herpes simplex virus rarely causes pneumonia, except in groups such as: newborns, persons with cancer, transplant recipients, and people with significant burns.[34] People following organ transplantation or those otherwise-immunocompromised present high rates of cytomegalovirus pneumonia.[32][34] Those with viral infections may be secondarily infected with the bacteria Streptococcus pneumoniae,Staphylococcus aureus, or Haemophilus influenzae, particularly when other health problems are present.[21][32] Different viruses predominate at different periods of the year; during influenza season, for example, influenza may account for over half of all viral cases.[32] Outbreaks of other viruses also occasionally occur, including hantaviruses and coronavirus.[32]

Fungi

Main article: Fungal pneumonia

Fungal pneumonia is uncommon, but occurs more commonly in individuals with weakened immune systems due to AIDS, immunosuppressive drugs, or other medical problems.[17][35] It is most often caused by Histoplasma capsulatum, blastomyces, Cryptococcus neoformans, Pneumocystis jiroveci (pneumocystis pneumonia), and Coccidioides immitis. Histoplasmosis is most common in the Mississippi River basin, and coccidioidomycosis is most common in the Southwestern United States.[17] The number of cases has been increasing in the later half of the 20th century due to increasing travel and rates of immunosuppression in the population.[35]

Parasites

Main article: Parasitic pneumonia

A variety of parasites can affect the lungs, including Toxoplasma gondii, Strongyloides stercoralis, Ascaris lumbricoides, and Plasmodium malariae.[36] These organisms typically enter the body through direct contact with the skin, ingestion, or via an insect vector.[36]Except for Paragonimus westermani, most parasites do not affect specifically the lungs but involve the lungs secondarily to other sites.[36] Some parasites, in particular those belonging to the Ascaris and Strongyloides genera, stimulate a strong eosinophilic reaction, which may result in eosinophilic pneumonia.[36] In other infections, such as malaria, lung involvement is due primarily to cytokine-induced systemic inflammation.[36] In the developed world these infections are most common in people returning from travel or in immigrants.[36] Around the world, these infections are most common in the immunodeficient.[37]

Idiopathic

Idiopathic interstitial pneumonia or noninfectious pneumonia[38] is 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.[39]

Mechanisms

A schematic diagram of the human lungs with an empty circle on the left representing a normal alveola and one on the right showing an alveola full of fluid as in pneumonia

Pneumonia fills the lung’s alveoli with fluid, hindering oxygenation. The alveolus on the left is normal, whereas the one on the right is full of fluid from pneumonia.

Pneumonia frequently starts as an upper respiratory tract infection that moves into the lower respiratory tract.[40] It is pneumonitis (lung inflammation) combined with consolidation (liquid in spaces normally inflated with air).[41]

Viral

Viruses may reach the lung by a number of different routes. Respiratory syncytial virus is typically contracted when people touch contaminated objects and then they touch their eyes or nose.[32] Other viral infections occur when contaminated airborne droplets are inhaled through the mouth or nose.[21] Once in the upper airway, the viruses may make their way in the lungs, where they invade the cells lining the airways, alveoli, orlung parenchyma.[32] Some viruses such as measles and herpes simplex may reach the lungs via the blood.[42] The invasion of the lungs may lead to varying degrees of cell death.[32] When the immune system responds to the infection, even more lung damage may occur.[32] Primarily white blood cells, mainly mononuclear cells, generate the inflammation.[42] As well as damaging the lungs, many viruses simultaneously affect other organs and thus disrupt other body functions. Viruses also make the body more susceptible to bacterial infections; in this way, bacterial pneumonia can arise as a co-morbid condition.[33]

Bacterial

Most bacteria enter the lungs via small aspirations of organisms residing in the throat or nose.[21] Half of normal people have these small aspirations during sleep.[25] While the throat always contains bacteria,potentially infectious ones reside there only at certain times and under certain conditions.[25] A minority of types of bacteria such as Mycobacterium tuberculosis and Legionella pneumophila reach the lungs via contaminated airborne droplets.[21] Bacteria can spread also via the blood.[22] Once in the lungs, bacteria may invade the spaces between cells and between alveoli, where the macrophages and neutrophils(defensive white blood cells) attempt to inactivate the bacteria.[43] The neutrophils also release cytokines, causing a general activation of the immune system.[44] This leads to the fever, chills, and fatigue common in bacterial pneumonia.[44] The neutrophils, bacteria, and fluid from surrounding blood vessels fill the alveoli, resulting in the consolidation seen on chest X-ray.[45]

Diagnosis

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Crackles heard in the lungs of a person with pneumonia using a stethoscope.

Problems playing this file? See media help.

Pneumonia is typically diagnosed based on a combination of physical signs and a chest X-ray.[46] However, the underlying cause can be difficult to confirm, as there is no definitive test able to distinguish between bacterial and non-bacterial origin.[13][46] The World Health Organization has defined pneumonia in children clinically based on either a cough or difficulty breathing and a rapid respiratory rate, chest indrawing, or a decreased level of consciousness.[47] 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 2 months to 1 year old, or greater than 40 breaths per minute in children 1 to 5 years old.[47] In children, increased respiratory rate and lower chest indrawing are more sensitive than hearing chest crackles with a stethoscope.[20] Grunting and nasal flaring may be other useful signs in children less than five.[48]

In general, in adults, investigations are not needed in mild cases.[49] There is a very low risk of pneumonia if all vital signs and auscultation are normal.[50] In persons requiring hospitalization, pulse oximetry, chest radiography and blood tests—including a complete blood count, serum electrolytes, C-reactive protein level, and possibly liver function tests—are recommended.[49] The diagnosis of influenza-like illness can be made based on the signs and symptoms; however, confirmation of an influenza infection requires testing.[51] Thus, treatment is frequently based on the presence of influenza in the community or a rapid influenza test.[51]

Physical exam

Physical examination may sometimes reveal low blood pressure, high heart rate, or low oxygen saturation.[21] The respiratory rate may be faster than normal, and this may occur a day or two before other signs.[21][25] Examination of the chest may be normal, but it 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.[21] Crackles (rales) may be heard over the affected area during inspiration.[21] Percussion may be dulled over the affected lung, and increased, rather than decreased, vocal resonance distinguishes pneumonia from a pleural effusion.[19]

Imaging

Right middle lobe pneumonia in a child as seen on plain X ray

A black-and-white image shows the internal organs in cross-section as generated by CT. Where one would expect black on the left, one sees a whiter area with black sticks through it.

CT of the chest demonstrating right-side pneumonia (left side of the image)

A chest radiograph is frequently used in diagnosis.[20] In people with mild disease, imaging is needed only in those with potential complications, those not having improved with treatment, or those in which the cause is uncertain.[20][49] If a person is sufficiently sick to require hospitalization, a chest radiograph is recommended.[49] Findings do not always match the severity of disease and do not reliably separate between bacterial infection and viral infection.[20]

X-ray presentations of pneumonia may be classified as lobar pneumonia, bronchopneumonia (also known as lobular pneumonia), and interstitial pneumonia.[52] Bacterial, community-acquired pneumonia classically show lung consolidation of one lung segmental lobe, which is known as lobar pneumonia.[30] However, findings may vary, and other patterns are common in other types of pneumonia.[30] Aspiration pneumonia may present with bilateral opacities primarily in the bases of the lungs and on the right side.[30] Radiographs of viral pneumonia may appear normal, appear hyper-inflated, have bilateral patchy areas, or present similar to bacterial pneumonia with lobar consolidation.[30] Radiologic findings may not be present in the early stages of the disease, especially in the presence of dehydration, or may be difficult to be interpreted in the obese or those with a history of lung disease.[21] ACT scan can give additional information in indeterminate cases.[30]

Microbiology

In patients managed in the community, determining the causative agent is not cost-effective and typically does not alter management.[20] For people that do not respond to treatment, sputum culture should be considered, and culture for Mycobacterium tuberculosis should be carried out in persons with a chronic productive cough.[49] Testing for other specific organisms may be recommended during outbreaks, for public health reasons.[49] In those hospitalized for severe disease, both sputum and blood cultures are recommended,[49] as well as testing the urine for antigens to Legionella and Streptococcus.[53] Viral infections can be confirmed via detection of either the virus or its antigens with culture or polymerase chain reaction (PCR), among other techniques.[13] The causative agent is determined in only 15% of cases with routine microbiological tests.[19]

Classification

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.[54] Pneumonia is most commonly classified by where or how it was acquired: community-acquired, aspiration, healthcare-associated, hospital-acquired, and ventilator-associated pneumonia.[30] It may also be classified by the area of lung affected: lobar pneumonia, bronchial pneumonia and acute interstitial pneumonia;[30] or by the causative organism.[55] Pneumonia in children may additionally be classified based on signs and symptoms as non-severe, severe, or very severe.[56]

The setting in which pneumonia develops is important to treatment,[57][58] as it correlates to which pathogens are likely suspects,[57] which mechanisms are likely, which antibiotics are likely to work or fail,[57] and which complications can be expected based on the person’s health status.

Community

Community-acquired pneumonia (CAP) is acquired in the community,[57][58] outside of health care facilities. Compared with health care–associated pneumonia, it is less likely to involve multidrug-resistant bacteria. Although the latter are no longer rare in CAP,[57] they are still less likely.

Health care

Health care–associated pneumonia (HCAP) is any pneumonia associated with any health care,[57] whether in a hospital, outpatient clinic, nursing home care, or home care.[58] The latter two settings could be viewed as community settings except that they are usually correlated with health care via proximity to, and interaction with, others who have recently visited health care facilities, such as nurses, doctors, and nursing home neighbors. There is recognition in the 2010s that these types of pneumonia are now better viewed as HCAP than as CAP.[57]

HCAP is sometimes called MCAP (medical care–associated pneumonia).

Hospital

Hospital-acquired pneumonia is acquired in a hospital[57] (specifically, pneumonia that occurs 48 hours or more after admission, which was not incubating at the time of admission[58]), and as such is likely to involve hospital-acquired infections, with higher risk ofmultidrug-resistant pathogens. Also, because hospital patients are often ill (which is why they are present in the hospital), comorbidities are an issue.

Ventilator

Ventilator-associated pneumonia occurs in people breathing with the help of mechanical ventilation[57] (specifically, it is pneumonia that arises more than 48 to 72 hours after endotracheal intubation[58]). Like any medical device, ventilators involve some risk of infection because of how difficult it is to prevent bacteria from colonizing the internal parts and surfaces, even with diligent cleaning. People who need venitlators typically are rather ill to begin with, so a superimposed pneumonia is not always easily managed.Immunodeficiency may be involved because of poor nutritional status and whichever disorders are comorbid.

Nursing home

Nursing home–acquired pneumonia is acquired in nursing home care.[57] A nursing home is a place where even if a resident has not visited a hospital recently, neighbors have, and visiting health professionals have. This, coupled with the comorbidities that typically are associated with advanced age, is why NHAP is now best viewed as a form of HCAP[57] and has a higher chance of resembling HAP in its causes and features than CAP generally does, requiring broader antibiotic coverage.[57]

Differential diagnosis

Several diseases can present with similar signs and symptoms to pneumonia, such as: chronic obstructive pulmonary disease (COPD), asthma, pulmonary edema, bronchiectasis, lung cancer, and pulmonary emboli.[19] 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.[19]

Prevention

Prevention includes vaccination, environmental measures and appropriate treatment of other health problems.[20] It is believed that, if appropriate preventive measures were instituted globally, mortality among children could be reduced by 400,000; and, if proper treatment were universally available, childhood deaths could be decreased by another 600,000.[22]

Vaccination

Vaccination prevents against certain bacterial and viral pneumonias both in children and adults. Influenza vaccines are modestly effective at preventing symptoms of influenza.[13][59] The Center for Disease Control and Prevention (CDC) recommends yearly vaccination for every person 6 months and older.[60] Immunizing health care workers decreases the risk of viral pneumonia among their patients.[53]

Vaccinations against Haemophilus influenzae and Streptococcus pneumoniae have good evidence to support their use.[40] Vaccinating children against Streptococcus pneumoniae has led to a decreased incidence of these infections in adults, because many adults acquire infections from children. A Streptococcus pneumoniae vaccine is available for adults, and has been found to decrease the risk of invasive pneumococcal disease.[61] Other vaccines for which there is support for a protective effect against pneumonia includepertussis, varicella, and measles.[62]

Medications

When influenza outbreaks occur, medications such as amantadine or rimantadine may help prevent the condition; however are associated with side effects.[63] Zanamivir or oseltamivir decrease the chance that those exposed will develop symptoms; however, it is recommended that potential side effects are taken into account.[64]

Other

Smoking cessation[49] and reducing indoor air pollution, such as that from cooking indoors with wood or dung, are both recommended.[20][22] Smoking appears to be the single biggest risk factor for pneumococcal pneumonia in otherwise-healthy adults.[53] Hand hygiene and coughing into one’s sleeve may also be effective preventative measures.[62] Wearing surgical masks by the sick may also prevent illness.[53]

Appropriately treating underlying illnesses (such as HIV/AIDS, diabetes mellitus, and malnutrition) can decrease the risk of pneumonia.[22][62][65] In children less than 6 months of age, exclusive breast feeding reduces both the risk and severity of disease.[22] In those with HIV/AIDS and a CD4 count of less than 200 cells/uL the antibiotic trimethoprim/sulfamethoxazole decreases the risk of Pneumocystis pneumonia[66] and is also useful for prevention in those that are immunocomprised but do not have HIV.[67]

Testing pregnant women for Group B Streptococcus and Chlamydia trachomatis, and administering antibiotic treatment, if needed, reduces rates of pneumonia in infants;[68][69] preventive measures for HIV transmission from mother to child may also be efficient.[70]Suctioning the mouth and throat of infants with meconium-stained amniotic fluid has not been found to reduce the rate of aspiration pneumonia and may cause potential harm,[71] thus this practice is not recommended in the majority of situations.[71] In the frail elderly good oral health care may lower the risk of aspiration pneumonia.[72] Zinc supplementation in children 2 months to five years old appears to reduce rates of pneumonia.[73]

