PECOBAAN

Posted on Jumat, 13 Mei 2011

Pneumonia can be generally defined as inflammation of the lung parenchyma, in which consolidation of the affected part and a filling of the alveolar air spaces with exudate, inflammatory cells, and fibrin is characteristic.[1] Infection by bacteria or viruses is the most common cause, although inhalation of chemicals, trauma to the chest wall, or infection by other infectious agents such as rickettsiae, fungi, and yeasts may occur.[1] (See images below.)
Bacterial pneumonia is caused by a pathogenic infection of the lungs and may present as a primary disease process or as the final coup de grace in the individual who is already debilitated. For example, historical review of the 1918-19 influenza pandemic suggests that the majority of deaths were not a direct effect of the influenza virus, but they were from bacterial coinfection.[2]

Discussion of bacterial pneumonia involves classification and categorization schemes based on various characteristics of the illness, such as anatomic or radiologic distribution, the setting, or mechanism of acquisition, and the pathogen responsible. A major part of what distinguishes these various categories from each other is the varying risk of exposure to multidrug-resistant (MDR) organisms

Bacterial Pneumonia

Posted on Rabu, 11 Mei 2011

Pneumonia can be generally defined as inflammation of the lung parenchyma, in which consolidation of the affected part and a filling of the alveolar air spaces with exudate, inflammatory cells, and fibrin is characteristic.^[1]Infection by bacteria or viruses is the most common cause, although inhalation of chemicals, trauma to the chest wall, or infection by other infectious agents such as rickettsiae, fungi, and yeasts may occur.^[1](See images below.)
Bacterial pneumonia is caused by a pathogenic infection of the lungs and may present as a primary disease process or as the final coup de grace in the individual who is already debilitated. For example, historical review of the 1918-19 influenza pandemic suggests that the majority of deaths were not a direct effect of the influenza virus, but they were from bacterial coinfection.^[2]
Discussion of bacterial pneumonia involves classification and categorization schemes based on various characteristics of the illness, such as anatomic or radiologic distribution, the setting, or mechanism of acquisition, and the pathogen responsible. A major part of what distinguishes these various categories from each other is the varying risk of exposure to multidrug-resistant (MDR) organisms.^{[3, 4, 5]}
Anatomic or radiologic distribution of pneumonia includes the following (see Chest Radiography for details):

Lobar - Known as focal or nonsegmental pneumonia (see the images below)
Multifocal/lobular (bronchopneumonia)
Interstitial (focal diffuse)Bacterial pneumonia. Radiographic images in a patient with right upper lobe pneumonia. Note the increased anteroposterior chest diameter, which is suggestive of chronic obstructive pulmonary disease (COPD). Bacterial pneumonia. Radiographic images in a patient with bilateral lower lobe pneumonia. Note the spine sign, or loss of progression of radiolucency of the vertebral bodies Bacterial pneumonia. Radiographic images in a patient with early right middle lobe pneumonia.

The setting of pneumonia includes the community, Institutional (healthcare/nursing home setting), and nosocomial (hospital).

Community-acquired pneumonia

Community-acquired pneumonia (CAP) is defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital. CAP should not meet the criteria for healthcare-associated pneumonia (HCAP), as defined below.
Go to Community-Acquired Pneumonia for complete information on this topic.

Institutional-acquired pneumonia

Institutional-acquired pneumonia (IAP) includes HCAP and nursing home–associated pneumonia (NHAP).
HCAP is defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital in patients with increased risk of exposure to MDR bacteria as a cause of infection. Risk factors for exposure to MDR bacteria in HCAP include the following:

Hospitalization for 2 or more days in an acute care facility within 90 days of current illness
Exposure to antibiotics, chemotherapy, or wound care within 30 days of current illness
Residence in a nursing home or long-term care facility
Hemodialysis at a hospital or clinic
Home nursing care (infusion therapy, wound care)
Contact with a family member or other close person with infection due to MDR bacteria

NHAP is generally included in the category of HCAP because of the high incidence of infection with gram-negative bacilli and Staphylococcus aureus. However, some authors accept NHAP as a separate entity because of distinct epidemiologic associations with infection in nonhospital healthcare settings.^[1]Pneumonia in patients in nursing homes and long-term care facilities has been associated with greater mortality than in patients with CAP. These differences may be due to factors such as disparities in functional status, likelihood of exposure to infectious agents, and variations in pathogen virulence, among others.
It is important to note that nursing home patients with pneumonia are less likely to present with classic signs and symptoms of the typical pneumonia presentation, such as fever, chills, chest pain, and productive cough, but instead these individuals often have delirium and altered mental status. Thus, the degree to which the HCAP definition applies to such settings is not yet clear.^{[3, 4]}
Go to Nursing Home Acquired Pneumonia for complete information on this topic.

Nosocomial pneumonia

Nosocomial infections are generally described as those acquired in the hospital setting. The term nosocomial pneumonia has evolved into the more succinct clinical entities of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP); however, the term nosocomial pneumonia still has an appropriate place in the descriptive language of pneumonia. Nosocomial infections have been viewed as a "tribute to pay to the more aggressive management of the population, characterized by the use of sophisticated technologies and invasive devices," an important consideration in the pulmonary care of critically ill patients.^[6]
Go to Ventilator-Associated Pneumonia and Nosocomial Pneumonia for complete information on these topics.

Hospital-acquired pneumonia

HAP is defined as pneumonia that develops at least 48 hours after admission to a hospital and, as in HCAP, is characterized by increased risk of exposure to MDR organisms,^[3]as well as gram-negative organisms.^[7]Risk factors for exposure to such organisms in HAP include the following^[3]:

Antibiotic therapy within 90 days of the hospital-acquired infection
Current length of hospitalization of 5 days or more
High frequency of antibiotic resistance in the local community or within the specific hospital unit
Immunosuppressive disease or therapy
Presence of HCAP risk factors for exposure to MDR bacteria

Common mechanisms for the acquisition of pneumonia include ventilator use and aspiration.

Ventilator-associated pneumonia

VAP is defined as pneumonia that develops more than 48 hours after endotracheal intubation or within 48 hours of extubation. Risk factors for exposure to MDR bacteria that cause VAP are the same as those for HCAP and/or HAP.^{[3, 5]}VAP may occur in as many as 10-20% of patients who are on ventilators for more than 48 hours.^[8]
Go to Ventilator-Associated Pneumonia for complete information on this topic.

Aspiration pneumonia

Aspiration pneumonia develops after the inhalation of oropharyngeal secretions and colonized organisms. Although organisms frequently implicated in CAP, such as Haemophilus influenzae and Streptococcus pneumoniae, can colonize the nasopharynx and oropharynx and their aspiration can contribute to the development of CAP, the term aspiration pneumonia refers specifically to the development of an infectious infiltrate in patients who are at increased risk of oropharyngeal aspiration.
Patients may be at increased risk of aspiration and/or the development of aspiration pneumonia for a number of reasons, as follows:

Decreased ability to clear oropharyngeal secretions - Poor cough or gag reflex, impaired swallowing mechanism (eg, dysphagia in stroke patients), impaired ciliary transport (eg, from smoking)
Increased volume of secretions
Increased bacterial burden of secretions
Presence of other comorbidities - Anatomic abnormalities, gastroesophageal reflux disease (GERD), achalasia.

Critically ill patients are at notably increased risk of aspiration due to the following:

The challenge of appropriate, risk-minimizing positioning
Gastroparesis/dysmotility
Impaired cough/gag/swallow reflexes (illness- or drug-induced)
Impaired immune response
Intubation/extubation

Historically, the bacteria implicated in aspiration pneumonia have been the anaerobic oropharyngeal colonizers such as Peptostreptococcus, Bacteroides, Fusobacterium, and Prevotella species. However, now evident is that the vast majority of cases of aspiration pneumonia result from the same pathogens implicated in CAP and HAP, depending on the setting in which the aspiration event occurred. The clinical course of aspiration pneumonia is, thus, similar to that of CAP or HAP.^[9]However, recurrence of aspiration pneumonia is common unless the risk factors for underlying aspiration are treated or minimized.
Go to Aspiration Pneumonia for complete information on this topic.

Pathophysiology

The causes for the development of pneumonia are extrinsic or intrinsic, and various bacterial causes are noted. Extrinsic factors include exposure to a causative agent, exposure to pulmonary irritants, or direct pulmonary injury. Intrinsic factors are related to the host. Loss of protective upper airway reflexes allows aspiration of contents from the upper airways into the lung. Various causes for this loss include altered mental status due to intoxication and other metabolic states and neurologic causes, such as stroke and endotracheal intubation.
Bacteria from the upper airways or, less commonly, from hematogenous spread, find their way to the lung parenchyma. Once there, a combination of factors (including virulence of the infecting organism, status of the local defenses, and overall health of the patient) may lead to bacterial pneumonia. The patient may be made more susceptible to infection because of an overall impairment of the immune response (eg, human immunodeficiency virus [HIV] infection, chronic disease, advanced age) and/or dysfunction of defense mechanisms (eg, smoking, chronic obstructive pulmonary disease [COPD], tumors, inhaled toxins, aspiration). Poor dentition or chronic periodontitis is another predisposing factor.
Thus, during pulmonary infection, acute inflammation results in the migration of neutrophils out of capillaries and into the air spaces, forming a marginated pool of neutrophils that is ready to respond when needed. These neutrophils phagocytize microbes and kill them with reactive oxygen species, antimicrobial proteins, and degradative enzymes; they also extrude a chromatin meshwork containing antimicrobial proteins that trap and kill extracellular bacteria, known as neutrophil extracellular traps (NETs). Various membrane receptors and ligands are involved in the complex interaction between microbes, cells of the lung parenchyma, and immune defense cells.^[10]

