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Mengatasi Luka Bakar pada Anak Filed under: Uncategorized — Tinggalkan komentar Februari 17, 2011

Mengatasi Luka Bakar pada Anak Luka bakar dapat disebabkan oleh cairan panas, radiasi dan uap panas, sengatan listrik, atau bahan kimia yang bersifat asam kuat. Luka bakar berbahaya karena merusak kulit yang berfungsi melindungi kita dari kotoran dan infeksi. Kulit juga berperan dalam pengaturan suhu tubuh dan pembuangan limbah melalui keringat. Jika banyak permukaan tubuh yang terbakar, ada banyak bahaya yang mengancam jiwa karena kerusakan pembuluh darah, obstruksi jalan pernapasan, ketidakseimbangan elektrolit dan suhu tubuh, serta gangguan fungsi saraf. Selain mengakibatkan bahaya fisik, luka bakar juga dapat menimbulkan masalah emosional dan psikologis yang bertahan lama karena trauma dan ketidaksempurnaan penampilan.

Bila anak Anda mengalami luka bakar Kebanyakan kecelakaan yang menyebabkan luka bakar terjadi di rumah. Untungnya selalu ada air di sekitarnya. Segeralah mendinginkan kulit terbakar anak Anda dengan air dingin, tetapi tidak terlalu dingin (bukan air es). Untuk area yang lebih luas, rendamlah atau guyurlah anak dengan air di kamar mandi selama minimal lima menit. Jangan mengoleskan pasta gigi, salep, minyak atau mentega ke area yang terbakar. Mengoleskan bahan tersebut akan membatasi keluarnya panas dari kulit. Setelah luka bakar memiliki cukup waktu untuk mendingin, silakan menggunakan salep untuk membantu mencegah infeksi. Jika Anda harus membuka pakaian yang lengket di kulit, jangan menariknya. Siramkan air dalam kondisi anak tetap berpakaian. Lepaskan pelan-pelan pakaian dan tutuplah luka dengan perban steril. Untuk luka bakar yang parah, segeralah memanggil bantuan ambulans atau dokter.

Kapan harus memeriksakan diri ke dokter? Tergantung pada tingkat keparahan luka bakar, yang dinyatakan dalam derajat. Derajat 1: cedera dangkal yang hanya melibatkan lapisan luar kulit (epidermis), misalnya karena berjemur di bawah terik matahari. Kulit memerah dan sangat menyakitkan. Luka bakar akan sembuh sendiri tanpa jaringan parut dalam waktu dua sampai lima hari. Derajat 2: terjadi ketika kulit terbakar hingga lapisan kedua. Kulit tampak melepuh dan lecet berwarna merah sehingga terlihat belang-belang dan terasa sangat perih menyakitkan. Luka bakar derajat dua dianggap belum berbahaya jika melibatkan kurang dari 15 persen dari permukaan tubuh pada orang dewasa dan kurang dari 10 persen pada anak-anak. Bila ditangani dengan benar, luka bakar derajat dua akan sembuh tanpa banyak menimbulkan jaringan parut. Penyembuhan biasanya memakan waktu hingga tiga minggu. Derajat 3: melibatkan semua lapisan kulit sehingga kulit rusak parah berwarna coklat, kadang-kadang diselingi kelupasan putih atau hitam. Luka bakar derajat tiga mungkin sangat menyakitkan, namun beberapa pasien dapat sedikit atau tidak merasa sakit karena ujung-ujung sarafnya telah hancur. Penyembuhan sempurna luka bakar derajat ini mungkin memerlukan pencangkokan kulit. Derajat luka bakar tergantung pada lama pemaparan dan suhu cairan, udara atau benda yang mengenainya. Jenis sumber yang mengenai juga berpengaruh. Misalnya, minyak panas biasanya menyebabkan derajat luka bakar lebih parah daripada air panas karena suhunya lebih tinggi dan lebih lengket di kulit. Jika anak Anda mengalami luka bakar derajat 2 atau lebih pada bagian tubuh yang luas atau berbahaya, segera periksakan ke dokter.