Management

CURB-65
Symptom Points
Confusion
1
Urea>7 mmol/l
1
Respiratory rate>30
1
SBP<90mmHg, DBP<60mmHg
1
Age>=65
1

Oral antibiotics, rest, simple analgesics, and fluids usually suffice for complete resolution.[49] However, those with other medical conditions, the elderly, or those with significant trouble breathing may require more advanced care. If the symptoms worsen, the pneumonia does not improve with home treatment, or complications occur, hospitalization may be required.[49] Worldwide, approximately 7–13% of cases in children result in hospitalization,[20] whereas in the developed world between 22 and 42% of adults with community-acquired pneumonia are admitted.[49] The CURB-65 score is useful for determining the need for admission in adults.[49] 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 3–5, hospitalization is recommended.[49] In children those with respiratory distress or oxygen saturations of less than 90% should be hospitalized.[74] The utility of chest physiotherapy in pneumonia has not yet been determined.[75] Non-invasive ventilation may be beneficial in those admitted to the intensive care unit.[76] Over-the-counter cough medicine has not been found to be effective[77] nor has the use of zinc in children.[78] There is insufficient evidence for mucolytics.[77]

Bacterial

Antibiotics improve outcomes in those with bacterial pneumonia.[14] Antibiotic choice depends initially on the characteristics of the person affected, such as age, underlying health, and the location the infection was acquired. In the UK, treatment before culture results with amoxicillin is recommended as the first line for community-acquired pneumonia, with doxycycline or clarithromycin as alternatives.[49] In North America, where the “atypical” forms of community-acquired pneumonia are more common, macrolides (such as azithromycin or erythromycin), and doxycycline have displaced amoxicillin as first-line outpatient treatment in adults.[31][79] In children with mild or moderate symptoms, amoxicillin remains the first line.[74] The use of fluoroquinolones in uncomplicated cases is discouraged due to concerns about side-effects and generating resistance in light of there being no greater clinical benefit.[31][80]

For those who require hospitalization and caught their pneumonia in the community the use of a β-lactam such as cephazolin plus macrolide such as azithromycin or a fluoroquinolones is recommended.[81] The addition of corticosteroids also appears to improve outcomes.[82][83]

The duration of treatment has traditionally been seven to ten days, but increasing evidence suggests that shorter courses (three to five days) are similarly effective.[84] Recommended for hospital-acquired pneumonia include third- and fourth-generationcephalosporins, carbapenems, fluoroquinolones, aminoglycosides, and vancomycin.[85] These antibiotics are often given intravenously and used in combination.[85] In those treated in hospital, more than 90% improve with the initial antibiotics.[25]

Viral

Neuraminidase inhibitors may be used to treat viral pneumonia caused by influenza viruses (influenza A and influenza B).[13] No specific antiviral medications are recommended for other types of community acquired viral pneumonias including SARS coronavirus,adenovirus, hantavirus, and parainfluenza virus.[13] Influenza A may be treated with rimantadine or amantadine, while influenza A or B may be treated with oseltamivir, zanamivir or peramivir.[13] These are of most benefit if they are started within 48 hours of the onset of symptoms.[13] Many strains of H5N1 influenza A, also known as avian influenza or “bird flu”, have shown resistance to rimantadine and amantadine.[13] The use of antibiotics in viral pneumonia is recommended by some experts, as it is impossible to rule out a complicating bacterial infection.[13] The British Thoracic Society recommends that antibiotics be withheld in those with mild disease.[13] The use of corticosteroids is controversial.[13]

Aspiration

In general, aspiration pneumonitis is treated conservatively with antibiotics indicated only for aspiration pneumonia.[86] 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 beta-lactam antibiotic and metronidazole, or an aminoglycoside.[87] Corticosteroids are sometimes used in aspiration pneumonia, but there is limited evidence to support their effectiveness.[86]

Prognosis

With treatment, most types of bacterial pneumonia will stabilize in 3–6 days.[88] It often takes a few weeks before most symptoms resolve.[88] X-ray finding typically clear within four weeks and mortality is low (less than 1%).[21][89] In the elderly or people with other lung problems, recovery may take more than 12 weeks. In persons requiring hospitalization, mortality may be as high as 10%, and in those requiring intensive care it may reach 30–50%.[21] Pneumonia is the most common hospital-acquired infection that causes death.[25]Before the advent of antibiotics, mortality was typically 30% in those that were hospitalized.[17]

Complications may occur in particular in the elderly and those with underlying health problems.[89] This may include, among others: empyema, lung abscess, bronchiolitis obliterans, acute respiratory distress syndrome, sepsis, and worsening of underlying health problems.[89]

Clinical prediction rules

Clinical prediction rules have been developed to more objectively predict outcomes of pneumonia.[25] These rules are often used in deciding whether or not to hospitalize the person.[25]

Pleural effusion, empyema, and abscess

An X-ray showing a chest lying horizontal. The lower black area, which is the right lung, is smaller with a whiter area below it of a pulmonary effusion. There are red arrows marking the size of these.

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 may form in the space that surrounds the lung.[91] Occasionally, microorganisms will infect this fluid, causing an empyema.[91] To distinguish an empyema from the more common simpleparapneumonic effusion, the fluid may be collected with a needle (thoracentesis), and examined.[91] If this shows evidence of empyema, complete drainage of the fluid is necessary, often requiring a drainage catheter.[91] In severe cases of empyema, surgery may be needed.[91] 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 must be drained only if it is causing symptoms or remains unresolved.[91]

In rare circumstances, bacteria in the lung will form a pocket of infected fluid called a lung abscess.[91] Lung abscesses can usually be seen with a chest X-ray but frequently require a chest CT scan to confirm the diagnosis.[91]Abscesses typically occur in aspiration pneumonia, and often contain several types of bacteria. Long-term antibiotics are usually adequate to treat a lung abscess, but sometimes the abscess must be drained by a surgeon orradiologist.[91]

Respiratory and circulatory failure

Pneumonia can 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 stiff. This stiffness, combined with severe difficulties extracting oxygen due to the alveolar fluid, may require long periods of mechanical ventilation for survival.[32]

Sepsis is a potential complication of pneumonia but occurs usually in people with poor immunity or hyposplenism. The organisms most commonly involved are Streptococcus pneumoniae, Haemophilus influenzae, andKlebsiella pneumoniae. Other causes of the symptoms should be considered such as a myocardial infarction or a pulmonary embolism.[92]

Epidemiology

A map of the world with a far bit of dark-red in Africa, orange colors in parts of Asia and South America, and yellow in Europe and North America

Age-standardized death rate: lower respiratory tract infections per 100,000 inhabitants in 2004[93]

  no data
  <100
  100–700
  700–1400
  1400–2100
  2100–2800
  2800–3500
  3500–4200
  4200–4900
  4900–5600
  5600–6300
  6300–7000
  >7000

Pneumonia is a common illness affecting approximately 450 million people a year and occurring in all parts of the world.[13] It is a major cause of death among all age groups resulting in 4 million deaths (7% of the world’s total death) yearly.[13][14] Rates are greatest in children less than five, and adults older than 75 years.[13] It occurs about five times more frequently in the developing world than in thedeveloped world.[13] Viral pneumonia accounts for about 200 million cases.[13] In the United States, as of 2009, pneumonia is the 8th leading cause of death.[21]

Children

In 2008, pneumonia occurred in approximately 156 million children (151 million in the developing world and 5 million in the developed world).[13] In 2010, it resulted in 1.3 million deaths, or 18% of all deaths in those under five years, of which 95% occurred in the developing world.[13][20][94] Countries with the greatest burden of disease include India (43 million), China (21 million) and Pakistan (10 million).[95] It is the leading cause of death among children in low income countries.[13][14] Many of these deaths occur in the newborn period. The World Health Organization estimates that one in three newborn infant deaths is due to pneumonia.[96] Approximately half of these deaths can be prevented, as they are caused by the bacteria for which an effective vaccine is available.[97] In 2011, pneumonia was the most common reason for admission to the hospital after an emergency department visit in the U.S. for infants and children.[98]

History

A poster with a shark in the middle of it, which reads "Pneumonia Strikes Like a Man Eating Shark Led by its Pilot Fish the Common Cold"

WPA poster, 1936/1937

Pneumonia has been a common disease throughout human history.[99] The symptoms were described by Hippocrates (c. 460 BC – 370 BC):[99] “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.”[100] However, Hippocrates referred to pneumonia as a disease “named by the ancients”. He also reported the results of surgical drainage of empyemas. Maimonides (1135–1204 AD) observed: “The basic symptoms that occur in pneumonia and that are never lacking are as follows: acute fever, sticking pleuritic pain in the side, short rapid breaths, serrated pulse and cough.”[101] 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.

Edwin Klebs was the first to observe bacteria in the airways of persons having died of pneumonia in 1875.[102] Initial work identifying the two common bacterial causes, Streptococcus pneumoniae and Klebsiella pneumoniae, was performed by Carl Friedländer[103] and Albert Fränkel[104] in 1882 and 1884, respectively. Friedländer’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 to differentiate the two bacteria, and showed that pneumonia could be caused by more than one microorganism.[105]

Sir William Osler, known as “the father of modern medicine”, appreciated the death and disability caused 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).[106][107] Osler also described pneumonia as “the old man’s friend” as death was often quick and painless when there were many slower and more painful ways to die.[17]

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 20th 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.[108] Vaccination against Streptococcus pneumoniae in adults began in 1977, and in children in 2000, resulting in a similar decline.[109]

Society and culture

Awareness

Due to the relatively low awareness of the disease, 12 November was declared as the annual World Pneumonia Day, a day for concerned citizens and policy makers to take action against the disease, in 2009.[110][111]

Costs

The global economic cost of community-acquired pneumonia has been estimated at $17 billion annually.[21] Other estimates are considerably higher. In 2012 the estimated aggregate costs of treating pneumonia in the United States were $20 billion;[112] the median cost of a single pneumonia-related hospitalization is over $15,000.[113] According to data released by the Centers for Medicare and Medicaid Services, average 2012 hospital charges for inpatient treatment of uncomplicated pneumonia in the U.S. were $24,549 and ranged as high as $124,000. The average cost of an emergency room consult for pneumonia was $943 and the average cost for medication was $66.[114] Aggregate annual costs of treating pneumonia in Europe have been estimated at €10 billion.[115]

This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumococcal pneumonia [Streptococcus pneumoniae pneumonia]
Bronchopneumonia due to Streptococcus pneumoniae · Left lower zone pneumonia · Left upper zone pneumonia · Lingular pneumonia · Lobar pneumonia · Lobar pneumonia left lower lobe · Lobar pneumonia left upper lobe · Lobar pneumonia lingula · Lobar pneumonia right lower lobe · Lobar pneumonia right middle lobe · Lobar pneumonia right upper lobe · Lobar pneumonia, LLL · Lobar pneumonia, LUL · Lobar pneumonia, RLL · Lobarpneumonia, RML · Lobar pneumonia, RUL · Pneumococcal bronchopneumonia · Pneumococcal pneumonia · Right lower zone pneumonia · Right middle zone pneumonia · Right upper zone pneumonia · A febrile disease caused by streptococcus pneumoniae….
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumonia due to Klebsiella pneumoniae
Bronchopneumonia due to Klebsiella pneumoniae · Klebsiella pneumoniae bronchopneumonia · Klebsiella pneumoniae pneumonia
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumonia due to mycoplasma pneumoniae
Bronchopneumonia due to Mycoplasma pneumoniae · Mycoplasma bronchopneumonia · Mycoplasma pneumonia · Pneumonia due to Mycoplasma pneumoniae
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumonia in aspergillosis
Aspergillosis pneumonia · Aspergillus pneumonia
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumonia due to Klebsiella pneumoniae
Bronchopneumonia due to Klebsiella pneumoniae · Klebsiella pneumoniae bronchopneumonia · Klebsiella pneumoniae pneumonia · Pneumonia (acute) (double) (migratory) (purulent) (septic) (unresolved) J18.9 Friedländer’s bacillus J15.0 Klebsiella (pneumoniae) J15.0 broncho-, bronchial (confluent) (croupous) (diffuse) (disseminated) (hemorrhagic) (involving lobes) (lobar) (terminal) J18.0 Friedländer’s bacillus J15.0 Klebsiella (pneumoniae) J15.0 in (due to) Friedländer’s bacillus J15.0 Klebsiella (pneumoniae) J15.0 lobar (disseminated) (double) (interstitial) J18.1 Friedländer’s bacillus J15.0 Klebsiella (pneumoniae) J15.0…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumonia due to Mycoplasma pneumoniae
Eaton’s agent J15.7 Mycoplasma (pneumoniae) J15.7 pleuro-pneumonia-like… (pneumoniae) J15.7 pleuro-pneumonia-like-organism (PPLO) J15.7 · …Bronchopneumonia due to Mycoplasma pneumoniae · Mycoplasma bronchopneumonia · Mycoplasma pneumonia · Interstitial pneumonia caused by extensive infection of the lungs (lung) and bronchi, particularly the lower lobes of the lungs, by mycoplasma pneumoniae in humans. In sheep, it is caused by mycoplasma ovipneumoniae. In cattle, it may be caused by mycoplasma dispar. · Interstitial pneumonia caused by extensive… species. · Pneumonia (acute) (double) (migratory) (purulent) (septic) (unresolved) J18.9 Eaton’s agent J15.7 Mycoplasma (pneumoniae) J15.7 pleuro-pneumonia-like organism (PPLO) J15.7 broncho-, bronchial (confluent) (croupous
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumonia due to Streptococcus pneumoniae
pneumonia due to S. pneumoniae (P23.6) · lobar pneumonia, unspecified organism (J18.1) · pneumonia due to other streptococci (J15.3-J15.4) · Bronchopneumonia due to Streptococcus pneumoniae · Pneumococcal bronchopneumonia · Pneumococcal pneumonia · A febrile disease caused by streptococcus pneumoniae. ·… pneumococcal A40.3 with pneumonia J13 Infection, infected, infective (opportunistic…) A40.3 with pneumonia J13Pneumonia (acute) (double) (migratory) (purulent…Bronchopneumonia due to S. pneumoniae · associated influenza, if applicable… pneumococcal (broncho) (lobar) J13 Streptococcus pneumoniae J13 broncho… streptococcal NEC J15.4 pneumoniae J13 in (due to) Diplococcus (pneumoniae) J13 pneumococcus J13 Streptococcus J15.4 pneumoniae J13

References

Pneumocystis pneumonia ICD-10 B20.6

Pneumocystis pneumonia

From Wikipedia, the free encyclopedia
Not to be confused with Pneumococcal pneumonia.
Pneumocystis jirovecii pneumonia
Pneumocystis.jpg

Pneumocystis jirovecii cysts from bronchoalveolar lavage, stained with Toluidine blue O stain
Classification and external resources
Specialty Pulmonology
ICD10 B20.6
ICD9-CM 136.3
DiseasesDB 10160
MedlinePlus 000671
eMedicine med/1850
MeSH D011020

Pneumocystis pneumonia (PCP) is a form of pneumonia, caused by the yeast-like fungus Pneumocystis jirovecii.[1]

Pneumocystis pneumonia is not commonly found in the lungs of healthy people, but, being a source of opportunistic infection, it can cause a lung infection in people with a weak immune system. Pneumocystis pneumonia is especially seen in people with cancer undergoing chemotherapy, HIV/AIDS, and the use of medications that suppress the immune system.