Bacterial virulence

General mechanisms of increased virulence include the following:

Genetic flexibility allowing the development of resistance to various classes of antibiotics
Flagellae and other bacterial appendages that facilitate spread of infection
Capsules resistant to attack by immune defense cells and that facilitate adhesion to host cells
Quorum sensing systems allow coordination of gene expression based on complex cell-signaling for adaptation to the local cellular environment
Iron scavenging

The following are examples of organism-specific virulence factors:

Streptococcus pneumoniae – Pneumolysin, a multifunctional virulence factor, is cytotoxic to respiratory epithelium and endothelium by disrupting pulmonary tissue barriers. This factor directly inhibits immune and inflammatory cells and activates complement, decreasing the clearance of the bacteria from the lung.^[11]
Pseudomonas aeruginosa - Pili play important role in the attachment to host cells. A type III secretion system allows injection of toxins into host cells.^[12]

Host resistance

Deficits in various host defenses and an inability to mount an appropriate acute inflammatory response can predispose patients to infection, as follows^[10]:

Deficits in neutrophil quantity, as in neutropenia
Deficits in neutrophil quality, as in chronic granulomatous disease
Deficiencies of complement
Deficiencies of immunoglobulins

Viral infection

With the recent H1N1 influenza virus pandemic, it is important to address the role that viral infection can have in bacterial pneumonia.
The association between infection with influenza virus and subsequent bacterial pneumonia became particularly apparent following the 1918 influenza pandemic, during which approximately 40-50 million people died.^[13]Historical investigations and current researchers argue that the vast majority of pulmonary-related deaths from past pandemic influenza viruses, most notably the pandemic of 1918, ultimately resulted from bacteriologic secondary or coinfection and poorly understood interactions between the infecting viral and bacterial organisms.^[14]Although influenza virus is the most commonly thought of agent in this co-infective context, other respiratory viruses, such as respiratory syncytial virus (RSV), parainfluenza viruses, adenovirus, and rhinoviruses, may also predispose to secondary bacterial infection.^[13]
The classic explanation behind the viral-bacterial interplay focuses on the disruption of the respiratory epithelium by the virus, clearing the way for bacterial infection. However, evidence depicts much more complex and possibly synergistic interactions between viruses and bacteria, including alteration of pulmonary physiology, downregulation of the host immune defense, changes in expression of receptors to which bacteria adhere, and enhancement of the inflammatory process.^[13]

Etiology

Although pneumonia may be caused by myriad pathogens, a limited number of agents are responsible for most cases,^{[15, 16, 17, 18]}Most authors categorize bacterial pneumonias by their infectious agents, which include pneumococcal agents; Haemophilus influenzae; Klebsiella, Staphylococcus, and Legionella species; gram-negative organisms; and aspirated materials. Inhalation of infectious aerosols is probably the most common mode of infection. Some agents, notably Staphylococcus species, may be spread hematogenously.

Risk factors

Coinfection with H1N1 influenza increases the risk of secondary bacterial pneumonia, with S pneumoniae the most likely coinfection.^[19]However, pregnant patients with H1N1 influenza in the 2009 pandemic were at increased risk of developing secondary Klebsiella pneumonia with poor clinical outcome.^[20]
Other risk factors include local lung pathologies (eg, tumors, chronic obstructive pulmonary disease [COPD], bronchiectasis), chronic gingivitis and periodontitis, and smoking, which impair resistance to infection. Furthermore, any individual with an altered sensorium (eg, seizures, alcohol or drug intoxication) or central nevous system (CNS) impairment (eg, stroke) may have a reduced gag reflex, which allows aspiration of stomach or oropharyngeal contents and which enables aspiration pneumonias.

Typical organisms

Although several of the organisms discussed in this section may be implicated in pneumonia, only a few of them are responsible for the vast majority of cases.
Gram-positive bacteria that can cause pneumonia include the following:

Streptococcus pneumoniae: This organism is a facultative anaerobe identified by its chainlike staining pattern. Pneumococcosis is by far the most common cause of typical bacterial pneumonia.
Staphylococcus aureus: S aureus is a facultative anaerobe identified by its clusterlike staining pattern. S aureus pneumonia is observed in intravenous drug abusers (IVDAs) and other individuals with debilitations. In patients who abuse intravenous drugs, the infection probably is spread hematogenously to the lungs from contaminated injection sites. Methicillin-resistant S aureus (MRSA) has had a large impact on empiric antibiotic choices at many institutions.
Enterococcus (E faecalis, E faecium): These organisms are group D streptococci that are well-known normal gut florae that can be identified by their pair-and-chain staining pattern. The emergence of vancomycin-resistant Enterococcus (VRE) is indicative of the importance of appropriate antibiotic use.
Actinomyces israelii: This is a beaded, filamentous anaerobic organism that grows as normal flora in the gastrointestinal (GI) tract. A israelii is known to form abscesses and sulfur granules.
Nocardia asteroides: N asteroides is a weakly gram-positive, partially acid-fast bacillus (AFB) that forms beaded, branching, thin filaments. It is known to cause lung abscesses and cavitations. Erosion into the pleura can also occur, resulting in hematologic spread of the organism.

Gram-negative pneumonias occur most often in individuals who are debilitated, immunocompromised, or recently hospitalized. Individuals living in long-term care facilities where other residents are intubated are also at risk for these infections. Gram-negative bacteria include the following:

Pseudomonas aeruginosa: P aeruginosa is an aerobic, motile bacillus often characterized by its distinct (grapelike) odor.
Klebsiella pneumoniae: K pneumoniae is a facultatively anaerobic, encapsulated bacillus that can lead to an aggressive, necrotizing, lobar pneumonia. Patients with chronic alcoholism, diabetes, or COPD are at increased risk.
Haemophilus influenzae: H influenzae is an aerobic bacillus that comes in both encapsulated and nonencapsulated forms. Several major subtypes have been identified, which have varying levels of pathogenicity; encapsulated type B (HiB) is known to be particularly virulent, although routine vaccination against this subtype has decreased the prevalence of severe disease caused by H influenzae.
Escherichia coli: E coli is a facultatively anaerobic, motile bacillus; it is well known to colonize the lower GI tract and produce the essential vitamin K.
Moraxella catarrhalis: M catarrhalis is an aerobic diplococcus known as a common colonizer of the respiratory tract.
Acinetobacter baumannii: A baumannii is a pathogen that has been well described in the context of ventilator-associated pneumonia (VAP).
Francisella tularensis: F tularensis is the causative agent of tularemia, or rabbit fever. F tularensis is a facultative intracellular bacterium that multiplies within macrophages and that is typically transmitted to humans via a tick bite; its reservoir animals include rodents, rabbits, and hares. F tularensis can also be transmitted in an airborne manner or contracted from handling dead, infected animals. It is commonly spoken of in terms of its potential use as a biologic weapon.^[21]
Bacillus anthracis: B anthracis is the agent responsible for inhalational anthrax.
Yersinia pestis: Y pestis infection is better known as the black plague, but other members of the Yersinia family are responsible for a wide variety of infectious presentations.

Atypical organisms

Atypical organisms are generally associated with a milder form of pneumonia, the so-called "walking pneumonia." A feature that makes these organisms atypical is the inability to detect them on Gram stain or to cultivate them in standard bacteriologic media.^{[15, 16]}Atypical organisms include the following:

Mycoplasma species: The mycoplasmas are the smallest known free-living organisms in existence; they lack cell walls (and therefore are not apparent after Gram stain) but have protective 3-layered cell membranes.
Chlamydophila species (C psittaci, C pneumoniae): Psittacosis, also known as parrot disease or parrot fever, is caused by C psittaci and is associated with the handling of various types of birds.
Legionella species: Legionella species are gram-negative bacteria found in freshwater and are known to grow in complex water distribution systems. Institutional water contamination is frequently noted in endemic outbreaks. Legionella species are the causative agents of Legionnaires disease.
Coxiella burnetii:C burnetii is the causative agent of Q fever. It is spread from animals to humans; person-to-person transmission is unusual. Animal reservoirs typically include cats, sheep, and cattle.
Bordetella pertussis:B pertussis is the agent responsible for pertussis or whooping cough.

Anaerobic organisms

Pneumonia due to anaerobes typically results from aspiration of oropharyngeal contents, as previously mentioned. These infections tend to be polymicrobial and may consist of the following anaerobic species, some of which have already been discussed above: Klebsiella, Peptostreptococcus, Bacteroides, Fusobacterium, and Prevotella.

source : emedicine.medscape.com

Pneumococcal Infections

Streptococcus pneumoniae is a gram-positive, catalase-negative cocci that has remained an extremely important human bacterial pathogen since its initial recognition in the late 1800s. The term pneumococcus gained widespread use by the late 1880s, when it was recognized as the most common cause of bacterial lobar pneumonia.
Worldwide, S pneumoniae remains the most common cause of community-acquired pneumonia (CAP), bacterial meningitis, bacteremia, and otitis media. S pneumoniae infection is also an important cause of sinusitis, septic arthritis, osteomyelitis, peritonitis, and endocarditis and an infrequent cause of other less-common diseases.
An image depicting pneumococcal pneumonia can be seen below.