Pencegahan luka bakar Banyak luka bakar yang disebabkan oleh air panas. Jauhkanlah ceret, panci, wajan berisi air panas dari jangkauan anak-anak. Luka bakar juga bisa diakibatkan ledakan kompor gas. (Terutama dari gas bersubsidi yang belakangan ramai dibicarakan orang). Jika Anda mencium bau gas atau melihat jilatan api dari kompor, segera cabut selang gas, buka jendela lebar-lebar, dan bawa tangki gas ke ruangan terbuka. Jangan pernah berjalan membawa panci berisi masakan panas tanpa penutup yang aman.

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Blunt Abdominal Trauma Filed under: Uncategorized — Tinggalkan komentar

Blunt Abdominal Trauma The care of the trauma patient is demanding and requires speed and efficiency. Evaluating patients who have sustained blunt abdominal trauma remains one of the most challenging and resource-intensive aspects of acute trauma care. Missed intra-abdominal injuries and concealed hemorrhage are frequent causes of increased morbidity and mortality, especially in patients who survive the initial phase after an injury. Physical examination findings are notoriously unreliable for several reasons; a few examples are the presence of distracting injuries, an altered mental state, and drug and alcohol intoxication in the patient. Coordinating a trauma resuscitation demands a thorough understanding of the pathophysiology of trauma and shock, excellent clinical and diagnostic acumen, skill with complex procedures, compassion, and the ability to think rationally in a chaotic milieu. Blunt abdominal trauma usually results from motor vehicle collisions, assaults, recreational accidents, or falls. The most commonly injured organs are the spleen, liver, retroperitoneum, small bowel, kidneys (see image below), bladder, colorectum, diaphragm, and pancreas. Men tend to be affected slightly more often than women.

Blunt abdominal trauma. Right kidney injury with blood in the perirenal space. Injury resulted from a high-speed motor vehicle collision. [ CLOSE WINDOW ]

Blunt abdominal trauma. Right kidney injury with blood in the perirenal space. Injury resulted from a high-speed motor vehicle collision.

Frequency United States By nearly every measure, injury ranks as one of this nation’s most pressing health issues. More than 150,000 people die each year as a result of injuries, such as motor vehicle crashes, fires, falls, drowning, poisoning, suicide, and homicide. Injuries are the leading cause of death and disability for US children and young adults. According to the 2000 statistics from the National Center for Injury Prevention and Control, trauma (unintentional and intentional) was the leading cause of death in persons aged 1-44 years. Further review of the data reveals that in those aged 15-25 years, 14,113 persons died from unintentional injuries, 73% of which were related to vehicular trauma. In individuals aged 25-34 years, 57% of the 11,769 deaths reported were from motor vehicle collisions. In 2001, approximately 30 million people visited emergency departments for the treatment of nonfatal injuries and more than 72,000 people were disabled by injuries. Injury imposes exceptional costs, both in health care dollars and in human losses, to society. International In 1990, approximately 5 million people died worldwide as a result of injury. The risk of death from injury varied strongly by region, age, and sex. Approximately 2 male deaths due to violence were reported for every female death. Injuries accounted for approximately 12.5% of all male deaths, compared with 7.4% of female deaths. Globally, injury accounts for 10% of all deaths; however, injuries in sub-Saharan Africa are far more destructive than in other areas. In sub-Saharan Africa, the risk of death from trauma is highest in those aged 15-60 years, and the proportion of such deaths from trauma is higher than in any other region of the world. In South Africa, for instance, the traffic death rate per unit of distance traveled is only surpassed by Korea, Kenya, and Morocco. Estimates indicate that by 2020, 8.4 million people will die yearly from injury, and injuries from traffic collisions will be the third most common cause of disability worldwide and the second most common cause in the developing world.