Signs and symptoms[edit]

Signs and symptoms of PCP include fever, non-productive cough (because sputum is too viscous to become productive), shortness of breath (especially on exertion), weight loss, and night sweats. There is usually not a large amount of sputum with PCP unless the patient has an additional bacterial infection. The fungus can invade other visceral organs (such as the liver, spleen, and kidney), but only in a minority of cases.

Pneumothorax is a well-known complication of PCP.[2] An acute history of chest pain with breathlessness and diminished breath sounds is typical of pneumothorax.[citation needed]

Disease course[edit]

The risk of PCP increases when CD4 positive T-cell levels are less than 200 cells/μL. In these immunosuppressed individuals the manifestations of the infection are highly variable.[3] The disease attacks the interstitial, fibrous tissue of the lungs, with marked thickening of the alveolar septa and alveoli, leading to significant hypoxia which can be fatal if not treated aggressively. In this situation LDH levels increase and gas exchange is compromised. Oxygen is less able to diffuse into the blood, leading to hypoxia. Hypoxia, along with high arterial carbon dioxide (CO2) levels, stimulates hyper-ventilatory effort, thereby causing dyspnea (breathlessness).

Diagnosis[edit]

X-ray of Pneumocystis jiroveciipneumonia. There is increased opacification (whiteness) in the lower lungs on both sides, characteristic ofPneumocystis pneumonia

The diagnosis can be confirmed by the characteristic appearance of the chest x-ray, which shows widespread pulmonary infiltrates, and an arterial oxygen level (PaO2) that is strikingly lower than would be expected from symptoms. Gallium 67 scans are also useful in the diagnosis. They are abnormal in approximately 90% of cases and are often positive before the chest x-ray becomes abnormal. The diagnosis can be definitively confirmed by histological identification of the causative organism in sputum or bronchio-alveolar lavage (lung rinse). Staining with toluidine blue, silver stain, periodic-acid schiff stain, or an immunofluorescence assay will show the characteristic cysts.[4] The cysts resemble crushed ping-pong balls and are present in aggregates of 2 to 8 (and not to be confused with Histoplasma or Cryptococcus, which typically do not form aggregates of spores or cells). A lung biopsy would show thickened alveolar septa with fluffy eosinophilic exudate in the alveoli. Both the thickened septa and the fluffy exudate contribute to dysfunctional diffusion capacity which is characteristic of this pneumonia.

Pneumocystis infection can also be diagnosed by immunofluorescent or histochemical staining of the specimen, and more recently by molecular analysis of polymerase chain reaction products comparing DNA samples. Notably, simple molecular detection of Pneumocystis jirovecii in lung fluids does not mean that a person has Pneumocystis pneumonia or infection by HIV. The fungus appears to be present in healthy individuals in the general population.[5]

Prevention and treatment[edit]

In immunocompromised patients, prophylaxis with co-trimoxazole (trimethoprim/sulfamethoxazole),[6] atovaquone, or regular pentamidine inhalations may help prevent PCP.

Antipneumocystic medication is used with concomitant steroids in order to avoid inflammation, which causes an exacerbation of symptoms about four days after treatment begins if steroids are not used. By far the most commonly used medication is trimethoprim/sulfamethoxazole, but some patients are unable to tolerate this treatment due to allergies. Other medications that are used, alone or in combination, include pentamidine,trimetrexate, dapsone, atovaquone, primaquine, pafuramidine maleate (under investigation), and clindamycin. Treatment is usually for a period of about 21 days.

Pentamidine is less often used as its major limitation is the high frequency of side effects. These include acute pancreatic inflammation, kidney failure, liver toxicity, decreased white blood cell count, rash, fever, and low blood sugar.

Epidemiology[edit]

Pneumocystis jirovecii

The disease PCP is relatively rare in people with normal immune systems, but common among people with weakened immune systems, such as premature or severely malnourished children, the elderly, and especially persons living with HIV/AIDS (in whom it is most commonly observed).[1][7] PCP can also develop in patients who are taking immunosuppressive medications. It can occur in patients who have undergone solid organ transplantation orbone marrow transplantation and after surgery.[8] Infections with Pneumocystis pneumonia are also common in infants with hyper IgM syndrome, an X-linked or autosomal recessive trait.

The causative organism of PCP is distributed worldwide[9] and Pneumocystis pneumonia has been described in all continents except Antarctica.[9] Greater than 75% of children are seropositive by the age of 4, which suggests a high background exposure to the organism. A post-mortem study conducted in Chile of 96 persons who died of unrelated causes (suicide, traffic accidents, and so forth) found that 65 (68%) of them had pneumocystis in their lungs, which suggests that asymptomatic pneumocystis infection is extremely common.[10]

Pneumocystis jirovecii was originally described as a rare cause of pneumonia in neonates. It is commonly believed to be a commensal organism (dependent upon its human host for survival). The possibility of person-to-person transmission has recently gained credence, with supporting evidence coming from many different genotyping studies of Pneumocystis jirovecii isolates from human lung tissue.[11][12] For example, in one outbreak of 12 cases among transplant patients in Leiden, it was suggested as likely, but not proven, that human-to-human spread may have occurred.[13]

PCP and AIDS[edit]

Since the start of the AIDS epidemic, PCP has been closely associated with AIDS. Because it only occurs in an immunocompromised host, it may be the first clue to a new AIDS diagnosis if the patient has no other reason to be immunocompromised (e.g. taking immunosuppressive drugs for organ transplant). An unusual rise in the number of PCP cases in North America, noticed when physicians began requesting large quantities of the rarely used antibiotic pentamidine, was the first clue to the existence of AIDS in the early 1980s.[14][15]

Prior to the development of more effective treatments, PCP was a common and rapid cause of death in persons living with AIDS. Much of the incidence of PCP has been reduced by instituting a standard practice of using oral co-trimoxazole (Bactrim / Septra) to prevent the disease in people with CD4 counts less than 200/μL. In populations that do not have access to preventive treatment, PCP continues to be a major cause of death in AIDS.[citation needed]

Nomenclature[edit]

Both Pneumocystis pneumonia and pneumocystis pneumonia[16] are orthographically correct; one uses the genus name per se and the other uses the common noun based on it. (This is the same reason, for example, why “group A Streptococcus” and “group A streptococcus” are both valid.) Synonyms for PCP include pneumocystosis[16] (pneumocystis + -osis), pneumocystiasis[16] (pneumocystis + -iasis), and interstitial plasma cell pneumonia.[16]

The older species name Pneumocystis carinii (which now applies only to the Pneumocystis species that is found in rats[17]) is still in common usage. As a result, Pneumocystis pneumonia (PCP) is also known as Pneumocystis jiroveci[i] pneumonia and (incorrectly) as Pneumocystis carinii pneumonia.[18][19][20]

Regarding nomenclature, when the name of Pneumocystis pneumonia (PCP) changed from P. carinii pneumonia to P. jirovecii pneumonia, it was at first felt that “PJP” should replace “PCP”. However, because the term PCP was already used among physicians that managed patients with Pneumocystis infection, it was rationalized that the term PCP could continue to be used, as it could stand for PneumoCystis (jirovecii) Pneumonia.[21]

Pneumocystosis
Pneumonia due to Pneumocystis carinii · Pneumonia due to Pneumocystis jiroveci · Pneumocystis pneumonia · Pneumocystosis jiroveci pneumonia · Pneumocystosis pneumonia · A pulmonary disease in humans occurring in immunodeficient… Pneumocystis (carinii) (jiroveci) B59 in (due to) pneumocystosis (Pneumocystis…. Pneumocystis pneumonia is a frequently seen opportunistic infection in aids. It is caused… it is caused by related species of pneumocystis. · Pneumocystis carinii pneumonia (pcp). Pneumonia resulting from infection with pneumocystis carinii, frequently seen…, characterized by dyspnea, tachypnea, and hypoxemia; pneumocystispneumonia is a frequent…) B99.9 Pneumocystis carinii (pneumonia) B59 Pneumocystis jiroveci (pneumonia) B59 Pneumocystis carinii pneumonia B59 Pneumocystis jiroveci (pneumonia
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumocystosis
Pneumocystis pneumonia · Pneumocystosis jiroveci pneumonia · Pneumocystosis pneumonia · A pulmonary disease in humans occurring in immunodeficient or malnourished patients or infants, characterized by dyspnea, tachypnea, and hypoxemia. Pneumocystis pneumonia is a frequently seen opportunistic infection in aids. It is caused by the fungus pneumocystis jirovecii. The disease is also found in other mammals where it is caused by related species of pneumocystis. · Pneumonia resulting from infection with pneumocystis carinii, frequently seen in the immunologically compromised, such as persons with aids, or steroid-treated individuals, the elderly, or premature or debilitated babies during…; pneumocystis pneumonia is a frequent opportunistic infection in aids; also found in other mammals where it is caused by related species of pneumocystis….
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumococcal pneumonia [Streptococcus pneumoniae pneumonia]
Bronchopneumonia due to Streptococcus pneumoniae · Left lower zone pneumonia · Left upper zone pneumonia · Lingular pneumonia · Lobar pneumonia · Lobar pneumonia left lower lobe · Lobar pneumonia left upper lobe · Lobar pneumonia lingula · Lobar pneumonia right lower lobe · Lobar pneumonia right middle lobe · Lobar pneumonia right upper lobe · Lobar pneumonia, LLL · Lobar pneumonia, LUL · Lobar pneumonia, RLL · Lobarpneumonia, RML · Lobar pneumonia, RUL · Pneumococcal bronchopneumonia · Pneumococcal pneumonia · Right lower zone pneumonia · Right middle zone pneumonia · Right upper zone pneumonia · A febrile disease caused by streptococcus pneumoniae….
This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Idiopathic interstitial pneumonia
lymphoid interstitial pneumonia (J84.2) · pneumocystis pneumonia (B59)…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pneumonia in diseases classified elsewhere
) · schistosomiasis (B65.0-B65.9) · candidial pneumonia (B37.1) · chlamydial pneumonia (J16.0) · gonorrheal pneumonia (A54.84) · histoplasmosis pneumonia (B39.0-B39.2) · measles pneumonia (B05.2) · nocardiosispneumonia (A43.0) · pneumocystosis (B59) · pneumonia due to Pneumocystis carinii (B59) · pneumonia due to Pneumocystis jiroveci (B59) · pneumonia in actinomycosis (A42.0) · pneumonia in anthrax (A22.1) · pneumoniain ascariasis (B77.81) · pneumonia in aspergillosis (B44.0-B44.1) · pneumonia in coccidioidomycosis (B38.0-B38.2) · pneumonia in cytomegalovirus disease (B25.0) · pneumonia in toxoplasmosis (B58.3) · rubella pneumonia(B06.81) · salmonella pneumonia (A02.22) · spirochetal infection NEC with pneumonia (A69.8) · tularemia pneumonia

Pleurisy

Pleurisy

From Wikipedia, the free encyclopedia
This article is about the disease. For the plant known as “pleurisy root”, see Butterfly weed.
Pleurisy
Pleurisy and pneumothorax.jpg

Figure A shows the location of the lungs, airways, pleura, and diaphragm. The inset image shows a detailed view of the two pleural layers and pleural space. Figure B shows lungs with pleurisy and pneumothorax. The inset image shows a detailed view of an infected lung with thickened and inflamed pleural layers.
Classification and external resources
Specialty Pulmonology
ICD10 J90, R09.1
ICD9-CM 511
DiseasesDB 29361
MedlinePlus 001371
MeSH D010998

Pleurisy (also known as pleuritis) is an inflammation of the pleurae, the membranes of the pleural cavity surrounding the lungs.[1] There are many possible causes of pleurisy but viral infections spreading from the lungs to the pleural cavity are the most common.[2] The inflamed pleural layers rub against each other every time the lungs expand to breathe in air.[3] This can cause sharp pain when breathing, also called pleuritic chest pain.[4][5] The condition may either be primary or secondary and is often associated with a pleural effusion.[6]

Signs and symptoms[edit]

The defining symptom of pleurisy is a sudden sharp, stabbing, burning or dull pain in the right or left side of the chest during breathing, especially when one inhales and exhales.[7] It feels worse with deep breathing, coughing, sneezing, or laughing. The pain may stay in one place, or it may spread to the shoulder or back.[8] Sometimes, it becomes a fairly constant dull ache.[9]

Depending on its cause, pleuritic chest pain may be accompanied by other symptoms:[10]

Causes[edit]

Pleurisy

Pleural linings and space (marked in blue)

Pleural space can be invaded by fluid, air, and particles from different parts of the body which fairly complicates the diagnosis.[10][11] Viral infection (coxsackievirus, RSV, CMV, adenovirus, EBV, parainfluenza, influenza) is the most common cause of pleurisy. However, many other different conditions can cause pleuritic chest pain:[9]

When the space between two layers of pleura starts to fill with fluid in a case of pleural effusion, it can ease the chest pain, but instead creates a shortness of breath, since the lungs need room to expand during breathing. Some cases of pleuritic chest pain are idiopathic, which means that the exact cause cannot be determined.