Lobar consolidation with pneumococcal pneumonia. Posteroanterior film. Courtesy of R. Duperval, MD. Pneumococcal vaccination, particularly routine childhood pneumococcal conjugate vaccine (introduced in the United States in 2000), has led to decreased rates of invasive pneumococcal infections (>90%) caused by pneumococcal serotypes covered by the vaccine, as well as overall decreased rates of invasive disease (45% overall; 77% in children < 5 y). In addition, herd immunity has led to decreased rates of disease in older children and adults.^{[1, 2, 3]}
Many subsequent studies have shown increased rates of invasive and noninvasive disease caused by serotypes not covered by the vaccine, including serotypes 15, 19A, and 33F. Serotype 19A has received the most attention, not only because of increased disease rates associated with this serotype but also because of its increased association with drug resistance. Increased rates of invasive disease with such serotypes have caused the overall rates of invasive disease to remain somewhat steady since 2002, although still greatly reduced from rates prior to introduction of the conjugate vaccine.^{[1, 4, 5, 6, 7, 8, 9, 10, 3]}
Data from 2006-2007 revealed that only 2% of invasive pneumococcal disease in children younger than 5 years in the United States was caused by serotypes contained in pneumococcal conjugate vaccine 7 (PCV7), while an additional 6 serotypes accounted for almost two thirds of invasive disease in this age group.^[11]Development of a vaccine containing additional serotypes continued, and pneumococcal conjugate vaccine 13 (PCV13) was approved by the FDA February 24, 2010.^[12]
Despite an overall decreased incidence of otitis media caused by serotypes not covered by vaccination since the introduction of the conjugate pneumococcal vaccine, an increase in rates of disease caused by serotypes not covered by the vaccine has occurred, as well as an increase in rates of diseases caused by vaccine-covered serotypes in incompletely immunized children. The incidence of otitis media caused by serotype 19F has remained steady. Overall health care utilization for otitis media has decreased, as has the incidence of recurrent otitis media in some populations and studies.^{[2, 13, 14, 15]}

Pathophysiology

Adherence and invasion

S pneumoniae is an example of a typical extracellular bacterial pathogen. Pathogenicity requires adherence to host cells, along with the ability to replicate and to escape clearance and/or phagocytosis. The organism must then gain access to areas where it can manifest infection, either via direct extension or lymphatic or hematogenous spread.
The rates of pneumococcal colonization in healthy children and adults provide information about the success of adherence and replication of the pneumococcus. After colonization, organisms may gain access to areas of the upper and/or lower respiratory tracts (sinuses, bronchi, eustachian tubes) by direct extension. Under normal conditions in a healthy host, anatomic and ciliary clearance mechanisms prevent clinical infection. However, clearance may be inhibited by chronic (smoking, allergies, bronchitis) or acute (viral infection, allergies) factors, which can lead to infection. Alternatively, pneumococci may reach normally sterile areas, such as the blood, peritoneum, cerebrospinal fluid, or joint fluid, by hematogenous spread after mucosal invasion. In the absence of previously acquired serotype-specific antibodies (see below), clinically apparent infection is likely to occur.

Capsule

Other than some isolates associated with conjunctivitis outbreaks, essentially all clinical isolates of S pneumoniae are encapsulated. Repeating oligosaccharides that make up the capsule of an individual bacterial isolate are transported to the cell surface, where they bind tightly with the cell-wall polysaccharides. Based on antigenic differences within these capsular polysaccharides, 91 serotypes of S pneumoniae have been identified.
The virulence of each organism is determined in part by the makeup and amount of capsule present. In a pneumococcus-naive host (or in the absence of antibody to pneumococcal capsule) host-cell phagocytosis is severely limited because of the inhibition of phagocytosis and the inhibition of the activation of the classic complement pathway. In addition, in vitro and in vivo studies of clinical isolates have shown that pneumococci have the ability to obtain DNA from other pneumococci (or other bacteria) via transformation, allowing them to switch to serotypically distinct capsular types.
There are 2 recognized numbering systems based on pneumococcal serotypes. In the American system, the serotypes were numbered in order of discovery, with lower numbers corresponding to serotypes that more frequently cause clinical disease, meaning that they were identified earlier. The Danish numbering system is based on grouping of serotypes with similar antigenicity and is more widely accepted and used worldwide. Today, serotyping provides important epidemiological information, especially with the increasingly widespread use of vaccination, but rarely provides timely clinical information.
The Quellung reaction is demonstrated by combining sera of previously immunized animals with capsular antigen. Agglutination causes capsule refractility and the ability to observe the capsule microscopically.

Toxins and other virulence factors

Pneumococcal isolates produce few toxins; however, all serotypes produce pneumolysin, which is an important virulence factor that acts as a cytotoxin and activates the complement system. In addition, pneumolysin causes a release of tumor necrosis factor-alpha and interleukin-1.
Other potential virulence factors include cell surface proteins such as surface protein A and surface adhesin A and enzymes such as autolysin, neuraminidase, and hyaluronidase. The contributions of these substances to pneumococcal virulence are being studied extensively, and some are being investigated as potential vaccine constituents.^[16]

Complement activation

Much of the clinical severity of pneumococcal disease is due to the activation of the complement pathways and cytokine release, which induce a significant inflammatory response. S pneumoniae cell wall components, along with the pneumococcal capsule, activate the alternative complement pathway; antibodies to the cell wall polysaccharides activate the classic complement pathway. Cell wall proteins, autolysin, and DNA released from bacterial breakdown all contribute to the production of cytokines, inducing further inflammation.

source : emedicine.medscape.com

SOFTWARE MEMPERCEPAT INTERNET

Posted on Jumat, 06 Mei 2011

Inilah sebuah software mempercepat internet.

SpeedConnect Internet Accelerator adalah sebuah aplikasi Windows yang kuat dirancang untuk mengoptimalkan koneksi jaringan anda dan mempercepat semua aktivitas internet anda. Hal ini berarti koneksi internet lebih cepat, lebih cepat browsing dan email, download yang lebih cepat, lebih cepat game online, meningkatkan koneksi Skype.
Top internet accelerator (menurut PC Magazine), pengaturan jaringan optimasi untuk mempercepat koneksi yang ada Dial-Up Modem, DSL, Cable, Wireless, LAN, internet kecepatan tinggi.
Kecepatan koneksi jaringan Anda tidak hanya tergantung pada kecepatan dari perangkat keras Anda. Windows adalah sistem operasi yang dirancang untuk bekerja pada berbagai hardware yang berbeda dan setup jaringan. Karena sifat abstrak dari sistem operasi, itu tidak dapat dioptimalkan untuk setup hardware pengguna tertentu.
Tergantung pada jenis koneksi jaringan yang Anda miliki, Anda mungkin dapat men-tweak koneksi Anda sehingga kecepatan internet anda, serta jaringan area lokal Anda, akan lebih cepat. Dengan mengubah Registry Sistem dan mengoptimalkan TCP / IP parameter, SpeedConnect dapat menyempurnakan nilai-nilai untuk mengambil keuntungan dari lebih dapat diandalkan, koneksi Internet lebih cepat.

Free Download software

DAEMON TOOLS PRO ADVANCED V 4.10

Bagaimana menginstal:

1. Instal aplikasi menggunakan installer disediakan.

2. Jangan menjalankannya sampai Anda mengubah nama dan menempatkan celah di dir diinstal.

3. Pertama, mengubah nama asli cryptapi.dll dir diinstal ke cryptapi_.dll

4. Kemudian, menempatkan cryptapi.dll retak disediakan dan dtprohlp.dll

5. Jalankan aplikasi dan mendaftar dengan email Anda sendiri dan nama.

6. Aplikasi ini akan offline diaktifkan dan kunci akan dihasilkan berdasarkanpada perangkat keras Anda id.

Sangat mudah dan memerlukan waktu 1 menit!Setelah intsallation berhasil, Anda dapat menggunakannya untuk waktu tak terbatasJika pesan kesalahan mengatakan "tidak dapat menambahkan keistimewaan adaptor tidak cukup" cukup klik kanan dan jalankan sebagai administrator.Jika program ini tidak bekerja pada komputer anda maka itu adalah kesalahan komputer Anda, jangan langsung posting "tidak bekerja atau tidak menginstal"

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SOFTWARE TOTAL RECORD

Records PC audio dari hampir sumber manapun, termasuk streaming audio dari program-program seperti Windows Media Player. Hal ini juga dapat merekam audio konvensional dari CD, mikrofon, dan baris input lainnya pada kartu suara. Rekaman dapat disimpan ke hard drive dalam gelombang (tekanan atau dikompresi), WMA, MP3, FLAC, APE atau Ogg Vorbis format. Versi ini juga menggabungkan fitur luas untuk file editingaudio dan fitur penjadwalan ditingkatkan.

HF RF

ADOBE PHOTOSHOP CS5

Kemarin sempet nyari-nyari software photoshop 5 portable, dan akhirnya ketemu. Kebetulan saya harus menyelesaikan desain dan butuh photoshop. Sebagaimana kita ketahui photoshop merupakan software yang sering digunakan untuk desain grafis. Fitur-fitur yang dimilikinya cukup bagus dan mudah digunakan.

Photoshop portable bisa digunakan tanpa perlu instalasi, tinggal di jalankan saja file aplikasinya. Untuk file yang akan di download nanti berukuran sekitar 60 MB-an dan setelah di download dan kemudian di extract maka ukurannya sekitar 300MB –an.