Pathophysiology Vehicular trauma is by far the leading cause of blunt abdominal trauma in the civilian population. Auto-to-auto and auto-to-pedestrian collisions have been cited as causes in 50-75% of cases. Rare causes of blunt abdominal injuries include iatrogenic trauma during cardiopulmonary resuscitation, manual thrusts to clear an airway, and the Heimlich maneuver. Intra-abdominal injuries secondary to blunt force are attributed to collisions between the injured person and the external environment and to acceleration or deceleration forces acting on the person’s internal organs. Blunt force injuries to the abdomen can generally be explained by 3 mechanisms. The first is when rapid deceleration causes differential movement among adjacent structures. As a result, shear forces are created and cause hollow, solid, visceral organs and vascular pedicles to tear, especially at relatively fixed points of attachment. For example, the distal aorta is attached to the thoracic spine and decelerates much more quickly than the relatively mobile aortic arch. As a result, shear forces in the aorta may cause it to rupture. Similar situations can occur at the renal pedicles and at the cervicothoracic junction of the spinal cord. The second is when intra-abdominal contents are crushed between the anterior abdominal wall and the vertebral column or posterior thoracic cage. This produces a crushing effect, to which solid viscera (eg, spleen, liver, kidneys) are especially vulnerable. The third is external compression forces that result in a sudden and dramatic rise in intra-abdominal pressure and culminate in rupture of a hollow viscous organ (ie, in accordance with the principles of Boyle law).

Presentation History The initial assessment of a trauma patient begins at the scene of the injury, with information provided by the patient, family, bystanders, or paramedics. Important factors relevant to the care of a patient with blunt abdominal trauma, specifically those involving motor vehicles, include the following: The extent of vehicular damage Whether prolonged extrication was required Whether the passenger space was intruded Whether a passenger died Whether the person was ejected from the vehicle The role of safety devices such as seat belts and airbags The presence of alcohol or drug use The presence of a head or spinal cord injury Whether psychiatric problems were evident Priorities in resuscitation and diagnosis are established based on hemodynamic stability and the degree of injury. The goal of the primary survey, as directed by the Advanced Trauma Life Support protocol, is to identify and expediently treat life-threatening injuries. The protocol includes the following: Airway, with cervical spine precautions Breathing Circulation Disability Exposure Key elements of the pertinent history include the following: Allergies Medications Past medical and surgical history Time of last meal Immunization status Events leading to the incident Social history, including history of substance abuse Information from family and friends Resuscitation is performed concomitantly and continues as the physical examination is completed. The secondary survey is the identification of all injuries via a head-to-toe examination. It is imperative for all personnel involved in the direct care of a trauma patient to exercise universal precautions against body fluid exposure. The incidence of infectious diseases (eg, HIV, hepatitis) is significantly higher in trauma patients than in the general public, with some centers reporting rates as high as 19%. Even in medical centers with relatively low rates of communicable diseases, safely determining who is infected with such pathogens is impossible. The standard barrier precautions include a hat, eye shield, face mask, gown, gloves, and shoe covers. Unannounced trauma arrival is probably the most common situation that leads to a breach in barrier precautions. Personnel must be instructed to adhere to these guidelines at all times, even if it means a 30-second delay in patient care. Physical examination The evaluation of a patient with blunt abdominal trauma must be accomplished with the entire patient in mind, with all injuries prioritized accordingly. This implies that injuries involving the head, the respiratory system, or the cardiovascular system may take precedence over an abdominal injury. The abdomen should neither be ignored nor the sole focus of the treating clinician and surgeon. In an unstable patient, the question of abdominal involvement must be expediently addressed. This is accomplished by identifying free intra-abdominal fluid using diagnostic peritoneal lavage (DPL) or the Focused Assessment with Sonography for Trauma (FAST) examination. The objective is to rapidly identify patients who need a laparotomy. The initial clinical assessment of patients with blunt abdominal trauma is often difficult and notably inaccurate. Associated injuries often cause tenderness and spasms in the abdominal wall and make diagnosis difficult. Lower rib fractures, pelvic fractures, and abdominal wall contusions may mimic the signs of peritonitis. In a collected series of 955 patients, Powell et al reported that clinical evaluation alone has an accuracy rate of only 65% for detecting the presence or absence of intraperitoneal blood.1 In general, accuracy increases if the patient is examined repeatedly and at frequent intervals. However, repeated examinations may not be feasible in patients who need general anesthesia and surgery for other injuries. The greatest compromise of the physical examination occurs in the setting of neurologic dysfunction, which may be caused by head injury or substance abuse. The most reliable signs and symptoms in alert patients are pain, tenderness, gastrointestinal hemorrhage, hypovolemia, and evidence of peritoneal irritation. However, large amounts of blood can accumulate in the peritoneal and pelvic cavities without any significant or early changes in the physical examination findings. The abdominal examination must be systematic. The abdomen is inspected for abrasions or ecchymosis. The seat belt sign, ie, a contusion or abrasion across the lower abdomen, is highly correlated with intraperitoneal pathology. Visual inspection for abdominal distention, which may be due to pneumoperitoneum, gastric dilatation, or ileus produced by peritoneal irritation, is important. Ecchymosis involving the flanks (Grey Turner sign) or the umbilicus (Cullen sign) indicates retroperitoneal hemorrhage, but this is usually delayed for several hours to days. Rib fractures involving the lower chest may be associated with splenic or liver injuries. Auscultation of bowel sounds in the thorax may indicate the presence of a diaphragmatic injury. Palpation may reveal local or generalized tenderness, guarding, rigidity, or rebound tenderness, which suggests peritoneal injury. A rectal examination should be performed to search for evidence of bony penetration resulting from a pelvic fracture, and the stool should be evaluated for gross or occult blood. The evaluation of rectal tone is important for determining the patient’s neurologic status, and palpation of a high-riding prostate suggests urethral injury. A nasogastric tube should be placed routinely (in the absence of contraindications, eg, basilar skull fracture) to decompress the stomach and to assess for the presence of blood. If the patient has evidence of a maxillofacial injury, an orogastric tube is preferred. As the assessment continues, a Foley catheter is placed and a sample of urine is sent for analysis for microscopic hematuria. If injury to the urethra or bladder is suggested because of an associated pelvic fracture, then a retrograde urethrogram is performed before catheterization. Because of the wide spectrum of injuries, frequent reevaluation is an essential component in the management of patients with blunt abdominal trauma. Pediatric patients are assessed and treated at least initially as adults with respect to the primary and secondary surveys. However, obvious anatomical and clinical differences exist and these must be kept in mind: the child’s physiologic response to injury is different; communication is not always possible; physical examination findings become more important; the pediatric patient’s blood volume is less, predisposing them to rapid exsanguination; technical procedures tend to be more time consuming and challenging; and a child’s relatively large body surface area contributes to rapid heat loss. Perhaps, the most significant difference between pediatric and adult blunt trauma is that, for the most part, pediatric patients can be resuscitated and treated nonoperatively. Some pediatric surgeons often transfuse up to 40 mL/kg of blood products in an effort to stabilize a pediatric patient. Obviously, if this fails and the child continues to be unstable, laparotomy is indicated. Tertiary examination This concept was first introduced by Enderson et al to assist in the diagnosis of any injuries that may have been missed during the primary and secondary surveys.2 The tertiary survey involves a repetition of the primary and secondary surveys and a revision of all laboratory and radiographic studies. In one study, a tertiary trauma survey detected 56% of injuries missed during the initial assessment within 24 hours of admission.