Diagnosis[edit]

A diagnosis of pleurisy or another pleural condition is based on a medical history, physical examinations, and diagnostic tests.[10] The goals are to rule out other sources of the symptoms and to find the cause of the pleurisy so that the underlying disorder can be treated.

Physical examination[edit]

A doctor uses a stethoscope to listen to the breathing. This method detects any unusual sounds in the lungs. A person with pleurisy may have inflamed layers of the pleura that make a rough, scratchy sound as they rub against each other during breathing. This is called pleural friction rub.

Diagnostic tests[edit]

Depending on the results of the physical examination, diagnostic tests are sometimes performed.

Chest x-ray[edit]

A chest x-ray takes a picture of the heart and lungs. It may show air or fluid in the pleural space. It also may show the cause (e.g., pneumonia, a fractured rib, or a lung tumor) of the pleurisy.

Sometimes an x-ray is taken while lying on the painful side. This may show fluid, as well as changes in fluid position, that did not appear in the vertical x-ray.

Blood test[edit]

Blood tests can detect bacterial or viral infections, pneumonia, rheumatic fever, a pulmonary embolism, or lupus.

ECG[edit]

Electrocardiography test can determine if a heart condition contributes to the symptoms.

Ultrasound[edit]

Ultrasonography uses sound waves to create an image. It may show where fluid is located in the chest. It also can show some tumors. Although ultrasound may detect fluid around the lungs, also known as a pleural effusion, sound waves are scattered by air. Therefore, an actual picture of the lungs cannot be obtained with ultrasonography.

Computed tomography (CT) scan[edit]

A CT scan provides a computer-generated picture of the lungs that can show pockets of fluid. It also may show signs of pneumonia, a lung abscess, or a tumor.

Magnetic resonance imaging (MRI)[edit]

Magnetic resonance imaging (MRI), also called nuclear magnetic resonance (NMR) scanning, uses powerful magnets to show pleural effusions and tumors.

Arterial blood gas[edit]

In arterial blood-gas sampling, a small amount of blood is taken from an artery, usually in the wrist. The blood is then checked for oxygen and carbon-dioxide levels. This test shows how well the lungs are taking in oxygen.

Thoracentesis[edit]

The illustration shows a person undergoing thoracentesis. The person sits upright and leans on a table. Excess fluid from the pleural space is drained into a bag.

Once the presence of an excess fluid in the pleural cavity, or pleural effusion, is suspected and location of fluid is confirmed, a sample of fluid can be removed for testing.[12] The procedure to remove fluid in the chest is called a diagnostic thoracentesis.[13] The doctor inserts a small needle or a thin, hollow, plastic tube in the chest wall and withdraws fluid.[14]

Thoracentesis can be done in the doctor’s office or at the hospital. Ultrasound is used to guide the needle to the fluid that is trapped in small pockets around the lungs.

Thoracentesis usually does not cause serious complications. Generally, a chest x-ray is done after the procedure to evaluate the lungs. Possible complications of thoracentesis include the following:

  • Bleeding and bruising where the needle went in. In rare cases, bleeding may occur in or around the lung. The doctor can use a chest tube to drain the blood. In some cases, surgery is needed.
  • Infection where the needle went in
  • Injury to the liver or spleen (in rare cases)
  • Pain.
  • Pneumothorax, or buildup of air in the pleural space, with a collapsed or partially collapsed lung. Sometimes air comes in through the needle or the needle makes a hole in the lung. Usually, a hole will seal itself. But sometimes air can build up around the lung and make it collapse. A chest tube can remove the air and let the lung expand again.

The lung fluid is examined under a microscope and is evaluated for the presence of chemicals and for its color and texture. The degree of clarity is an indicator of infection, cancer, or other conditions that may be causing the buildup of fluid or blood in the pleural space.

Biopsy[edit]

If tuberculosis or cancer is suspected, a small piece of the pleura may be examined under a microscope to make a definitive diagnosis. This is called a biopsy.

Several approaches to taking tissue samples are available

  1. Insertion of a needle through the skin on the chest to remove a small sample of the outer layer of the pleura.
  2. Insertion of a small tube with a light on the end (endoscope) into tiny cuts in the chest wall in order to visualize the pleura. Small pieces of tissue can be biopsied though the endoscope.
  3. Removal of a sample of the pleura through a small cut in the chest wall. This is called an open pleural biopsy. It is usually done if the sample from the needle biopsy is too small for an accurate diagnosis.

Treatment[edit]

Treatment has several goals:[10]

  • Relief of symptoms
  • Removal of the fluid, air, or blood from the pleural space
  • Treatment of the underlying condition

Procedures[edit]

If large amounts of fluid, air, or blood are not removed from the pleural space, they may cause the lung to collapse.

The surgical procedures used to drain fluid, air, or blood from the pleural space are as follows:

  • During thoracentesis, a needle or a thin, hollow, plastic tube is inserted through the ribs in the back of the chest into the chest wall. A syringe is attached to draw fluid out of the chest. This procedure can remove more than 6 cups (1.5 litres) of fluid at a time.
  • When larger amounts of fluid must be removed, a chest tube may be inserted through the chest wall. The doctor injects a local painkiller into the area of the chest wall outside where the fluid is. A plastic tube is then inserted into the chest between two ribs. The tube is connected to a box that suctions the fluid out. A chest x-ray is taken to check the tube’s position.
  • A chest tube is also used to drain blood and air from the pleural space. This can take several days. The tube is left in place, and the patient usually stays in the hospital during this time.
  • Sometimes the fluid contains thick pus or blood clots, or it may have formed a hard skin or peel. This makes it harder to drain the fluid. To help break up the pus or blood clots, the doctor may use the chest tube to put certain medicines into the pleural space. These medicines are called fibrinolytics. If the pus or blood clots still do not drain out, surgery may be necessary.

Medications[edit]

A couple of medications are used to relieve pleurisy symptoms:

There may be a role for the use of corticosteroids (for tuberculous pleurisy), tacrolimus (Prograf) and methotrexate (Trexall, Rheumatrex) in the treatment of pleurisy. Further studies are needed.

Lifestyle changes[edit]

The following may be helpful in the management of pleurisy:

  • Lying on the painful side may be more comfortable
  • Breathing deeply and coughing to clear mucus as the pain eases. Otherwise, pneumonia may develop.
  • Getting rest

Treating the cause[edit]

Ideally, the treatment of pleurisy is aimed at eliminating the underlying cause of the disease.

  • If the pleural fluid is infected, treatment involves antibiotics and draining the fluid. If the infection is tuberculosis or from a fungus, treatment involves long-term use of antibiotics or antifungal medicines.
  • If the fluid is caused by tumors of the pleura, it may build up again quickly after it is drained. Sometimes anti-tumor medicines will prevent further fluid buildup. If they don’t, the doctor may seal the pleural space. This is called pleurodesis. Pleurodesis involves the drainage of all the fluid out of the chest through a chest tube. A substance is inserted through the chest tube into the pleural space. This substance irritates the surface of the pleura. This causes the two layers of the pleura to squeeze shut so there is no room for more fluid to build up.
  • Chemotherapy or radiation treatment also may be used to reduce the size of the tumors.
  • If congestive heart failure is causing the fluid buildup, treatment usually includes diuretics and other medicines.

The treatment for pleurisy depends on its origin and is prescribed by a physician on a base of an individual assessment.[16] Paracetamol (acetaminophen) and amoxicillin, or other antibiotics in case of bacterial infections, are common remedies dispensed by doctors to relieve the initial symptoms and pain in the chest, while viral infections are self-limited. Non-steroidal anti-inflammatory drugs (NSAIDs), preferably indometacin, are usually employed as pain control agents.[10]

Alternative treatments[edit]

A number of alternative or complementary medicines are being investigated for their anti-inflammatory properties, and their use in pleurisy. At this time, clinical trials of these compounds have not been performed.

Extracts from the Brazilian folk remedy Wilbrandia ebracteata (“Taiuia”) have been shown to reduce inflammation in the pleural cavity of mice.[17][18] The extract is thought to inhibit the same enzyme, cyclooxygenase-2 (COX-2), as the non-steroidal anti-inflammatory drugs.[18] Similarly, an extract from the roots of the Brazilian Petiveria alliacea plant reduced inflammation in a rat model of pleurisy.[19] The extract also reduced pain sensations in the rats. An aqueous extract from Solidago chilensis has been shown to reduce inflammation in a mouse model of pleurisy.[20]

Pleurisy root Asclepias tuberosa is another example of a herbal solution for this inflammation.

Related problems[edit]

Pleurisy is often associated with complications that affect the pleural space.

Pleural effusion[edit]

In some cases of pleurisy, excess fluid builds up in the pleural space. This is called a pleural effusion. The buildup of fluid usually forces the two layers of the pleura apart so they don’t rub against each other when breathing. This can relieve the pain of pleurisy. A large amount of extra fluid can push the pleura against the lung until the lung, or a part of it, collapses. This can make it hard to breathe.

In some cases of pleural effusion, the extra fluid gets infected and turns into an abscess. This is called an empyema.

Pleural effusion involving fibrinous exudates in the fluid may be called fibrinous pleurisy. It sometimes occurs as a later stage of pleurisy.

A person can develop a pleural effusion in the absence of pleurisy. For example, pneumonia, heart failure, cancer, or a pulmonary embolism can lead to a pleural effusion.

Pneumothorax[edit]

Air or gas also can build up in the pleural space. This is called a pneumothorax. It can result from acute lung injury or a lung disease like emphysema. Lung procedures, like surgery, drainage of fluid with a needle, examination of the lung from the inside with a light and a camera, or mechanical ventilation, also can cause a pneumothorax.

The most common symptom is sudden pain in one side of the lung and shortness of breath. A pneumothorax also can put pressure on the lung and cause it to collapse.

If the pneumothorax is small, it may go away on its own. If large, a chest tube is placed through the skin and chest wall into the pleural space to remove the air.

Hemothorax[edit]

Blood also can collect in the pleural space. This is called hemothorax. The most common cause is injury to the chest from blunt force or surgery on the heart or chest. Hemothorax also can occur in people with lung or pleural cancer.

Hemothorax can put pressure on the lung and force it to collapse. It also can cause shock, a state of hypoperfusion in which an insufficient amount of blood is able to reach the organs.

Prognosis[edit]

Pleurisy and other disorders of the pleura can be serious, depending on what caused them. Generally, pleurisy treatment has an excellent prognosis, but if left untreated it can cause severe complications. For example, a resulting pulmonary heart disease cor pulmonale, which manifests itself with an inflammation of the arms and legs, can lead to heart failure. If the conditions that caused the pleurisy or other pleural disorders were adequately diagnosed and treated early, one can expect a full recovery. Help of a pulmonologist (respiratory physician in the U.K. and Australia) may be enlisted to address the underlying cause and chart post-illness rehabilitation.

Notable cases[edit]

This code is a specific code that can be used to specify a diagnosis or procedure.

Pleurisy
pleurisy with effusion (J90) · Inflammation of pleura, the lining of the lung. When parietal pleura is involved, there is pleuritic chest pain. · Inflammation of the lining of the lung (pleura) · Inflammation of the pleura, with exudation into its cavity and upon its surface; may occur as either an acute or a chronic process. · Inflammation of the pleura. It is usually caused by infections. Chest pain while breathing or coughing is the presenting symptom. · Pleurisy (acute) (adhesive) (chronic) (costal) (diaphragmatic) (double) (dry) (fibrinous) (fibrous) (interlobar) (latent) (plastic) (primary) (residual) (sicca) (sterile) (subacute) (unresolved) R09.1…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pleurisy with effusion, with mention of a bacterial cause other than tuberculosis
Bacterial pleural effusion · Bacterial pleurisy w effusion · Bacterial pleurisy with effusion · Pleural effusion bacterial, nontuberculosis · Pleural effusion due to bacterial infection · Pneumococcal pleurisy w effusion · Pneumococcal pleurisy with effusion · Strep pleurisy with effusion · Streptococcal pleurisy w effusion · Streptococcal pleurisy with effusion…
This code is a specific code that can be used to specify a diagnosis or procedure.

Tuberculous pleurisy
Tuberculosis of pleura Tuberculous empyema · primary respiratory tuberculosis (A15.7) · Tb (tuberculosis) of lung, pleura · TB of pleura · Tuberculosis of pleura · Tuberculous pleural effusion · Tuberculosis of the serous membrane lining the thoracic cavity and surrounding the lungs. · Adhesions, adhesive (postinfective) K66.0 pleura, pleuritic J94.8 tuberculous NEC A15.6 Effusion pleura, pleurisy, pleuritic, pleuropericardial J90 tuberculous NEC A15.6 Empyema (acute) (chest) (double) (pleura) (supradiaphragmatic) (thorax) J86.9 tuberculous A15.6 Fistula (cutaneous) L98.8 pleura…) J94.8 tuberculous NEC (non primary) A15.6 Pleurisy (acute) (adhesive… hydrothorax A15.6 pleura, pleural, pleurisy, pleuritis (fibrinous) (obliterative) (purulent
This code is a specific code that can be used to specify a diagnosis or procedure.

Pleurisy without mention of effusion or current tuberculosis
Asbestos pleurisy · Asbestos-induced pleural plaque · Calcification of pleura · Disorder of pleura · Fibrosis of pleura · Fibrothorax · Pleural calcification · Pleural disease · Pleural disease due to asbestos · Pleural plaque · Pleural plaque due to asbestos exposure · Pleural thickening · Pleurisy · Thickening of pleura…

Empyema ICD-10 J86.9

Empyema

From Wikipedia, the free encyclopedia
Empyema
Classification and external resources
ICD10 J86.9
MedlinePlus 000123
MeSH D004653

An empyema (from Greek ἐμπύημα, “abscess”) is a collection or gathering of pus within a naturally existing anatomical cavity. For example, pleural empyema is empyema of the pleural cavity. It must be differentiated from an abscess, which is a collection of pus in a newly formed cavity.