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CARA MENGUNCI FILE TANPA SOFTWARE

Akhirnya saya punya ide untuk buat artikel baru.....karena komputer saya suka dipake maen game,dan mengerjakan tugas sekolah, jadi saya mencoba bagaimana cara agar file game dan tugas-tugas tersebut hanya saya yang tahu,supaya yang lain tidak bisa membukanya ....alhamdulillah saya temukan caranya.....nyari-nyari cara buat ngunci file eh ketemudeh di salah satu web.........
Nah langsung aja.....rata-rata ketika kita ingin menyimpan data dan memproteksinya kita membutuhkan sebuah software, tapi kali ini berbeda.....dari sebuah notepad bisa membuat hal baru........
Caranya:

1. Buka Notepad anda dan copy paste kode di bawah ini :

cls
@ECHO OFF
title Folder FolderRahasia
if EXIST "Control Panel.{21EC2020-3AEA-1069-A2DD-08002B30309D}" goto UNLOCK
if NOT EXIST FolderRahasia goto MDLOCKER
:CONFIRM
echo Apakah anda ingin mengunci FolderRahasia tersebut ? (Y/N)
set/p "cho=>"
if %cho%==Y goto LOCK
if %cho%==y goto LOCK
if %cho%==n goto END
if %cho%==N goto END
echo Ketik Y atau N.
goto CONFIRM
:LOCK
ren FolderRahasia "Control Panel.{21EC2020-3AEA-1069-A2DD-08002B30309D}"
attrib +h +s "Control Panel.{21EC2020-3AEA-1069-A2DD-08002B30309D}"
echo FolderRahasia Terkunci
goto End
:UNLOCK
echo Masukkan Password untuk membuka kunci
set/p "pass=>"
if NOT %pass%== masukkanpassword goto FAIL
attrib -h -s "Control Panel.{21EC2020-3AEA-1069-A2DD-08002B30309D}"
ren "Control Panel.{21EC2020-3AEA-1069-A2DD-08002B30309D}" FolderRahasia
echo FolderRahasia sudah di buka
goto End
:FAIL
echo Password salah
goto end
:MDLOCKER
md FolderRahasia
echo FolderRahasia Sukses di buat
goto End
:End

2. Anda dapat mengganti tulisan “masukkanpassword” dengan password yang anda inginkan.

3. Save As File tersebut dengan Nama “Kunci.bat” (Tanpa tanda kutip)

4. Klik file Kunci.bat ( Dia akan membuat Folder pribadi dengan nama “FolderRahasia” )

5. Klik kembali file Kunci.bat dan masukkan “y” untuk mengunci folder tersebut.

6. Untuk membuka nya anda bisa mengklik file Kunci.bat kembali dan masukkan password anda.

Selamat mencoba.

Sumber inspirasi http://finderonly.com/2008/08/10/membuat-folder-pribadi-tanpa-menggunakan-software/
disana kalian bakalan dapat info IT yang cukup bagus

Catatan: jangan salah gunakan cara ini untuk hal-hal yang negatif.....

Menonaktifkan Balon Notifikasi pada Windows 7 dan Vista

Apakah anda merasa terganggu dengan balon notifikasi yang kerap muncul di system tray windows? berikut ini tips singkat yang akan menunjukan bagaimana cara menonaktifkan balon notifikasi tersebut.

Buka Registry Editor, ketik 'regedit' melalui textbox search programs and files (run)
Ikutilah navigasi ini HKEY_CURRENT_USER\Software\Microsoft\Windows\CurrentVersion\Explorer\Advanced
Klik kanan dan buatlah 32-bit DWORD EnableBallonTips seperti gambar diatas dan berikan value : 0
Restart komputer anda

Selamat komputer anda sudah bebas dari notifikasi anda bisa menghidupkan kembali kembali dengan value : 1, selamat mencoba!

TuneUp Utilities 2011 v10.0.4010.20

TuneUp Utilities 2011 v10.0.4010.20 provides quick and easy access to the most critical optimization functions, A single yet comprehensive appraisal of your PC current performance and overall system health and gives easy optimization in just a few clicks. There is a new start page feature it is a concise appraisal of system performance and health on startup and new intelligent recommendations for your unique PC optimization.
FEATURES:
Enables one-click maintenance of the most important functions
Cleans the Windows registry
Deletes temporary files and folders
Increases the system performance through integrated defragmentation
Streamlines your desktop and simplifies folder shortcuts with one click
Identifies unused programs and resource-draining functions
Recommends tools for optimal PC performance
Review an assessment of your Windows PC System Health every time you log on
Learn how system issues impact your PC, and how to fix them
Increase the speed of your PC using detailed system recommendations
Improve load times for your operating system, games and other programs
Speed up overall Windows PC response time and performance
Maintain an organized hard drive
Identifies hidden programs in your start-up folder and removes them.
——-NOTE——–
ALL Lz0, CORE, ZWT keygens will get ya blacklisted and expire Tuneup Utilities with nags, this is due to the fact that the server-side serial check needs to be patched. Use this release to prevent blacklisting… if ya have been blacklisted, this release will still work.

RF HF

Aortic regurgitation (AR)

Posted on Senin, 02 Mei 2011

Aortic regurgitation (AR) is the abnormal retrograde flow of blood through the aortic valve during cardiac diastole.
AR may be caused by either valvular or aortic root pathology. Valvular abnormalities that may result in AR include bicuspid aortic valve (the most common congenital cause), rheumatic fever, infective endocarditis, collagen vascular diseases, and degenerative aortic valve disease.
Abnormalities of the ascending aorta, in the absence of valve pathology, may also cause AR, such as may occur with longstanding uncontrolled hypertension, Marfan syndrome, idiopathic aortic dilation, cystic medial necrosis, senile aortic ectasia and dilation, syphilitic aortitis, giant cell arteritis, Takayasu arteritis, ankylosing spondylitis, Whipple disease, and other spondyloarthropathies.

Pathophysiology

AR causes a volume load of the left ventricle (LV); in diastole, the LV fills antegrade from the left atrium and retrograde from the aorta through the leaky aortic valve. The pathophysiology depends upon whether the AR is acute or chronic. In acute AR, the LV does not have time to dilate in response to the volume load, whereas in chronic AR, the LV may undergo a series of adaptive (and maladaptive) changes.

Acute aortic regurgitation

Acute AR of significant severity leads to increased blood volume in the LV during diastole. The LV does not have sufficient time to dilate in response to the sudden increase in volume. As a result, LV end-diastolic pressure increases rapidly, causing an increase in pulmonary venous pressure. As pressure increases throughout the pulmonary circuit, the patient develops dyspnea and pulmonary edema. In severe cases, heart failure may develop and potentially deteriorate to cardiogenic shock. Early surgical intervention should be considered (particularly if AR is due to aortic dissection, in which case surgery should be performed immediately).

Chronic aortic regurgitation

Chronic AR causes gradual left ventricular (LV) volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy. LV dilation occurs through addition of sarcomeres in series (resulting in longer myocardial fibers) as well as rearrangement of myocardial fibers. As a result, the LV becomes larger and more compliant, with greater capacity to deliver a large stroke volume that can compensate for the regurgitant volume. The resulting hypertrophy is necessary to accommodate the increased wall tension and stress that results from LV dilation (Laplace law).
During the early phases of chronic AR, the LV ejection fraction (EF) is normal or even increased (due to the increased preload and the Frank-Starling mechanism). Patients may remain asymptomatic during this period. As AR progresses, LV enlargement surpasses preload reserve on the Frank-Starling curve with the EF falling to normal and then subnormal levels. The LV end-systolic volume rises and is a sensitive indicator of progressive myocardial dysfunction. Eventually, the LV reaches its maximal diameter and diastolic pressure begins to rise, resulting in symptoms (dyspnea) that may be worse during exercise. Increasing LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis. Grossly, the LV gradually transforms from an elliptical to a spherical configuration.

Source : emedicine.medscape.com

Alpha2-Plasmin Inhibitor Deficiency

Platelet disorders and inherited or acquired deficiencies of hemostatic factors (eg, factor VIII, factor IX, or von Willebrand factor [vWF]) lead to excessive bleeding, as is widely recognized. Widespread experience with the use of thrombolytic agents in acute myocardial infarction currently indicates that excess plasmin, generated by thrombolytic drugs, increases bleeding risk. However, the fact that a deficiency of alpha2-plasmin inhibitor (alpha 2-PI, a2-PI), a physiologic inhibitor of fibrinolysis, can lead to excessive bleeding is not widely appreciated.
To date, only 15 cases of congenital homozygous alpha 2-plasmin inhibitor deficiency (alpha 2-PI deficiency, a2-PI deficiency) and 7 molecular defects of the alpha 2-PI gene have been reported. The first reported case involved a 25-year-old Japanese homozygous male born of consanguineous parents.^[1]He had a lifelong history of severe bleeding, starting with bleeding from the umbilical cord at birth. The patient experienced hematomas, prolonged bleeding from cuts and after dental extraction, and muscle and joint bleeds following minor trauma.^[1]Central nervous system (CNS) bleeding has also been described in a Dutch patient who was homozygously deficient.^[2]
In 3 homozygous patients (sisters) from another Japanese family, bleeding was milder, with umbilical bleeding at birth followed by hematomas, gingival bleeding, and epistaxis without joint bleeding. The levels of alpha 2-PI were undetectable in all of the patients.
Most reported heterozygous patients did not have clinically significant bleeding, although some had a bleeding disorder. Currently, the reasons for variability in bleeding manifestations in heterozygous persons with alpha 2-plasmin inhibitor deficiency (alpha 2-PI deficiency, a2-PI deficiency) are unclear.