Classification[edit]

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
  • ICD-9-CM 510.0 converts approximately to:

    Note: approximate conversions between ICD-9-CM codes and ICD-10-CM codes may require clinical interpretation in order to determine the most appropriate conversion code(s) for your specific coding situation.

    Source: 2016 ICD-10-CM CMS General Equivalence Mappings.

  • ICD-9-CM 510.9 converts approximately to:

    Note: approximate conversions between ICD-9-CM codes and ICD-10-CM codes may require clinical interpretation in order to determine the most appropriate conversion code(s) for your specific coding situation.

    Source: 2016 ICD-10-CM CMS General Equivalence Mappings.

Pleural effusion 2016 ICD-10-CM Code J90

Pleural effusion

From Wikipedia, the free encyclopedia
Pleural effusion
Diagram showing a build up of fluid in the lining of the lungs (pleural effusion) CRUK 054.svg

Diagram of fluid buildup in the pleura
Classification and external resources
Specialty Pulmonology
ICD10 J90J91
ICD9-CM 511.9
MedlinePlus 000086
MeSH D010996

A pleural effusion is excess fluid that accumulates in the pleural cavity, the fluid-filled space that surrounds the lungs. This excess can impair breathing by limiting the expansion of the lungs. Various kinds of pleural effusion, depending on the nature of the fluid and what caused its entry into the pleural space, are hydrothorax (serous fluid), hemothorax (blood), urinothorax (urine), chylothorax (chyle), or pyothorax (pus). Apneumothorax is the accumulation of air in the pleural space, and is commonly called a “collapsed lung.”

Types[edit]

Various methods can be used to classify pleural fluid.

By the origin of the fluid:

By pathophysiology:

  • Transudative pleural effusion
  • Exudative pleural effusion

By the underlying cause (see next section).

Causes[edit]

Pleural effusion

Transudative[edit]

The most common causes of transudative pleural effusions in the United States are heart failure and cirrhosis. Nephrotic syndrome, leading to the loss of large amounts of albumin in urine and resultant low albumin levels in the blood and reduced colloid osmotic pressure is another, less common, cause. Pulmonary emboli were once thought to cause transudative effusions, but have been recently shown to be exudative.[1] The mechanism for the transudative pleural effusion is probably related to increased permeability of the capillaries in the lung, which results from the release of cytokines or inflammatory mediators (e.g. vascular endothelial growth factor) from theplatelet-rich blood clots. The excessive interstitial lung fluid traverses the visceral pleura and accumulates in the pleural space.

Conditions associated with transudative pleural effusions include:[2]

Exudative[edit]

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

When a pleural effusion has been determined to be exudative, additional evaluation is needed to determine its cause, and amylase, glucose, pH and cell counts should be measured.

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, andpulmonary embolism.

Another common cause is after heart surgery, when incompletely drained blood can lead to an inflammatory response that causes exudative pleural fluid.

Conditions associated with exudative pleural effusions:[2]

Other/ungrouped[edit]

Other causes of pleural effusion include tuberculosis (though stains of pleural fluid are only rarely positive for acid-fast bacilli, this is the most common cause of pleural effusions 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 abscesses, rheumatoid arthritis, asbestos pleural effusion, mesothelioma, Meigs’ syndrome (ascites and pleural effusion due to a benign ovarian tumor), and ovarian hyperstimulation syndrome.

Pleural effusions may also occur through medical or 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.

Pathophysiology[edit]

Pleural fluid is secreted by the parietal layer of the pleura and reabsorbed by the lymphatics in the most dependent parts of the parietal pleura, primarily the diaphragmatic and mediastinal regions. Exudative pleural effuisions occur when the pleura is damaged, e.g., by trauma, infection or malignancy, and transudative pleural effusions develop when there is either excessive production of pleural fluid or the resorption capacity is exceeded.

Diagnosis[edit]

A large left sided pleural effusion as seen on an upright chest X-ray

A pleural effusion is usually diagnosed on the basis of medical history and physical exam, and confirmed by a chest X-ray. Once accumulated fluid is more than 300 mL, there are usually detectable clinical signs, such as decreased movement of the chest on the affected side, 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 sounds and egophony. A large effusion there may cause 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 showed that dullness to conventional percussion was most accurate for diagnosing pleural effusion (summary positive likelihood ratio, 8.7; 95% confidence interval, 2.2–33.8), while the absence of reduced tactile vocal fremitus made pleural effusion less likely (negative likelihood ratio, 0.21; 95% confidence interval, 0.12–0.37).[4]

Imaging[edit]

A pleural effusion appears as an area of whiteness on a standard posteroanterior chest X-ray.[5] Normally, the space between 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 water, it can be seen on radiographs. Since the effusion has greater density than the rest of the lung, it gravitates towards the lower portions of thepleural cavity. The pleural effusion behaves according to basic fluid dynamics, conforming to the shape of pleural space, which is determined by the lung and chest wall. If the pleural space contains both air and fluid, then an air-fluid level that is horizontal will be present, instead of conforming to the lung space.[6] Chest radiographs in the lateral decubitus position (with the patient lying on the side of the pleural effusion) are more sensitive and can detect as little as 50 mL of fluid. At least 300 mL of fluid must be present before upright chest X-rays can detect a pleural effusion (e.g., blunted costophrenic angles).

Chest computed tomography is more accurate for diagnosis and may be obtained to better characterize the presence, size, and characteristics of a pleural effusion. Lung ultrasound, nearly as accurate as CT and more accurate than chest X-ray, is increasingly being used at the point of care to diagnose pleural effusions, with the advantage that it is a safe, dynamic, and repeatable imaging modality.[7]

Thoracentesis[edit]

Once a pleural effusion is diagnosed, its cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis, and it should be done in almost all patients who have pleural fluid that is at least 10 mm in thickness on CT, ultrasonography, or lateral decubitus X-ray and that is new or of uncertain etiology. In general, the only patients who do not require thoracentesis are those who have heart failure with symmetric pleural effusions and no chest pain or fever; in these patients, diuresiscan be tried, and thoracentesis avoided unless effusions persist for more than 3 days.[8] In a 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 use of ultrasound to guide the procedure is now standard of care as it increases accuracy and decreases complications.[9][10] After removal, the fluid may then be evaluated for:

  1. Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pH, and glucose
  2. Gram stain and culture to identify possible bacterial infections
  3. White and red blood cell counts and differential white blood cell counts
  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, tuberculosis cultures, lupus cell prep, specific immunoglobulins

Light’s criteria[edit]

Transudate vs. exudate

Transudate Exudate
Main causes hydrostatic
pressure
,
colloid
osmotic pressure
Inflammation-Increased vascular permeability
Appearance Clear[11] Cloudy[11]
Specific gravity < 1.012 > 1.020
Protein content < 2.5 g/dL > 2.9 g/dL[12]
fluid protein/
serum protein
< 0.5 > 0.5[13]
SAAG = Serum [albumin] – Effusion [albumin] > 1.2 g/dL < 1.2 g/dL[14]
fluid LDH
upper limit for serum
< 0.6 or < 23 > 0.6[12] or > 23[13]
Cholesterol content < 45 mg/dL > 45 mg/dL[12]

Instruments for needle biopsy of the pleura.[15]

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, and oncotic pressure (effective pressure due to the composition of the pleural fluid and blood)–are altered in many diseases, e.g., left ventricular failure, kidney failure, liver 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).[16]

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:[17]

  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 [12] or 23[17] times the normal upper limit for serum. Different laboratories have different values for the upper limit of serum LDH, but examples include 200[18] and 300[18] IU/l.[19]

The sensitivity and specificity of Light’s criteria for detection of exudates have been measured in many studies and are usually reported to be around 98% and 80%, respectively.[20][21] This means that although Light’s criteria are relatively accurate, twenty percent of patients that are identified by Light’s criteria as having exudative pleural effusions actually have transudative 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.[14] 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 to the 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.[4] Instruments in picture while in shape are accurate most hospitals use disposable trocar’s as they are safer since they are always sharp since they are single use and have a much smaller risk of cross patient contamination.

Treatment[edit]

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 if scarring occurs. 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 PleurX Pleural Catheter 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 to 1000 mL of fluid, and 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.

See also[edit]

This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant pleural effusion
underlying neoplasm · Neoplastic pleural effusion · Pleural effusion due to malignancy · A collection of fluid in the pleural cavity as a result of malignant disease. Malignant pleural effusion fluid often contains free-floating malignant cells. · A condition in which cancer causes an abnormal amount of fluid to collect between the thin layers of tissue (pleura) lining the outside of the lung and the wall of the chest cavity. Lung cancer, breast cancer, lymphoma, and leukemia cause most malignant pleural effusions. · Presence of fluid in the pleural cavity as a complication of malignant disease. Malignant pleural effusions often contain actual malignant cells. · Effusionmalignant pleural J91.0 pleura, pleurisy, pleuritic, pleuropericardial J90 malignant J91.0…
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant pleural effusion
Neoplastic pleural effusion · Pleural effusion due to malignancy · A collection of fluid in the pleural cavity as a result of malignant disease. Malignant pleural effusion fluid often contains free-floating malignant cells. · A condition in which cancer causes an abnormal amount of fluid to collect between the thin layers of tissue (pleura) lining the outside of the lung and the wall of the chest cavity. Lung cancer, breast cancer, lymphoma, and leukemia cause most malignant pleural effusions. · Presence of fluid in the pleural cavity as a complication of malignant disease. Malignant pleural effusions often contain actual malignant cells….
This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Pleural effusion in conditions classified elsewhere
pleural effusion in heart failure (I50.-) · pleural effusion in systemic lupus erythematosus (M32.13)…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pleural effusion, not elsewhere classified
Encysted pleurisy · Pleural effusion NOS · Pleurisy with effusion (exudative) (serous) · chylous (pleural) effusion (J94.0) · malignant pleural effusion (J91.0)) · pleurisy NOS (R09.1) · tuberculous pleural effusion (A15.6) · Bacterial pleural effusion · Bacterial pleurisy w effusion · Bacterial pleurisy with effusion · Exudative pleural effusion · Loculated pleural effusion · Pleural effusion · Pleural effusion (fluid around lung) · Pleural effusionbacterial, nontuberculosis · Pleural effusion due to bacterial… in amounts of fluid within the pleural cavity. Symptoms include shortness of breath, cough… amounts of fluid within the pleural cavity. Symptoms include shortness of breath, cough, and chest pain. It is usually caused by lung infections, congestive heart failure, pleural
This code is a specific code that can be used to specify a diagnosis or procedure.

Unspecified pleural effusion
Chylothorax · Chylous effusion · Exudative pleural effusion · Loculated pleural effusion · Pleural effusion · Pleural effusion (fluid around lung) · A disorder characterized by an increase in amounts of fluid within the pleuralcavity. Symptoms include shortness of breath, cough and marked chest discomfort. ·… the lung and the wall of the chest cavity. · Increased amounts of fluid within the pleural… by lung infections, congestive heart failure,pleural and lung tumors, connective tissue disorders, and trauma. · Presence of fluid in the pleural cavity resulting from excessive transudation or exudation from the pleural surfaces. It is a sign of disease and not a diagnosis in itself. · Presence of fluid in the pleural cavity resulting from excessive transudation or exudation from the pleural surfaces; it is a sign of disease

Platelet Function Disorders

  • D69.1 is a specific ICD-10-CM code that can be used to specify a diagnosis.
  • Reimbursement claims with a date of service on or after October 1, 2015 require the use of ICD-10-CM codes.
  • This is the American ICD-10-CM version of D69.1. Other international ICD-10 versions may differ.
  • Clinical Information

    • A congenital bleeding disorder with prolonged bleeding time, absence of aggregation of platelets in response to most agents, especially adp, and impaired or absent clot retraction. Platelet membranes are deficient in or have a defect in the glycoprotein iib-iiia complex (platelet glycoprotein gpiib-iiia complex).
    • A rare inherited bleeding disorder characterized by the decrease or absence of the platelet alpha-granules and their proteins in the peripheral blood platelets.
    • A rare, autosomal recessive inherited and less frequently acquired platelet disorder. It is characterized by deficient or dysfunctional glycoprotein iib/iiia complex. It leads to defective platelet aggregation, resulting in bleeding.
    • A rare, inherited platelet disorder characterized by a selective deficiency in the number and contents of platelet alpha-granules. It is associated with thrombocytopenia, enlarged platelets, and prolonged bleeding time.
    • Platelet abnormality characterized by defective clot formation, impaired aggregation, and prolonged bleeding time; other manifestations include nosebleeds, inappropriate bruising, and excessive bleeding.

    Applicable To

    • Bernard-Soulier [giant platelet] syndrome
    • Glanzmann’s disease
    • Grey platelet syndrome
    • Thromboasthenia (hemorrhagic) (hereditary)
    • Thrombocytopathy

    Approximate Synonyms

    • Drug induced platelet dysfunction
    • Platelet disorder
    • Platelet disorder, qualitative
    • Platelet dysfunction due to drugs
    • Platelet dysfunction, drug induced
    • Qualitative platelet disorder

    Type 1 Excludes

    • von Willebrand’s disease (D68.0)

    ICD-10-CM D69.1 is grouped within Diagnostic Related Group (MS-DRG v32.0):

    • 813 Coagulation disorders

    Convert ICD-10-CM D69.1 to ICD-9-CM

    The following ICD-10-CM Index entries contain back-references to ICD-10-CM D69.1:

    platelets, qualitative D69.1
    platelet NEC D69.1
    Bernard-Soulier (thrombopathy) D69.1
    Glanzmann’s (hereditary hemorrhagic thrombasthenia) D69.1
    Naegeli’s D69.1
    platelets D69.1
    platelets D69.1
    giant platelet (Bernard-Soulier) D69.1
    gray or grey (newborn) P93.0
    platelet D69.1
    • Thrombasthenia (Glanzmann) (hemorrhagic) (hereditary) D69.1
    • Thromboasthenia (Glanzmann) (hemorrhagic) (hereditary) D69.1
    • Thrombocytasthenia (Glanzmann) D69.1
    • Thrombocytopathy (dystrophic) (granulopenic) D69.1
    • Thrombopathy (Bernard-Soulier) D69.1

Pituitary Tumors

Pituitary Adenoma

From Wikipedia, the free encyclopedia
  (Redirected from Pituitary tumors)
Pituitary adenoma
Adenome hypophyse.JPG
Classification and external resources
Specialty Oncology, endocrinology
ICD10 D35.2
ICD9-CM 237.0
ICD-O M8272/0
MedlinePlus 000704
eMedicine neuro/312
MeSH D010911

Pituitary adenomas are tumors that occur in the pituitary gland. Pituitary adenomas are generally divided into three categories dependent upon their biological functioning: benign adenoma, invasive adenoma, andcarcinomas, with carcinomas accounting for 0.1% to 0.2%, approximately 35% being invasive adenomas and most being benign adenomas. Pituitary adenomas represent from 10% to 25% of all intracranial neoplasms [1]and the estimated prevalence rate in the general population is approximately 17%.[2]

Non-invasive and non-secreting pituitary adenomas are considered to be benign in the literal as well as the clinical sense; however a recent meta-analysis (Fernández-Balsells, et al. 2011) of available research has shown there are to date scant studies – of poor quality – to either support or refute this assumption.

Adenomas which exceed 10 millimetres (0.39 in) in size are defined as macroadenomas, with those smaller than 10 mm referred to as microadenomas. Most pituitary adenomas are microadenomas, and have an estimated prevalence of 16.7% (14.4% in autopsy studies and 22.5% in radiologic studies).[2][3] A majority of pituitary microadenomas often remain undiagnosed and those that are diagnosed are often found as anincidental finding, and are referred to as incidentalomas.

Pituitary macroadenomas are the most common cause of hypopituitarism, and in the majority of cases they are non-secreting adenomas.[4]

The Pituitary gland is in close proximity to the brain, invasive adenomas may invade the dura mater, cranial bone, or sphenoid bone. While Pituitary adenomas are extremely common, affecting approximately one in 6 of the general population, clinically active pituitary adenomas requiring surgical treatment are more rare, affecting approximately one in 1000 of the general population.[5]

Signs and symptoms[edit]

Physical[edit]

Binocular image with the outer halves of each circle removed

Visual field loss in bitemporal hemianopsia: peripheral vision loss affecting both eyes, resulting from a tumor-typically a pituitary adenoma- putting pressure on the optic chiasm.

Hormone secreting pituitary adenomas cause one of several forms of hyperpituitarism. The specifics depend on the type of hormone. Some tumors secrete more than one hormone, the most common combination being GH and prolactin.

A pituitary adenoma may present with visual field defects, classically bitemporal hemianopsia. It arises from the compression of the optic nerve by the tumor. The specific area of the visual pathway at which compression by these tumours occurs is at the optic chiasma.

The anatomy of this structure causes pressure on it to produce a defect in the temporal visual field on both sides, a condition called bitemporal hemianopsia. If originating superior to the optic chiasm, more commonly in acraniopharyngioma of the pituitary stalk, the visual field defect will first appear as bitemporal inferior quadrantanopia, if originating inferior to the optic chiasm the visual field defect will first appear as bitemporal superior quadrantanopia. Lateral expansion of a pituitary adenoma can also compress the abducens nerve, causing a lateral rectus palsy.

Also, a pituitary adenoma can cause symptoms of increased intracranial pressure.

Prolactinomas often start to give symptoms especially during pregnancy, when the hormone progesterone increases the tumor’s growth rate.

Various types of headaches are common in patients with pituitary adenomas. The adenoma may be the prime causative factor behind the headache or may serve to exacerbate a headache caused by other factors. Amongst the types of headaches experienced are both chronic and episodic migraine, and more uncommonly various unilateral headaches; primary stabbing headache,[6] short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)[7] – another type of stabbing headache characterized by short stabs of pain -, cluster headache,[8] and hemicrania continua (HS).[9]

Psychiatric[edit]

Various psychiatric manifestations have been associated with pituitary disorders including pituitary adenomas. Psychiatric symptoms such as depression, anxiety[10] apathy, emotional instability, easy irritability and hostility have been noted.[11]

Complications[edit]

Morphological facial changes caused by acromegaly; frontal bossing, enlarged nose, prognathism andmaxillary widening with separation of teeth and unseen, enlargement of the tongue (macroglossia).

  • Acromegaly is a syndrome that results when the anterior pituitary gland produces excess growth hormone (GH). Approximately 90-95% of acromegaly cases are caused by a pituitary adenoma and it most commonly affects middle aged adults,[12] Acromegly can result in severe disfigurement, serious complicating conditions, and premature death if unchecked. The disease which is often also associated with gigantism, is difficult to diagnose in the early stages and is frequently missed for many years, until changes in external features, especially of the face, become noticeable with the median time from the development of initial symptoms to diagnosis being twelve years.[13]
  • Cushing’s syndrome is a hormonal disorder that causes hypercortisolism, which is elevated levels of cortisol in the blood. Cushing’s disease (CD) is the most frequent cause of Cushing’s syndrome, responsible for approximately 70% of cases.[14] CD results when a pituitary adenoma causes excessive secretion of adrenocorticotropic hormone (ACTH) that stimulates the adrenal glands to produce excessive amounts of cortisol.[15]
Cushing’s disease may cause fatigue, weight gain, fatty deposits around the abdomen and lower back (truncal obesity) and face (“moon face”), stretch marks (striae) on the skin of the abdomen, thighs, breasts and arms,hypertension, glucose intolerance and various infections. In women it may cause excessive growth of facial hair (hirsutism) and in men erectile dysfunction. Psychiatric manifestations may include depression, anxiety, easy irritability and emotional instability. It may also result in various cognitive difficulties.
  • Hyperpituitarism is a disease of the anterior lobe of the pituitary gland which is usually caused by a functional pituitary adenoma and results in hypersecretion of adenohypophyseal hormones such as growth hormone; prolactin; thyrotropin; luteinizing hormone; follicle stimulating hormone; and adrenocorticotropic hormone.
  • Pituitary apoplexy is a condition that occurs when pituitary adenomas suddenly hemorrhage internally, causing a rapid increase in size or when the tumor outgrows its blood supply which causes tissue necrosis and subsequent swelling of the dead tissue. Pituitary apoplexy often presents with visual loss and sudden onset headache and requires timely treatment often with corticosteroids and if necessary surgical intervention.[16]
  • Central diabetes insipidus is caused by diminished production of the antidiuretic hormone vasopressin that causes severe thirst and excessive production of very dilute urine (polyuria) which can lead to dehydration. Vasopressin is produced in the hypothalamusand is then transported down the pituitary stalk and stored in the posterior lobe of the pituitary gland which then secretes it into the bloodstream.[17]
The diagnosis of CDI is based on the results of urine and blood tests, and a water deprivation test which tests the body’s ability to concentrate urine. CDI is often treated with desmopressin acetate a synthetic vasopressin known as DDAVP administered via nasal spray.

Risk factors[edit]

Multiple endocrine neoplasia[edit]

Adenomas of the anterior pituitary gland are a major clinical feature of multiple endocrine neoplasia type 1 (MEN1), a rare inherited endocrine syndrome that affects 1 person in every 30,000. MEN causes various combinations of benign or malignant tumors in various glands in the endocrine system or may cause the glands to become enlarged without forming tumors. It often affects the parathyroid glands, pancreatic islet cells, and anterior lobe of the pituitary gland. MEN1 may also cause non-endocrine tumors such as facial angiofibromas, collagenomas, lipomas, meningiomas, ependymomas, and leiomyomas. Approximately 25 percent of patients with MEN1 develop pituitary adenomas.[18][19]

Carney complex[edit]

Carney complex (CNC), also known as LAMB syndrome[20] and NAME syndrome[20] is an autosomal dominant condition comprising myxomas of the heart and skin, hyperpigmentation of the skin (lentiginosis), and endocrine overactivity and is distinct fromCarney’s triad.[21][22] Approximately 7% of all cardiac myxomas are associated with Carney complex.[23] Patients with CNC develop growth hormone (GH)-producing pituitary tumors and in some instances these same tumors also secrete prolactin. There are however no isolated prolactinomas or any other type of pituitary tumor. In some patients with CNC, the pituitary gland is characterized by hyperplastic areas with the hyperplasia most likely preceding the formation of GH-producing adenomas.[24]

Familial isolated pituitary adenoma[edit]

Familial isolated pituitary adenoma (FIPA) is a term that used to identify a condition that displays an autosomal dominant inheritance and is characterised by the presence of two or more related patients affected by adenomas of the pituitary gland only, with no other associated symptoms that occur in Multiple endocrine neoplasia Type 1 or Carney complex.[25][26]

Mechanism[edit]

Pituitary gland

The pituitary gland or hypophysis is often referred to as the “master gland” of the human body. Part of the hypothalamic-pituitary axis, it controls most of the body’s endocrine functions via the secretion of various hormones into the circulatory system. The pituitary gland is located below the brain in a depression (fossa) of the sphenoid bone known as the sella turcica. Although anatomically and functionally connected to the brain, the pituitary gland[27]sits outside the blood–brain barrier. It is separated from the subarachnoid space by the diaphragma sella, therefore the arachnoid mater and thus cerebral spinal fluid cannot enter the sella turcica.

The pituitary gland is divided into two lobes, the anterior lobe (which accounts for two thirds of the volume of the gland), and the posterior lobe (one third of the volume) separated by the pars intermedia.

The posterior lobe (the neural lobe or neurohypophysis) of the pituitary gland is not, despite its name, a true gland. The posterior lobe contains axons of neurons that extend from the hypothalamus to which it is connected via the pituitary stalk. The hormones vasopressin and oxytocin, produced by the neurons of the supraoptic and paraventricular nuclei of the hypothalamus, are stored in the posterior lobe and released from axon endings (dendrites) within the lobe.[28]

The pituitary gland’s anterior lobe (adenohypophysis) is a true gland which produces and secretes six different hormones: thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone(FSH), luteinizing hormone (LH), growth hormone (GH), and prolactin (PRL).[29]

Diagnosis[edit]

Diagnosis of pituitary adenoma can be made, or at least suspected, by a constellation of related symptoms presented above.

Tumors which cause visual difficulty are likely to be a macroadenoma greater than 10 mm in diameter; tumors less than 10 mm are microadenoma.

The differential diagnosis includes pituitary tuberculoma, especially in developing countries and in immumocompromised patients.[30] The diagnosis is confirmed by testing hormone levels, and by radiographic imaging of the pituitary (for example, by CT scan or MRI).

Classification[edit]

Unlike tumors of the posterior Pituitary, Pituitary adenomas are classified as endocrine tumors (not brain tumors). Pituitary adenomas are classified based upon anatomical, histological and functional criteria.[31]

  • Anatomically pituitary tumors are classified by their size based on radiological findings; either microadenomas (less than <10 mm) or macroadenomas (equal or greater than ≥10 mm).
Classification based on radioanatomical findings places adenomas into 1 of 4 grades (I–IV):[32]
Stage I: microadenomas (<1 cm) without sella expansion.
Stage II: macroadenomas (≥1 cm) and may extend above the sella.
Stage III: macroadenomas with enlargement and invasion of the floor or suprasellar extension.
Stage IV is destruction of the sella.
  • Histological classification utilizes an immunohistological characterization of the tumors in terms of their hormone production.[31] Historically they were classed as either basophilic, acidophilic, or chromophobic on the basis of whether or not they took up thetinctorial stains hematoxylin and eosin. This classification has fallen into disuse, in favor of a classification based on what type of hormone is secreted by the tumor. Approximately 20-25% of adenomas do not secrete any readily identifiable active hormones (‘non-functioning tumors’) yet they are still sometimes referred to as ‘chromophobic’.
  • Functional classification is based upon the tumors endocrine activity as determined by serum hormone levels and pituitary tissue cellular hormone secretion detected via immunohistochemical staining.[33] The “Percentage of hormone production cases” values are the fractions of adenomas producing each related hormone of each tumor type as compared to all cases of pituitary tumors, and does not directly correlate to the percentages of each tumor type because of smaller or greater incidences of absence of secretion of the expected hormone. Thus, nonsecretive adenomas may be either null cell adenomas or a more specific adenoma that, however, remains nonsecretive.
Type of adenoma Secretion Staining Pathology Percentage of hormone production cases
lactotrophic adenomas(prolactinomas) secrete prolactin acidophilic galactorrhea, hypogonadism, amenorrhea, infertility, andimpotence 30%[34]
somatotrophic adenomas secrete growth hormone (GH) acidophilic acromegaly in adults; gigantism in children 15%[34]
corticotrophic adenomas secrete adenocorticotropic hormone (ACTH) basophilic Cushing’s disease
gonadotrophic adenomas secrete luteinizing hormone (LH), follicle-stimulating hormone (FSH) and their subunits basophilic usually doesn’t cause symptoms 10%[34]
thyrotrophic adenomas (rare) secrete thyroid-stimulating hormone (TSH) basophilic to chromophobic occasionally hyperthyroidism,[35] usually doesn’t cause symptoms Less than 1%[34]
null cell adenomas do not secrete hormones may stain positive forsynaptophysin 25% of pituitary adenomas are nonsecretive[34]

Pituitary incidentalomas[edit]

Pituitary incidentalomas are pituitary tumors that are characterized as an incidental finding. They are often discovered by computed tomography (CT) or magnetic resonance imaging (MRI), performed in the evaluation of unrelated medical conditions such as suspected head trauma, in cancer staging or in the evaluation of nonspecific symptoms such as dizziness and headache. It is not uncommon for them to be discovered at autopsy. In a meta-analysis, adenomas were found in an average of 16.7% in postmortem studies, with most being microadenomas (<10mm); macrodenomas accounted for only 0.16% to 0.2% of the decedents.[2] While non-secreting, noninvasive pituitary microadenomas are generally considered to be literally as well as clinically benign, there are to date scant studies of low quality to support this assertion.[36]