Pathophysiology

Alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) is the most important physiologic inhibitor of plasmin, which is the principal protease of the fibrinolytic pathway. Plasminogen activators convert the zymogen plasminogen to the active enzyme plasmin, which then hydrolyzes susceptible arginine and lysine bonds in a variety of proteins.^{[3, 4, 5]}
Plasmin has a broad range of actions. Plasmin not only degrades fibrin, which is its principal substrate, but it also degrades fibrinogen, factors V and VIII, proteins involved in platelet adhesion (glycoprotein I and vWF), platelet aggregation (glycoprotein IIb/IIIa) and maintenance of platelet aggregates (thrombospondin, fibronectin, histidine-rich glycoprotein), and the attachment of platelets and fibrin to the endothelial surface.
A positive feedback mechanism exists whereby plasmin acts to further increase the generation of plasmin by converting Glu-plasminogen to Lys-plasminogen; Lys-plasminogen is more susceptible to activation by plasminogen activators. In addition, other noncoagulation proteins, such as complement, growth hormone, corticotropin, and glucagon, are substrates for plasmin. Therefore, the reasons for the bleeding disorder that develops due to the actions of excess unfettered and unneutralized plasmin are easily comprehended.
Alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) belongs to the serpin family of inhibitors, is synthesized by the liver, and is present in plasma as a single-chain protein in approximately half the concentration of plasminogen. Two forms of alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) are present in blood; 70% of alpha 2-PI binds plasminogen and has inhibitory activity, whereas the remaining 30% is in a nonbinding form. The nonbinding form is a degradation product of the binding form and has little inhibitory activity.
A small amount of alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) present in platelets contributes to inhibition of fibrinolysis in platelet-containing thrombi. Activated factor XIII (FXIIIa) cross-links alpha 2-PI to the a-chains of fibrin(ogen), thus making a cross-linked fibrin clot more resistant to lysis by plasmin.
Alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) reacts very rapidly with plasmin to form a stable plasmin-inhibitor complex. This interaction is central to the physiologic control of fibrinolysis and irreversibly inhibits plasmin activity, which in turn, partially degrades alpha 2-PI. The plasmin-alpha 2-PI complex is cleared more rapidly from the circulation. The half-life of the complex is approximately 12 hours compared with the longer half-life of 3 days for native alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI).
Alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) performs several functions. Alpha 2-PI inhibits free plasmin rapidly and more readily than fibrin-bound plasmin. Alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) is cross-linked to fibrin, thus conferring resistance to degradation by plasmin, and it interferes with the adsorption of plasminogen to fibrin. As a result, recent clots are more susceptible than older clots to degradation by plasmin.
Several other proteins are also involved in the complex process of regulation of fibrinolysis in vivo. Physiologically, the end result is that the hemostatic plug (fibrin and platelet clot) is protected from premature breakdown, leaving the fibrin meshwork intact so that it functions not only in hemostasis but also in wound repair as a scaffold for regenerating cells.
As the principal inhibitor of plasmin, alpha 2-PI plays a key role in the physiologic control of fibrinolysis by helping localize reactions to the sites where they are needed and by helping prevent systemic spillover. When the amount of plasmin generated exceeds the capacity of alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) to neutralize plasmin (since, in plasma, plasminogen levels are twice those of alpha 2-PI) alpha 2-macroglobulin can function as a less efficient backup inhibitor. Note the image below.

The role of alpha2-plasmin inhibitor (alpha2-antiplasmin) in fibrinolysis. Conceptually, alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) neutralizes plasmin at various sites of plasmin production, including in the fibrin clot, on the surface of cells, and in the fluid phase (For an excellent diagram showing these details, see Figure 2 in Castellino FJ, Ploplis VA. Plasminogen and streptokinase. In: Bachmann F, ed. Fibrinolytics and Antifibrinolytics. Berlin: Springer-Verlag; 2001:26-56.)^[6]
Other inhibitors, such as antithrombin, alpha 1-antitrypsin, and C1 inactivator of complement, have in vitro antiplasmin activity, but these inhibitors may play only a minimal role in vivo.
In the absence of alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI), plasmin degrades the primary hemostatic platelet-fibrin plug, thereby interfering with adequate primary hemostasis. Although fibrin formation is unimpaired, subsequent accelerated lysis of the formed fibrin plug (fibrinolysis) leads to the onset of delayed bleeding.
In pathologic states, in which there is an endogenous excessive activation of plasminogen or a secondary infusion of activators, such as tissue plasminogen activator (t-PA) and streptokinase, sudden generation of large amounts of plasmin overwhelms the neutralizing capacity of alpha 2-PI. In addition to degrading the primary fibrin-platelet plug, excess plasmin degrades circulating fibrinogen (fibrinogenolysis) and factors V and VIII, adding to the hemorrhagic diathesis.
Most patients with an inherited homozygous alpha 2-plasmin inhibitor deficiency (alpha 2-PI deficiency, a2-PI deficiency) have a clinically significant bleeding disorder that is characterized by prolonged bleeding and bruising following minor trauma and bleeding into the joints, similar to the manifestations seen in patients with hemophilia.
Gene knockout mouse models of alpha 2-plasmin inhibitor deficiency (alpha 2-PI deficiency, a2-PI deficiency) show the expected accelerated clot lysis, but the mice do not manifest the bleeding disorder that is seen in humans.

Source : emedicine.medscape.com

Pregnancy, Ectopic

An ectopic pregnancy is any implantation of a fertilized ovum at a site other than the endometrial lining of the uterus. Virtually all ectopic pregnancies are considered nonviable and are at risk of eventual rupture. Rupture of an ectopic pregnancy and resulting hemorrhage is one of the leading causes of first-trimester maternal death in the developed world; therefore, early diagnosis and treatment (before rupture) is important to prevent morbidity and mortality.^[1]

An endovaginal sonogram demonstrates an early ectopic pregnancy. An echogenic ring (tubal ring) found outside of the uterus can be seen in this view.

Pregnancy, ectopic. An endovaginal sonogram reveals an intrauterine pregnancy at approximately 6 weeks. A yolk sac (ys), gestational sac (gs), and fetal pole (fp) are depicted.

Pathophysiology

The faulty implantation that occurs in ectopic pregnancy occurs because of a defect in the anatomy or normal function of either the fallopian tube (as in surgical or infectious scarring), the ovary (as in women undergoing fertility treatments), or the uterus (as in cases of bicornuate uterus, cesarean delivery scar).
Reflecting this, about 95% of ectopic pregnancies occur in the fallopian tube — 70% in the ampulla; 12%, isthmus; 11.1%, fimbria; and 2.4%, interstitium (or cornual region of the uterus). Some ectopic pregnancies implant in the cervix (< 1%), in prior cesarean delivery scars, or in a rudimentary uterine horn; although these may be technically in the uterus, they are not considered normal intrauterine pregnancies. About 3.2% of ectopic pregnancies occur in the ovary, and 1.3% occur in the abdomen.^[2]About 80% of ectopic pregnancies are found on the same side as the corpus luteum (the old ruptured follicle), when present.^[3]In the absence of modern prenatal care, abdominal pregnancies can present at an advanced stage (>28 wk) and have the potential for catastrophic rupture and bleeding.^[4]

^{Source : emedicine.medscape.com}

Normal Labor and Delivery

Labor is a physiologic process during which the products of conception (ie, the fetus, membranes, umbilical cord, and placenta) are expelled outside of the uterus. Labor is achieved with changes in the biochemical connective tissue and with gradual effacement and dilatation of the uterine cervix as a result of rhythmic uterine contractions of sufficient frequency, intensity, and duration.^{[1, 2]}
Labor is a clinical diagnosis. The onset of labor is defined as regular, painful uterine contractions resulting in progressive cervical effacement and dilatation. Cervical dilatation in the absence of uterine contraction suggests cervical insufficiency, whereas uterine contraction without cervical change does not meet the definition of labor.

Stages of Labor and Epidemiology

Stages of Labor

Obstetricians have divided labor into 3 stages that delineate milestones in a continuous process.

First stage of labor

The first stage begins with regular uterine contractions and ends with complete cervical dilatation at 10 cm. In Friedman’s landmark studies of 500 nulliparas^[3], he subdivided the first stage into an early latent phase and an ensuing active phase. The latent phase begins with mild, irregular uterine contractions that soften and shorten the cervix. The contractions become progressively more rhythmic and stronger. This is followed by the active phase of labor, which usually begins at about 3-4 cm of cervical dilation and is characterized by rapid cervical dilation and descent of the presenting fetal part. The first stage of labor ends with complete cervical dilation at 10 cm. According to Friedman, the active phase is further divided into an acceleration phase, a phase of maximum slope, and a deceleration phase.
Characteristics of the average cervical dilatation curve is known as the Friedman labor curve, and a series of definitions of labor protraction and arrest were subsequently established.^{[4, 5]}However, subsequent data of modern obstetric population suggest that the rate of cervical dilatation is slower and the progression of labor may be significantly different from that suggested by the Friedman labor curve.^{[6, 7, 8]}

Second stage of labor

The second stage begins with complete cervical dilatation and ends with the delivery of the fetus. The American College of Obstetricians and Gynecologists (ACOG) has suggested that a prolonged second stage of labor should be considered when the second stage of labor exceeds 3 hours if regional anesthesia is administered or 2 hours in the absence of regional anesthesia for nulliparas. In multiparous women, such a diagnosis can be made if the second stage of labor exceeds 2 hours with regional anesthesia or 1 hour without it.^[1]
Studies performed to examine perinatal outcomes associated with a prolonged second stage of labor revealed increased risks of operative deliveries and maternal morbidities but no differences in neonatal outcomes.^{[9, 10, 11, 12]}Maternal risk factors associated with a prolonged second stage include nulliparity, increasing maternal weight and/or weight gain, use of regional anesthesia, induction of labor, fetal occiput in a posterior or transverse position, and increased birthweight.^{[11, 12, 13, 14]}