It has been recommended in the current Clinical Practice Guidelines (2011) by the Endocrine Society – a professional, international medical organization in the field of endocrinology and metabolism – that all patients with pituitary incidentalomas undergo a completemedical history and physical examination, laboratory evaluations to screen for hormone hypersecretion and for hypopituitarism. If the lesion is in close proximity to the optic nerves or optic chiasm, a visual field examination should be performed. For those with incidentalomas which do not require surgical removal, follow up clinical assessments and neuroimaging should be performed as well follow-up visual field examinations for incidentalomas that abut or compress the optic nerve and chiasm and follow-up endocrine testing for macroincidentalomas.[37]

Ectopic pituitary adenoma[edit]

An ectopic (occurring in an abnormal place) pituitary adenoma is a rare type of tumor which occurs outside of the sella turcica, most often in the sphenoid sinus,[38] suprasellar region, nasopharynx and the cavernous sinuses.[39]

Metastases to the pituitary gland[edit]

Carcinomas that metastasize into the pituitary gland are uncommon and typically seen in the elderly,[40][41] with lung and breast cancers being the most prevalent,[42] In breast cancer patients, metastases to the pituitary gland occur in approximately 6-8% of cases.[43]

Symptomatic pituitary metastases account for only 7% of reported cases. In those who are symptomatic Diabetes insipidus often occurs with rates approximately 29-71%. Other commonly reported symptoms include anterior pituitary dysfunction, visual field defects, headache/pain, and ophthalmoplegia.[44]

Treatment[edit]

Treatment options depend on the type of tumor and on its size:

  • Prolactinomas are most often treated with bromocriptine or more recently, cabergoline or quinagolide which decrease tumor size as well as alleviates symptoms, both dopamine agonists, and followed by serial imaging to detect any increase in size. Treatment where the tumor is large can be with radiation therapy or surgery, and patients generally respond well. Efforts have been made to use a progesterone antagonist for the treatment of prolactinomas, but so far have not proved successful.
  • Somatotrophic adenomas respond to octreotide, a long-acting somatostatin analog, in many but not all cases according to a review of the medical literature. Unlike prolactinomas, thyrotrophic adenomas characteristically respond poorly to dopamine agonist treatment.[35]
  • Surgery is a common treatment for pituitary tumors. Trans-sphenoidal adenectomy surgery can often remove the tumor without affecting other parts of the brain. Endoscopic surgery has become common recently.[45]

See also[edit]

Benign neoplasm of pituitary gland
Adenoma of pituitary · Adenoma, pituitary · Benign neoplasm of pituitary · Benign neoplasm pituitary, macroadenoma · Benign neoplasm pituitary, microadenoma · Benign neoplasm, macroprolactinoma · Benign neoplasm, microprolactinoma · Benign neoplasm, pituitary · Macroprolactinoma · Microprolactinoma · Pituitary adenoma · Pituitary macroadenoma · Pituitary microadenoma · Prolactinoma · A neoplasm without metastatic potential arising from the anterior or the posterior lobe of the pituitary gland. The vast majority are adenomas. · Adenoma – see also Neoplasm, benign, by site acidophil unspecified site D35.2 acidophil-basophil, mixed unspecified site D35.2 basophil unspecified site D35.2 basophil-acidophil, mixed unspecified
This code is a specific code that can be used to specify a diagnosis or procedure.

Benign neoplasm of pituitary gland and craniopharyngeal duct
Adenoma of pituitary · Adenoma, pituitary · Benign neoplasm of craniopharyngeal duct · Benign neoplasm of pituitary · Benign neoplasm of pituitary gland · Benign neoplasm pituitary, macroadenoma · Benign neoplasmpituitary, microadenoma · Benign neoplasm, craniopharyngeal duct · Benign neoplasm, macroprolactinoma · Benign neoplasm, microprolactinoma · Benign neoplasm, pituitary · Macroprolactinoma · Microprolactinoma ·Pituitary adenoma · Pituitary macroadenoma · Pituitary microadenoma · Prolactinoma…
This code is a specific code that can be used to specify a diagnosis or procedure.

Infertility, female, of pituitary-hypothalamic origin
Female infertility due to pituitary disorder · Female infertility of pituitary origin…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pituitary-dependent Cushing’s disease
Overproduction of pituitary ACTH · Pituitary-dependent hypercorticalism · A disease of the pituitary gland characterized by the excess amount of adrenocorticotropic hormone secreted. This leads to hypersecretion of cortisol (hydrocortisone) by the adrenal…) (Cushing’s) (pituitary) E24.0 Cushing’s syndrome or disease E24.9 pituitary-dependent E24.0 Hyperadrenocorticism E24.9 pituitary-dependent E24.0 Hypercorticalism, pituitary-dependent E24.0 Hypersecretion ACTH (not associated with Cushing’s syndrome) E27.0 pituitary E24.0 hormone (s) ACTH (not associated with Cushing’s syndrome) E27.0 pituitary E24.0 Syndrome – see also Disease Cushing’s E24.9pituitary-dependent E24.0 due to overproduction of pituitary ACTH E24.0…
This code is a specific code that can be used to specify a diagnosis or procedure.

Disorder of pituitary gland, unspecified
Anterior pituitary disorder · Disease of pituitary gland · Disorder of anterior pituitary · Disorder of optic chiasm due to pituitary disorder · Disorder of pituitary gland · Optic chiasm disorder assoc w pituitary disorder · Optic chiasm disorder assoc with pituitary disorder · Pituitary disorder · Pituitary disorder, anterior · Disorders involving either the adenohypophysis… of pituitary hormones. Neoplastic pituitary masses can also cause compression of the optic chiasm and other adjacent structures. · Disorders of the anterior or posterior pituitary gland which usually manifest as hypersecretion or hyposecretion of pituitary hormones. · Your pituitary gland is a pea-sized gland at the base of your brain. The pituitary… and the functions of other glands in the body. With pituitary disorders, you often have too much

Pilonidal cyst 2016 ICD-10-CM Code L05.01

Pilonidal cyst

From Wikipedia, the free encyclopedia
  (Redirected from Pilonidal disease)
“Jeep seat” redirects here. For other uses, see Jeep.
Pilonidal cyst
Two pilonidal cysts in the natal cleft.jpg

Two pilonidal cysts that have formed in thegluteal cleft of an adult man.
Classification and external resources
Specialty General surgery; Colorectal surgery
ICD10 L05
ICD9-CM 685
DiseasesDB 31128
eMedicine emerg/771
MeSH D010864

A pilonidal cyst, also referred to as a pilonidal abscess, pilonidal sinus or sacrococcygeal fistula, is a cyst or abscess near or on the natal cleft of the buttocks that often contains hair and skin debris.[1]

Signs and symptoms[edit]

Pilonidal cysts are often very painful, and typically occur between the ages of 15 and 35.[2] Although usually found near the coccyx, the condition can also affect the navel, armpit or genital region,[3] though these locations are much rarer.

Symptoms include:[4]

  • Pain/discomfort or swelling above the anus or near the tailbone that comes and goes
  • Opaque yellow (purulent) or bloody discharge from the tailbone area
  • Unexpected moisture in the tailbone region
  • Discomfort with sitting on the tailbone, doing sit-ups or riding a bike (any activities that roll over the tailbone area)

Some people with a pilonidal cyst will be asymptomatic.[5]

Pilonidal sinus[edit]

A sinus tract, or small channel, may originate from the source of infection and open to the surface of the skin. Material from the cyst may drain through the pilonidal sinus. A pilonidal cyst is usually painful, but with draining, the patient might not feel pain.

Causes[edit]

One proposed cause of pilonidal cysts is ingrown hair.[6] Excessive sitting is thought to predispose people to the condition, as sitting increases pressure on the coccygeal region. Trauma is not believed to cause a pilonidal cyst; however, such an event may result in inflammation of an existing cyst. However, there are cases where this can occur months after a localized injury to the area. Some researchers have proposed that pilonidal cysts may be the result of a congenital pilonidal dimple.[7] Excessive sweating can also contribute to the cause of a pilonidal cyst. Moisture can fill a stretched hair follicle, which helps create a low-oxygen environment that promotes the growth of anaerobic bacteria, often found in pilonidal cysts. The presence of bacteria and low oxygen levels hamper wound healing and exacerbate a forming pilonidal cyst.[8]

The condition was widespread in the United States Army during World War II. The condition was termed “jeep seat” or “Jeep riders’ disease”, because a large portion of people who were being hospitalized for it rode in Jeeps, and prolonged rides in the bumpy vehicles were believed to have caused the condition due to irritation and pressure on the coccyx.

Differential diagnosis[edit]

A pilonidal cyst can resemble a dermoid cyst, a kind of teratoma (germ cell tumor). In particular, a pilonidal cyst in the gluteal cleft can resemble a sacrococcygeal teratoma. Correct diagnosis is important because all teratomas require complete surgical excision, if possible without any spillage, and consultation with an oncologist.

Treatment[edit]

Pilonidal cyst two days after surgery.

Treatment may include antibiotic therapy, hot compresses and application of depilatory creams. In more severe cases, the cyst may need to be lanced or treated surgically. Lancing is performed using a local anesthesia, with healing time generally under one week.[9] The most conservative surgical treatment, Bascom’s Pit Picking procedure, is a relatively simple outpatient option that can be performed in a physician’s office, involves minimal pain and requires only a few days healing.[10] Although this procedure is much less invasive than the alternatives, it is not regularly practiced in the US. The Pit Picking procedure provides good results, fast recovery, and in instances where it is unsuccessful, other options for more invasive surgery can still be performed.

The more common course for surgical treatment is for the cyst to be surgically excised (along with pilonidal sinus tracts). Post-surgical wound packing may be necessary, and packing typically must be replaced once daily for 4 to 8 weeks. In some cases, two years may be required for complete granulation to occur. Sometimes the cyst is resolved via surgical marsupialization.[11]

Surgeons can also excise the sinus and repair with a reconstructive flap technique, such as a “cleft lift” procedure or Z-plasty, usually done under general anesthetic. This approach is especially useful for complicated or recurring pilonidal disease, leaves little scar tissue and flattens the region between the buttocks, reducing the risk of recurrence.[8] This approach typically results in a more rapid recovery than the traditional surgery, however there are fewer surgeons trained in the cleft lift procedure and thus, it may not be as accessible to patients, depending on their geographic location.

Pilonidal cysts recur and do so more frequently if the surgical wound is sutured in the midline, as opposed to away from the midline, which obliterates the natal cleft and removes the focus of shearing stress. An incision lateral to the intergluteal cleft is therefore preferred, especially given the poor healing of midline incisions in this region. A minimally invasive surgical technique, was developed in Israel by Moshe Gips et al.,2008.[12] In this procedure, trephines or biopsy punches which only “core out” and remove the diseased tissue and cyst are used, leaving only small holes to heal. Work or school activities will be resumed in one or two days, without or with minimal postoperative pain. The procedure has been slightly modified and perfected in Rome (Italy) by Prof. L. Basso. An attractive minimally invasive technique is to treat pilonidal sinus with fibrin glue. This technique is less painful than traditional excisional techniques and flaps, can be performed under local or general anaesthesia, does not require dressings or packing and allows return to normal activities within 1 to 2 days. Long term outcome and recurrence rates are not dissimilar to more invasive techniques in 5 year follow up in a small randomised controlled trial.[13][14][15][16] Fibrin glue has also been shown to be better than more invasive alternatives in the treatment of pilonidal sinus disease in children, where a quick return to normal activities and minimal postoperative pain are especially important[17]

Etymology[edit]

Pilonidal cyst with abscess
Pilonidal cyst W abscess · Pilonidal sinus w abscess · Pilonidal sinus with abscess…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pilonidal cyst without abscess
Parasacral dimple · Pilonidal dimple · Postanal dimple · Pilonidal cyst NOS · Cyst – pilonidal · Pilonidal cyst · Pilonidal cyst, recurrent or chronic, without abscess · Pilonidal cyst, recurrent or chronic, wo abscess · Recurrent or chronic pilonidal cyst without abscess · Recurrent pilonidal cyst · Sacral dimple · A hair-containing cyst or sinus, occurring chiefly in the coccygeal region. · A sacral dimple, or pilonidal dimple, is a small hollow area or sinus present at birth and located just above the crease of the buttocks. In most cases, pilonidal dimples are benign and may just be accompanied by increased hair growth in the area. · Cyst (colloid) (mucous) (simple) (retention) pilonidal (infected) (rectum) L05.91…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pilonidal cyst with abscess
Parasacral dimple with abscess · Pilonidal abscess · Pilonidal dimple with abscess · Postanal dimple with abscess · Pilonidal cyst w abscess · Abscess (connective tissue) (embolic) (fistulous) (infective) (metastatic) (multiple) (pernicious) (pyogenic) (septic) L02.91 pilonidal L05.01 Cyst (colloid) (mucous) (simple) (retention) pilonidal (infected) (rectum) L05.91 with abscess L05.01…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pilonidal cyst without mention of abscess
Cyst – pilonidal · Dimple, sacral, w/o abscess · Pilonidal cyst · Pilonidal cyst, recurrent or chronic, without abscess · Pilonidal cyst, recurrent or chronic, wo abscess · Recurrent or chronic pilonidal cyst without abscess · Recurrent pilonidal cyst · Sacral dimple · Sacral dimple without abscess…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pilonidal sinus with abscess
Coccygeal fistula with abscess · Coccygeal sinus with abscess · Pilonidal fistula with abscess · Pilonidal sinus w abscess · Sinus – see also Fistula pilonidal (infected) (rectum) L05.92 with abscess L05.02…
This code is a specific code that can be used to specify a diagnosis or procedure.