Third stage of labor

The third stage of labor is defined by the time period between the delivery of the fetus and the delivery of the placenta and fetal membranes. During this period, uterine contraction decreases basal blood flow, which results in thickening and reduction in the surface area of the myometrium underlying the placenta with subsequent detachment of the placenta.^[15]Although delivery of the placenta often requires less than 10 minutes, the duration of the third stage of labor may last as long as 30 minutes.
Expectant management of the third stage of labor involves spontaneous delivery of the placenta. Active management often involves prophylactic administration of oxytocin or other uterotonics (prostaglandins or ergot alkaloids), early cord clamping/cutting, and controlled cord traction of the umbilical cord. A systematic review of the literature that included 5 randomized controlled trials comparing active and expectant management of the third stage reports that active management shortens the duration of the third stage and is superior to expectant management with respect to blood loss/risk of postpartum hemorrhage; however, active management is associated with an increased risk of unpleasant side effects.^[16]
The third stage of labor is considered prolonged after 30 minutes, and active intervention, such as manual extraction of the placenta, is commonly considered.^[2]

Epidemiology

As the childbearing population in the United States has changed, the clinical obstetric management of labor also has evolved since Friedman's studies. Data from number a studies have suggested that normal labor can progress at a rate much slower than that Friedman and Sachtleben^{[4, 5]}had described. Zhang et al examined the labor progression of 1,162 nulliparas who presented in spontaneous labor and constructed a labor curve that was markedly different from Friedman's: The average interval to progress from 4-10 cm of cervical dilatation was 5.5 hours compared with 2.5 hours of Friedman's labor curve.^[17]Kilpatrick et al^[6]and Albers et al^[7]also reported that the median lengths of first and second stages of labor were longer than those Friedman suggested.
A number of investigators have identified several maternal characteristics obstetric factors that are associated with the length of labor. One group reported that increasing maternal age was associated with a prolonged second stage but not first stage of labor.^[18]
While nulliparity is associated with a longer labor compared to multiparas, increasing parity does not further shorten the duration of labor.^[19]Some authors have observed that the length of labor differs among racial/ethnic groups. One group reported that Asian women have the longest first and second stages of labor compared with Caucasian or African American women^[20], and American Indian women had second stages shorter than those of non-Hispanic Caucasian women.^[7]However, others report conflicting findings.^{[21, 22]}Differences in the results may have been due to variations in study designs, study populations, labor management, or statistical power.
In one large retrospective study of the length of labor, specifically with respect to race and/or ethnicity, the authors observed no significant differences in the length of the first stage of labor among different racial/ethnic groups. However, the second stage was shorter in African American women than in Caucasian women for both nulliparas (-22 min) and multiparas (-7.5 min). Hispanic nulliparas, compared with their Caucasian counterparts, also had a shortened second stage, whereas no differences were seen for multiparas. In contrast, Asian nulliparas had a significantly prolonged second stage compared with their Caucasian counterparts, and no differences were seen for multiparas.^[23]

Mechanism of Labor

The ability of the fetus to successfully negotiate the pelvis during labor involves changes in position of its head during its passage in labor. The mechanisms of labor, also known as the cardinal movements, are described in relation to a vertex presentation, as is the case in 95% of all pregnancies. Although labor and delivery occurs in a continuous fashion, the cardinal movements are described as 7 discrete sequences, as discussed below.^[2]

Engagement

The widest diameter of the presenting part (with a well-flexed head, where the largest transverse diameter of the fetal occiput is the biparietal diameter) enters the maternal pelvis to a level below the plane of the pelvic inlet. On the pelvic examination, the presenting part is at 0 station, or at the level of the maternal ischial spines.

Descent

The downward passage of the presenting part through the pelvis. This occurs intermittently with contractions. The rate is greatest during the second stage of labor.

Flexion

As the fetal vertex descents, it encounters resistance from the bony pelvis or the soft tissues of the pelvic floor, resulting in passive flexion of the fetal occiput. The chin is brought into contact with the fetal thorax, and the presenting diameter changes from occipitofrontal (11.0 cm) to suboccipitobregmatic (9.5 cm) for optimal passage through the pelvis.

Internal rotation

As the head descends, the presenting part, usually in the transverse position, is rotated about 45° to anteroposterior (AP) position under the symphysis. Internal rotation brings the AP diameter of the head in line with the AP diameter of the pelvic outlet.

Extension

With further descent and full flexion of the head, the base of the occiput comes in contact with the inferior margin of the pubic symphysis. Upward resistance from the pelvic floor and the downward forces from the uterine contractions cause the occiput to extend and rotate around the symphysis. This is followed by the delivery of the fetus' head.

Restitution and external rotation

When the fetus' head is free of resistance, it untwists about 45° left or right, returning to its original anatomic position in relation to the body.

Expulsion

After the fetus' head is delivered, further descent brings the anterior shoulder to the level of the pubic symphysis. The anterior shoulder is then rotated under the symphysis, followed by the posterior shoulder and the rest of the fetus.

Clinical History and Physical Examination

History

The initial assessment of labor should include a review of the patient's prenatal care, including confirmation of the estimated date of delivery. Focused history taking should be conducted to include information, such as the frequency and time of onset of contractions, the status of the amniotic membranes (whether spontaneous rupture of the membranes has occurred, and if so, whether the amniotic fluid is clear or meconium stained), the fetus' movements, and the presence or absence of vaginal bleeding.
Braxton-Hicks contractions, which are often irregular and do not increase in frequency with increasing intensity, must be differentiated from true contractions. Braxton-Hicks contractions often resolve with ambulation or a change in activity. However, contractions that lead to labor tend to last longer and are more intense, leading to cervical change. True labor is defined as uterine contractions leading to cervical changes. If contractions occur without cervical changes, it is not labor. Other causes for the cramping should be diagnosed. Gestational age is not a part of the definition of labor.
In addition, Braxton-Hicks contractions occur occasionally, usually no more than 1-2 per hour, and they often occur just a few times per day. Labor contractions are persistent, they may start as infrequently as every 10-15 minutes, but they usually accelerate over time, increasing to contractions that occur every 2-3 minutes.
Patients may also describe what has been called lightening, ie, physical changes felt because the fetus' head is advancing into the pelvis. The mother may feel that her baby has become light. As the presenting fetal part starts to drop, the shape of the mother's abdomen may change to reflect descent of the fetus. Her breathing may be relieved because tension on the diaphragm is reduced, whereas urination may become more frequent due to the added pressure on the urinary bladder.

Physical examination

Physical examination should include documentation of the patient's vital signs, the fetus' presentation, and assessment of the fetal well-being. The frequency, duration, and intensity of uterine contractions should be assessed, particularly the abdominal and pelvic examinations in patients who present in possible labor.
Abdominal examination begins with the Leopold maneuvers described below^[2]:

The initial maneuver involves the examiner placing both of his or her hands on each upper quadrant of the patient's abdomen and gently palpating the fundus with the tips of the fingers to define which fetal pole is present in the fundus. If it is the fetus' head, it should feel hard and round. In a breech presentation, a large, nodular body is felt.
The second maneuver involves palpation in the paraumbilical regions with both hands by applying gentle but deep pressure. The purpose is to differentiate the fetal spine (a hard, resistant structure) from its limbs (irregular, mobile small parts) to determinate the fetus' position.
The third maneuver is suprapubic palpation by using the thumb and fingers of the dominant hand. As with the first maneuver, the examiner ascertains the fetus' presentation and estimates its station. If the presenting part is not engaged, a movable body (usually the fetal occiput) can be felt. This maneuver also allows for an assessment of the fetal weight and of the volume of amniotic fluid.
The fourth maneuver involves palpation of bilateral lower quadrants with the aim of determining if the presenting part of the fetus is engaged in the mother's pelvis. The examiner stands facing the mother's feet. With the tips of the first 3 fingers of both hands, the examiner exerts deep pressure in the direction of the axis of the pelvic inlet. In a cephalic presentation, the fetus' head is considered engaged if the examiner's hands diverge as they trace the fetus' head into the pelvis.

Pelvic examination is often performed using sterile gloves to decrease the risk of infection. If membrane rupture is suspected, examination with a sterile speculum is performed to visually confirm pooling of amniotic fluid in the posterior fornix. The examiner also looks for fern on a dried sample of the vaginal fluid under a microscope and checks the pH of the fluid by using a nitrazine stick or litmus paper, which turns blue if the amniotic fluid is alkalotic. If frank bleeding is present, pelvic examination should be deferred until placenta previa is excluded with ultrasonography. Furthermore, the pattern of contraction and the patient's presenting history may provide clues about placental abruption.
Digital examination of the vagina allows the clinician to determine the following: (1) the degree of cervical dilatation, which ranges from 0 cm (closed or fingertip) to 10 cm (complete or fully dilated), (2) the effacement (assessment of the cervical length, which is can be reported as a percentage of the normal 3- to 4-cm-long cervix or described as the actual cervical length); actual reporting of cervical length may decrease potential ambiguity in percent-effacement reporting, (3) the position, ie, anterior or posterior, and (4) the consistency, ie, soft or firm. Palpation of the presenting part of the fetus allows the examiner to establish its station, by quantifying the distance of the body (-5 to +5 cm) that is presenting relative to the maternal ischial spines, where 0 station is in line with the plane of the maternal ischial spines).^[2]
The pelvis can also be assessed either by clinical examination (clinical pelvimetry) or radiographically (CT or MRI). The pelvic planes include the following:

Pelvic inlet: The obstetrical conjugate is the distance between the sacral promontory and the inner pubic arch; it should measure 11.5 cm or more. The diagonal conjugate is the distance from the undersurface of the pubic arch to sacral promontory; it is 2 cm longer than the obstetrical conjugate. The transverse diameter of the pelvic inlet measures 13.5 cm.
Midpelvis: The midpelvis is the distance between the bony points of ischial spines, and it typically exceeds 12 cm.
Pelvic outlet: The pelvic outlet is the distance between the ischial tuberosities and the pubic arch. It usually exceeds 10 cm.