Pilonidal sinus without abscess
Coccygeal fistula · Coccygeal sinus without abscess · Pilonidal fistula · A hair-containing cyst or sinus, occurring chiefly in the coccygeal region. · Sinus – see also Fistula pilonidal (infected) (rectum) L05.92…

Pheochromocytoma D35.0, C74.1

Pheochromocytoma

From Wikipedia, the free encyclopedia
Pheochromocytoma/Phaeochromocytoma
Pheochromocytoma high mag.jpg

High magnification micrograph of a pheochromocytoma, showing the nested arrangement of cells (Zellballen) and stippled chromatin. H&E stain.
Classification and external resources
Specialty Oncology
ICD10 D35.0, C74.1
ICD9-CM 227.0, 194.0, 255.6
ICD-O M8700/0
OMIM 171300
DiseasesDB 9912
MedlinePlus 000340
eMedicine med/1816 radio/552 ped/1788
Patient UK Pheochromocytoma
MeSH D010673

A pheochromocytoma (from Greek phaios “dark”, chroma “color”, kytos “cell”, -oma “tumor”) or phaeochromocytoma (PCC) is a neuroendocrine tumor of the medulla of the adrenal glands (originating in thechromaffin cells), or extra-adrenal chromaffin tissue that failed to involute after birth,[1] that secretes high amounts of catecholamines, mostly norepinephrine, plus epinephrine to a lesser extent.[2] Extra-adrenalparagangliomas (often described as extra-adrenal pheochromocytomas) are closely related, though less common, tumors that originate in the ganglia of the sympathetic nervous system and are named based upon the primary anatomical site of origin.

Signs and symptoms[edit]

The signs and symptoms of a pheochromocytoma are those of sympathetic nervous system hyperactivity,[3] including:

A pheochromocytoma can also cause resistant arterial hypertension. A pheochromocytoma can be fatal if it causes a hypertensive emergency, that is, severely high blood pressure that impairs one or more organ systems (formerly called “malignant hypertension”). This hypertension is not well controlled with standard blood pressure medications.

Not all patients experience all of the signs and symptoms listed. The most common presentation is headache, excessive sweating, and increased heart rate, with the attack subsiding in less than one hour.

Tumors may grow large, but most are smaller than 10 centimetres (4 in).

Cause[edit]

Up to 25% of pheochromocytomas may be familial. Mutations of the genes VHL, RET, NF1 (Gene 17 Neurofibromatosis type 1), SDHB and SDHD are all known to cause familial pheochromocytoma, therefore this disease may be accompanied by Von Hippel–Lindau disease, neurofibromatosis,[4] or familial paraganglioma depending on the mutation.

Pheochromocytoma is a tumor of the multiple endocrine neoplasia syndrome, type IIA and type IIB (also known as MEN IIA and MEN IIB, respectively). The other component neoplasms of that syndrome include parathyroid adenomas, and medullary thyroid cancer.Mutations in the autosomal RET proto-oncogene drives these malignancies.[5] Common mutations in the RET oncogene may also account for medullary sponge kidney as well.[6]

Pheochromocytoma linked to MEN II can be caused by RET oncogene mutations. Both syndromes are characterized by pheochromocytoma as well as thyroid cancer (thyroid medullary carcinoma). MEN IIA also presents with hyperparathyroidism, while MEN IIB also presents with mucosal neuroma.

Diagnosis[edit]

Histopathology of adrenal pheochromocytoma. Adrenectomy specimen.

Pheochromocytoma (dark circular shadow near body center) localized byMIBG scintigraphy. Front and back views also show radioiodine collection in thyroid (neck) and bladder (pelvis)

The diagnosis can be established by measuring catecholamines and metanephrines in plasma (blood) or through a 24-hour urine collection. Care should be taken to rule out other causes of adrenergic (adrenalin-like) excess like hypoglycemia, stress, exercise, and drugs affecting the catecholamines like stimulants, methyldopa, dopamine agonists, or ganglion blocking antihypertensives. Various foodstuffs (e.g. coffee, tea, bananas, chocolate, cocoa, citrus fruits, and vanilla) can also affect the levels of urinary metanephrine and VMA (vanillylmandelic acid).[7]

Imaging by computed tomography or a T2 weighted MRI of the head, neck, and chest, and abdomen can help localize the tumor. Tumors can also be located using an MIBG scan, which is scintigraphy using iodine-123-marked metaiodobenzylguanidine. Even finer localization can be obtained in certain PET scan centers using PET-CT or PET-MRI with [18F] fluorodopamine[8] or FDOPA.[9]

Pheochromocytomas occur most often during young-adult to mid-adult life.

These tumors can form a pattern with other endocrine gland cancers which is labeled multiple endocrine neoplasia (MEN). Pheochromocytoma may occur in patients with MEN 2 and MEN 3 (MEN 2B). Von Hippel Lindau patients may also develop these tumors.[10]

Patients experiencing symptoms associated with pheochromocytoma should be aware that it is rare. However, it often goes undiagnosed until autopsy; therefore patients might wisely choose to take steps to provide a physician with important clues, such as recording whether blood pressure changes significantly during episodes of apparent anxiety.

Testing[edit]

  • Blood tests: Buters and others have suggested that analysis of free metanephrines (metadrenalines) (normetanephrine and metanephrine) in blood plasma is the most accurate test for detecting pheochromocytoma.
  • Urine tests: Although this test is slightly less effective than plasma testing it is still considered highly effective in diagnosis. Usually the metabolites of norepinephrine and epinephrine, normetanephrine (NMN) andmetanephrine (MN), are found in relatively small amounts in normal humans. The increased excretion of these metabolites is indicative of the disease, but does not completely rule out other diseases which may cause the same excretion values.
  • Other Tests:
  • One diagnostic test used in the past for a pheochromocytoma is to administer clonidine, a centrally-acting alpha-2 agonist used to treat high blood pressure. Clonidine mimics catecholamines in the brain, causing it to reduce the activity of the sympathetic nerves controlling the adrenal medulla. A healthy adrenal medulla will respond to the clonidine suppression test by reducing catecholamine production; the lack of a response is evidence of pheochromocytoma.

Tumor location[edit]

In adults, approximately 80% of pheochromocytomas are unilateral and solitary, 10% are bilateral, and 10% are extra-adrenal. In children, a quarter of tumors are bilateral, and an additional quarter are extra-adrenal. Solitary lesions inexplicably favor the right side. Although pheochromocytomas may grow to large size (>3 kg), most weigh <100 g and are <10 cm in diameter. Pheochromocytomas are highly vascular.

The tumors are made up of large, polyhedral, pleomorphic chromaffin cells. Fewer than 10% of these tumors are malignant. As with several other endocrine tumors, malignancy cannot be determined from the histologic appearance; tumors that contain large number of aneuploid or tetraploid cells, as determined by flow cytometry, are more likely to recur. Local invasion of surrounding tissues or distant metastases indicate malignancy.

Extra-adrenal pheochromocytomas: Extra-adrenal pheochromocytomas usually weigh 20 to 40 g and are <5 cm in diameter. Most are located within the abdomen in association with the celiac, superior mesenteric, and inferior mesenteric ganglia and the organ of Zuckerkandl. Approximately 10% are in the thorax, 1% are within the urinary bladder, and less than 3% are in the neck, usually in association with the sympathetic ganglia or the extracranial branches of the ninth cranial nerves.

Differential diagnosis[edit]

The differential diagnoses of pheochromocytoma include:

Treatment[edit]

Surgical resection of the tumor is the treatment of first choice, either by open laparotomy or laparoscopy.[13] Given the complexity of perioperative management, and the potential for catastrophic intra and postoperative complications, such surgery should be performed only at centers experienced in the management of this disorder. In addition to the surgical expertise that such centers can provide, they will also have the necessary endocrine and anesthesia resources. It may also be necessary to carry out adrenalectomy, a complete surgical removal of the affected adrenal gland(s).

Either surgical option requires prior treatment with the non-specific and irreversible alpha adrenoceptor blocker phenoxybenzamine or a short acting alpha antagonist (e.g. prazosin, terazosin, or doxazosin).[14] Doing so permits the surgery to proceed while minimizing the likelihood of severe intraoperative hypertension (as might occur when the tumor is manipulated). Some authorities would recommend that a combined alpha/beta blocker such as labetalol also be given in order to slow the heart rate. Regardless, a beta-1 receptor selective beta blocker such as atenolol must never be used in the presence of a pheochromocytoma due to the risk of such a treatment leading to unopposed alpha agonism and, thus, severe and potentially refractory hypertension. However some clinical guidelines permit beta-1 blockade use together with alpha blockers during surgery for control of tachycardia.

The patient with pheochromocytoma is invariably volume depleted. In other words, the chronically elevated adrenergic state characteristic of an untreated pheochromocytoma leads to near-total inhibition of reninangiotensin activity, resulting in excessive fluid loss in the urine and thus reduced blood volume. Hence, once the pheochromocytoma has been resected, thereby removing the major source of circulating catecholamines, a situation arises where there is both very low sympathetic activity and volume depletion. This can result in profound hypotension. Therefore, it is usually advised to “salt load” pheochromocytoma patients before their surgery. This may consist of simple interventions such as consumption of high salt food pre-operatively, direct salt replacement or through the administration of intravenous saline solution.

Malignant neoplasm of medulla of unspecified adrenal gland
Adrenal medulla cancer · Cancer, adrenal medulla · Cancer, pheochromocytoma · Malignant pheochromocytoma · Primary malignant neoplasm of adrenal medulla · Pheochromoblastoma unspecified site C74.10Pheochromocytoma malignant unspecified site C74.10..

Complications[edit]

Hypertension secondary to endocrine disorders
Hypertension, hypertensive (accelerated) (benign) (essential) (idiopathic) (malignant) (systemic) I10 due to endocrine disorders I15.2 pheochromocytoma I15.2 secondary NEC I15.9 due to endocrine disorders I15.2pheochromocytoma I15.2…

History of Illness 52 year old male code?

History of illness the patient is a 52-year-old male who was involved in an interpersonal altercation at approximately 1:30 AM in the morning he presented to the emergency department with complaints of pain and swelling to the right side of his face the patient had been struck multiple times by the butt end of a handgun he denied loss of consciousness the attack was witnessed in the witnesses also claimed there was no loss of consciousness he presented with pain and swelling to the right side of his face in the temporal region and in the right eye region he had a small abrasion to the top of his head and on his right for had no lacerations were noted he had no diplopia the past medical history and past surgical history were noncontributory the patient was talking and conscious. Taking no medications and had no allergies

hospital course admission x-rays and CT scan revealed a non-this displaced right zygoma fracture and an orbital floor fracture with slight limitation on physical examination of his upward gaze he was taken to the operating room for exploration and for placement of a silastic implant to the right orbital floor fracture which is accomplished without difficulty and without complication the patient tolerated the procedure well postoperative course was uncomplicated received IV antibiotics throughout his stay at the hospital

final diagnosis right orbital fracture right zygoma fracture abrasion to the head

ICD-9 CM principal diagnosis in code right orbital fracture 802.6 fracture orbit floor

ICD-9-CM 802.6 converts approximately to:

2016 ICD-10-CM S02.3XXA Fracture of orbital floor, initial encounter for closed fracture

Note: approximate conversions between ICD-9-CM codes and ICD-10-CM codes may require clinical interpretation in order to determine the most appropriate conversion code(s) for your specific coding situation.

Source: 2016 ICD-10-CM CMS General Equivalence Mappings.

ICD-9-CM other diagnosis and codes right zygoma fracture 802.4 fracture zygoma

ICD-9-CM 802.4 converts approximately to:

2016 ICD-10-CM S02.400A Malar fracture unspecified, initial encounter for closed fracture

or:

2016 ICD-10-CM S02.401A Maxillary fracture, unspecified, initial encounter for closed fracture

or:

2016 ICD-10-CM S02.402A Zygomatic fracture, unspecified, initial encounter for closed fracture

Note: approximate conversions between ICD-9-CM codes and ICD-10-CM codes may require clinical interpretation in order to determine the most appropriate conversion code(s) for your specific coding situation.

Source: 2016 ICD-10-CM CMS General Equivalence Mappings

abrasion to the head 910.0 injury superficial head

ICD-9-CM 910.0 converts approximately to:

2016 ICD-10-CM S00.01XA Abrasion of scalp, initial encounter

or:

2016 ICD-10-CM S00.31XA Abrasion of nose, initial encounter

or:

2016 ICD-10-CM S00.419A Abrasion of unspecified ear, initial encounter

or:

2016 ICD-10-CM S00.511A Abrasion of lip, initial encounter

or:

2016 ICD-10-CM S00.512A Abrasion of oral cavity, initial encounter

or:

2016 ICD-10-CM S00.91XA Abrasion of unspecified part of head, initial encounter

or:

2016 ICD-10-CM S10.11XA Abrasion of throat, initial encounter

or:

2016 ICD-10-CM S10.91XA Abrasion of unspecified part of neck, initial encounter

Note: approximate conversions between ICD-9-CM codes and ICD-10-CM codes may require clinical interpretation in order to determine the most appropriate conversion code(s) for your specific coding situation.

Source: 2016 ICD-10-CM CMS General Equivalence Mappings.

assault by striking E96 8.2 index to external causes assault weapon blonde

ICD-9 procedure codes 76.92 implant implant facial bone synthetic alloplastic

ICD 10 CM diagnosis codes as S02.3XXA fracture traumatic orbit floor blowout

2016 ICD-10-CM Code S02.3XXA[convert to ICD-9-CM]

Fracture of orbital floor, initial encounter for closed fracture

S02.44XA fracture traumatic zygoma not found

S00.01XA abrasion scalp 2016 ICD-10-CM Code S00.01XA[convert to ICD-9-CM]

Abrasion of scalp, initial encounter

S00.81XA abrasion for head 2016 ICD-10-CM Code S00.81XA[convert to ICD-9-CM]

Abrasion of other part of head, initial encounter

Y00.XXXA index to external causes assault weapon Blunt 2016 ICD-10-CM Code Y00.XXXA[convert to ICD-9-CM]

Assault by blunt object, initial encounter

CPT code 2016 would range 70010-76499Diagnostic Radiology (Diagnostic Imaging) Procedures

CT of head with contrast 70460

CT of head with contrast 70450

CT of head with and without contrast 70470

ICD-10 CM must do!

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