The shape of the mother's pelvis can also be assessed and classified into 4 broad categories based on the descriptions of Caldwell and Moloy: gynecoid, anthropoid, android, and platypelloid.^[24]Although the gynecoid and anthropoid pelvic shapes are thought to be most favorable for vaginal delivery, many women can be classified into 1 or more pelvic types, and such distinctions can be arbitrary.^[2]

Workup

High-risk pregnancies can account for up to 80% of all perinatal morbidity and mortality. The remaining perinatal complications arise in pregnancies without identifiable risk factors for adverse outcomes.^[25]Therefore, all pregnancies require a thorough evaluation of risks and close surveillance. As soon as the mother arrives at the Labor and Delivery suite, external tocometric monitoring for the onset and duration of uterine contractions and use of a Doppler device to detect fetal heart tones and rate should be started.
In the presence of labor progression, monitoring of uterine contractions by external tocodynamometry is often adequate. However, if a laboring mother is confirmed to have rupture of the membranes and if the intensity/duration of the contractions cannot be adequately assessed, an intrauterine pressure catheter can be inserted into the uterine cavity past the fetus to determine the onset, duration, and intensity of the contractions. Because the external tocometer records only the timing of contractions, an intrauterine pressure catheter can be used to measure the intrauterine pressure generated during uterine contractions if their strength is a concern. While it is considered safe, placental abruption has been reported as a rare complication of an intrauterine pressure catheter placed extramembraneously.^[26]
Often, fetal monitoring is achieved using cardiotography, or electronic fetal monitoring. Cardiotography as a form of fetal assessment in labor was reviewed using randomized and quasirandomized controlled trials involving a comparison of continuous cardiotocography with no monitoring, intermittent auscultation, or intermittent cardiotocography. This review concluded that continuous cardiotocography during labor is associated with a reduction in neonatal seizures but not cerebral palsy or infant mortality; however, continuous monitoring is associated with increased cesarean and operative vaginal deliveries.^[27]
If nonreassuring fetal heart rate tracings by cardiotography (eg, late decelerations) are noted, a fetal scalp electrode may be applied to generate sensitive readings of beat-to-beat variability. However, a fetal scalp electrode should be avoided if the mother has HIV, hepatitis B or hepatitis C infections, or if fetal thrombocytopenia is suspected. Recently, a framework has been suggested to classify and standardize the interpretation of a fetal heart rate monitoring pattern according to the risk of fetal acidemia with the intention of minimizing neonatal acidemia without excessive obstetric intervention.^[28]
The question of whether fetal pulse oximetry may be useful for fetal surveillance in labor was examined in a review of 5 published trials comparing fetal pulse oximetry and cardiotography with cardiotography alone. It concluded that existing data provide limited support for the use of fetal pulse oximetry when used in the presence of a nonreassuring fetal heart rate tracing to reduce caesarean delivery for nonreassuring fetal status. The addition of fetal pulse oximetry does not reduce overall caesarean deliveries.^[29]
Further evaluation of a fetus at risk for labor intolerance or distress can be accomplished with blood sampling from fetal scalp capillaries. This procedure allows for a direct assessment of fetal oxygenation and blood pH. A pH of < 7.20 warrants further investigation for the fetus' well-being and for possible resuscitation or surgical intervention.
Routine laboratory studies of the parturient, such as CBC analysis, blood typing and screening, and urinalysis, are usually performed. Intravenous (IV) access is established.

Intrapartum Management of Labor

First stage of labor

Cervical change occurs at a slow, gradual pace during the latent phase of the first stage of labor. Latent phase of labor is complex and not well-studied since determination of onset is subjective and may be challenging as women present for assessment at different time duration and cervical dilation during labor. In a cohort of women undergoing induction of labor, the median duration of latent labor was 384min with an interquartile range of 240-604 min. The authors report that cervical status at admission for labor induction, but not other risk factors typically associated with cesarean delivery, is associated with length of the latent phase.^[30]
Most women experience onset of labor without premature rupture of the membranes (PROM); however, approximately 8% of term pregnancies is complicated by PROM. Spontaneous onset of labor usually follows PROM such that 50% of women with PROM who were expectantly managed delivered within 5 hours, and 95% gave birth within 28 hours of PROM.^[31]Currently, the American College of Obstetricians and Gynecologists (ACOG) recommends that fetal heart rate monitoring should be used to assess fetal status and dating criteria reviewed, and group B streptococcal prophylaxis be given based on prior culture results or risk factors of cultures not available. Additionally, randomized controlled trials to date suggest that for women with PROM at term, labor induction, usually with oxytocin infusion, at time of presentation can reduce the risk of chorioamnionitis.^[32]
According to Friedman and colleagues,^[4]the rate of cervical dilation should be at least 1 cm/h in a nulliparous woman and 1.2 cm/h in a multiparous woman during the active phase of labor. However, labor management has changed substantially during the last quarter century. Particularly, obstetric interventions such as induction of labor, augmentation of labor with oxytocin administration, use of regional anesthesia for pain control, and continuous fetal heart rate monitoring are increasingly common practice in the management of labor in today’s obstetric population.^{[33, 34, 17]}Vaginal breech and mid- or high-forceps deliveries are now rarely performed.^{[35, 36, 37]}Therefore, subsequent authors have suggested normal labor may precede at a rate less rapid than those previously described.^{[6, 7, 17]}
Data collected from the Consortium on Safe Labor suggests that allowing labor to continue longer before 6-cm dilation may reduce the rate of intrapartum and subsequent cesarean deliveries in the United States.^[38]In the study, the authors noted that the 95^th percentile for advancing from 4-cm dilation to 5-cm dilation was longer than 6 hours; and the 95^th percentile for advancing from 5-cm dilation to 6-cm dilation was longer than 3 hours, regardless of the patient’s parity.
On admission to the Labor and Delivery suite, a woman having normal labor should be encouraged to assume the position that she finds most comfortable. Possibilities including walking, lying supine, sitting, or resting in a left lateral decubitus position. Of note, ambulating during labor did not change the progression of labor in a large randomized controlled study of >1000 women in active labor.^[39]
The patient and her family or support team should be consulted regarding the risks and benefits of various interventions, such as the augmentation of labor using oxytocin, artificial rupture of the membranes, methods and pharmacologic agents for pain control, and operative vaginal delivery (including forceps or vacuum-assisted vaginal deliveries) or cesarean delivery. They should be actively involved, and their preferences should be considered in the management decisions made during labor and delivery.^[2]
The frequency and strength of uterine contractions and changes in cervix and in the fetus' station and position should be assessed periodically to evaluate the progression of labor. Although progression must be monitored, vaginal examinations should be performed only when necessary to minimize the risk of chorioamnionitis, particularly in women whose amniotic membrane has ruptured. During the first stage of labor, fetal well-being can be assessed by monitoring the fetal heart rate at least every 15 minutes, particularly during and immediately after uterine contractions. In most labor and delivery units, the fetal heart rate is assessed continuously.^[40]
Two methods of augmenting labor have been established. The traditional method involves the use of low doses of oxytocin with long intervals between dose increments. For example, low-dose infusion of oxytocin is started at 1 mili IU/min and increased by 1-2 mili IU/min every 20-30 minutes until adequate uterine contraction is obtained.^[2]
The second method, or active management of labor, involves a protocol of clinical management that aims to optimize uterine contractions and shorten labor. This protocol includes strict criteria for admission to the labor and delivery unit, early amniotomy, hourly cervical examinations, early diagnosis of inefficient uterine activity (if the cervical dilation rate is < 1.0 cm/h), and high-dose oxytocin infusion if uterine activity is inefficient. Oxytocin infusion starts at 4 mili IU/min (or even 6 mili IU/min) and increases by 4 mili IU/min (or 6 mili IU/min) every 15 minutes until a rate of 7 contractions per 15 minutes is achieved or until the maximum infusion rate of 36 mili IU/min is reached.^{[41, 2]}
Although active management of labor was originally intended to shorten the length of labor in nulliparous women, its application at the National Maternity Hospital in Dublin produced a primary cesarean delivery rate of 5-6% in nulliparas.^[42]Data from randomized controlled trials confirmed that active management of labor shortens the first stage of labor and reduces the likelihood of maternal febrile morbidity, but it does not consistently decrease the probability of cesarean delivery.^{[43, 44, 45]}
Although the active management protocol likely leads to early diagnosis and interventions for labor dystocia, a number of risk factors are associated with a failure of labor to progress during the first stage. These risk factors include premature rupture of the membranes (PROM), nulliparity, induction of labor, increasing maternal age, and or other complications (eg, previous perinatal death, pregestational or gestational diabetes mellitus, hypertension, infertility treatment).^{[46, 47]}
While the ACOG defines labor dystocia as abnormal labor that results form abnormalities of the power (uterine contractions or maternal expulsive forces), the passenger (position, size, or presentation of the fetus), or the passage (pelvis or soft tissues), labor dystocia can rarely be diagnosed with certainty.^[1]Often, a "failure to progress" in the first stage is diagnosed if uterine contraction pattern exceeds 200 Montevideo units for 2 hours without cervical change during the active phase of labor is encountered.^[1]Thus, the traditional criteria to diagnose active-phase arrest are cervical dilatation of at least 4 cm, cervical changes of < 1 cm in 2 hours, and a uterine contraction pattern of >200 Montevideo units. These findings are also a common indication for cesarean delivery.
Proceeding to cesarean delivery in this setting, or the "2-hour rule," was challenged in a clinical trial of 542 women with active phase arrest.^[48]In this cohort of women diagnosed with active phase arrest, oxytocin was started, and cesarean delivery was not performed for labor arrest until adequate uterine contraction lasted at least 4 hours (>200 Montevideo units) or until oxytocin augmentation was given for 6 hours if this contraction pattern could not be achieved. This protocol achieved vaginal delivery rates of 56-61% in nulliparas and 88% in multiparas without severe adverse maternal or neonatal outcomes. Therefore, extending the criteria for active-phase labor arrest from 2 to at least 4 hours appears to be effective in achieving vaginal birth.^{[48, 1]}

Second stage of labor

When the woman enters the second stage of labor with complete cervical dilatation, the fetal heart rate should be monitored or auscultated at least every 5 minutes and after each contractions during the second stage.^[40]Although the parturient may be encouraged to actively push in concordance with the contractions during the second stage, many women with epidural anesthesia who do not feel the urge to push may allow the fetus to descend passively, with a period of rest before active pushing begins.
A number of randomized controlled trials have shown that, in nulliparous women, delayed pushing, or passive descend, is not associated with adverse perinatal outcomes or an increased risk for operative deliveries despite an often prolonged second stage of labor.^{[49, 50, 31]}Furthermore, investigators who recently compared obstetric outcomes associated with coached versus uncoached pushing during the second stage reported a slightly shortened second stage (13 min) in the coached group, with no differences in the immediate maternal or neonatal outcomes.^[51]
When a prolonged second stage of labor is encountered, clinical assessment of the parturient, the fetus, and the expulsive forces is warranted. A randomized controlled trial performed by Api et al determined that application of fundal pressure on the uterus does not shorten the second stage of labor.^[52]Although the 2003 ACOG practice guidelines state that the duration of the second stage alone does not mandate intervention by operative vaginal delivery or cesarean delivery if progress is being made, the clinician has several management options (continuing observation/expectant management, operative vaginal delivery by forceps or vacuum-assisted vaginal delivery, or cesarean delivery) when second-stage arrest is diagnosed.
The association between a prolonged second stage of labor and adverse maternal or neonatal outcome has been examined. While a prolonged second stage is not associated with adverse neonatal outcomes in nulliparas, possibly because of close fetal surveillance during labor, but it is associated with increased maternal morbidity, including higher likelihood of operative vaginal delivery and cesarean delivery, postpartum hemorrhage, third- or fourth-degree perineal lacerations, and peripartum infection.^{[9, 10, 11, 12]}Therefore, it is crucial to weigh the risks of operative delivery against the potential benefits of continuing labor in hopes to achieve vaginal delivery. The question of when to intervene should involve a thorough evaluation of the ongoing risks of further expectant management versus the risks of intervention with vaginal or cesarean delivery, as well as the patients' preferences.

Delivery of the fetus

When delivery is imminent, the mother is usually positioned supine with her knees bent (ie, dorsal lithotomy position), though delivery can occur with the mother in any position, including the lateral (Sims) position, the partial sitting or squatting position, or on her hands and knees.^[2]Although an episiotomy (an incision continuous with the vaginal introitus) used to be routinely performed at this time, the ACOG recommended in 2006 that its use be restricted to maternal or fetal indications. Studies have also shown that routine episiotomy does not decrease the risk of severe perineal lacerations during forceps or vacuum-assisted vaginal deliveries.^{[53, 54]}
Crowning is the word used to describe when the fetal head forcibly extends the vaginal outlet. A modified Ritgen maneuver can be performed to deliver the head. Draped with a sterile towel, the heel of the clinician's hand is placed over the posterior perineum overlying the fetal chin, and pressure is applied upward to extend the fetus' head. The other hand is placed over the fetus' occiput, with pressure applied downward to flex its head. Thus, the head is held in mid position until it is delivered, followed by suctioning of the oropharynx and nares. Check the fetus' neck for a wrapped umbilical cord, and promptly reduce it if possible. If the cord is wrapped too tightly to be removed, the cord can be double clamped and cut. Of note, some providers, in an attempt to avoid shoulder dystocia, deliver the anterior shoulder prior to restitution of the fetal head.
Next, the fetus' anterior shoulder is delivered with gentle downward traction on its head and chin. Subsequent upward pressure in the opposite direction facilitates delivery of the posterior shoulder. The rest of the fetus should now be easily delivered with gentle traction away from the mother. If not done previously, the cord is clamped and cut. The baby is vigorously stimulated and dried and then transferred to the care of the waiting attendants or placed on the mother's abdomen.

Third stage of labor - Delivery of the placenta and the fetal membranes

The labor process has now entered the third stage, ie, delivery of the placenta. Three classic signs indicate that the placenta has separated from the uterus: (1) The uterus contracts and rises, (2) the cord suddenly lengthens, and (3) a gush of blood occurs.^[2]
Delivery of the placenta usually happens within 5-10 minutes after delivery of the fetus, but it is considered normal up to 30 minutes after delivery of the fetus. Excessive traction should not be applied to the cord to avoid inverting the uterus, which can cause severe postpartum hemorrhage and is an obstetric emergency. The placenta can also be manually separated by passing a hand between the placenta and uterine wall. After the placenta is delivered, inspect it for completeness and for the presence of 1 umbilical vein and 2 umbilical arteries. Oxytocin can be administered throughout the third stage to facilitate placental separation by inducing uterine contractions and to decrease bleeding.
Expectant management of the third stage involves allowing the placenta to deliver spontaneously, whereas active management involves administration of uterotonic agent (usually oxytocin, an ergot alkaloid, or prostaglandins) before the placenta is delivered. This is done with early clamping and cutting of the cord and with controlled traction on the cord while placental separation and delivery are awaited.
A review of 5 randomized trials comparing active versus expectant management of the third stage demonstrated that active management was associated with lowered risks of maternal blood loss, postpartum hemorrhage, and prolongation of the third stage, but it increased maternal nausea, vomiting, and blood pressure (when ergometrine was used). However, given the reduced risk of complications, this review recommends that active management is superior to expectant management and should be the routine management of choice.^[16]A multicenter, randomized, controlled trial of the efficacy of misoprostol (prostaglandin E1 analog) compared with oxytocin showed that oxytocin 10 IU IV or given intramuscularly (IM) was preferable to oral misoprostol 600 mcg for active management of the third stage of labor in hospital settings.^[55]Therefore, if the risks and benefits are balanced, active management with oxytocin may be considered a part of routine management of the third stage.
After the placenta is delivered, the labor and delivery period is complete. Palpate the patient's abdomen to confirm reduction in the size of the uterus and its firmness. Ongoing blood loss and a boggy uterus suggest uterine atony. A thorough examination of the birth canal, including the cervix and the vagina, the perineum, and the distal rectum, is warranted, and repair of episiotomy or perineal/vaginal lacerations should be carried out.
Franchi et al found that topically applied lidocaine-prilocaine (EMLA) cream was an effective and satisfactory alternative to mepivacaine infiltration for pain relief during perineal repair. In a randomized trial of 61 women with either an episiotomy or a perineal laceration after vaginal delivery, women in the EMLA group had lower pain scores than those in the mepivacaine group (1.7 +/- 2.4 vs 3.9 +/- 2.4; P = .0002), and a significantly higher proportion of women expressed satisfaction with anesthesia method in the EMLA group than in the mepivacaine group (83.8% vs 53.3%; P = .01).^[56]

Pain Control

Laboring women often experience intense pain. Uterine contractions result in visceral pain, which is innervated by T10-L1. While in descent, the fetus' head exerts pressure on the mother's pelvic floor, vagina, and perineum, causing somatic pain transmitted by the pudendal nerve (innervated by S2-4).^[57]Therefore, optimal pain control during labor should relieve both sources of pain.
A number of opioid agonists and opioid agonist-antagonists can be given in intermittent doses for systemic pain control. These include meperidine 25-50 mg IV every 1-2 hours or 50-100 mg IM every 2-4 hours, fentanyl 50-100 mcg IV every hour, nalbuphine 10 mg IV or IM every 3 hours, butorphanol 1-2 mg IV or IM every 4 hours, and morphine 2-5 mg IV or 10 mg IM every 4 hours.^[57]As an alternative, regional anesthesia may be given. Options are epidural, spinal, or combined spinal epidural anesthesia. These provide partial to complete blockage of pain sensation below T8-10, with various degree of motor blockade. These blocks can be used during labor and for surgical deliveries.
Studies performed to compare the analgesic effect of regional anesthesia and parenteral agents showed that regional anesthesia provides superior pain relief.^{[58, 36, 59]}Although some researchers reported that epidural anesthesia is associated with a slight increase in the duration of labor and in the rate of operative vaginal delivery,^{[60, 61]}large randomized controlled studies did not reveal a difference in frequency of cesarean delivery between women who received parenteral analgesics compared with women who received epidural anesthesia^{[58, 59, 61]}given during early-stage or later in labor.^[62]Although regional anesthesia is effective as a method of pain control, common adverse effects include maternal hypotension, maternal temperature >100.4°F, postdural puncture headache, transient fetal heart deceleration, and pruritus (with added opioids).^[57]
Despite the many methods available for analgesia and anesthesia to manage labor pain, some women may not wish to use conventional pain medications during labor, opting instead for a natural childbirth. Although these women may use breathing and mental exercises to help alleviate labor pain, they should be assured that pain relief can be administered at any time during labor.
Of note, use of nonsteroidal anti-inflammatory drugs (NSAIDs) are relatively contraindicated in the third trimester of pregnancy. The repeated use of NSAIDs has been associated with early closure of the fetal ductus arteriosus in utero and with decreasing fetal renal function leading to oligohydramnios.

source : emedicine.medscape.com