Indications Aggressive radiographic and surgical investigation is indicated in patients with persistent hyperamylasemia or hyperlipasemia, conditions that suggest significant intra-abdominal injury. Stable patients with inconclusive physical examination findings should undergo radiographic studies of the abdomen. DPL is indicated in blunt trauma as follows: Patients with a spinal cord injury Those with multiple injuries and unexplained shock Obtunded patients with a possible abdominal injury Intoxicated patients in whom abdominal injury is suggested Patients with potential intra-abdominal injury who will undergo prolonged anesthesia for another procedure An indication for immediate blood transfusion is hemodynamic instability despite the administration of 2 L of fluid to adult patients; this instability indicates ongoing blood loss. Indications for laparotomy in a patient with blunt abdominal injury include the following: Signs of peritonitis Uncontrolled shock or hemorrhage Clinical deterioration during observation Hemoperitoneum findings after FAST or DPL examinations Finally, surgical intervention is indicated in patients with evidence of peritonitis based on physical examination findings.

Relevant Anatomy The abdomen can be arbitrarily divided into 4 areas. The first is the intrathoracic abdomen, which is the portion of the upper abdomen that lies beneath the rib cage. Its contents include the diaphragm, liver, spleen, and stomach. The rib cage makes this area inaccessible for palpation and complete examination. The second is the pelvic abdomen, which is defined by the bony pelvis. Its contents include the urinary bladder, urethra, rectum, small intestine, and, in females, the ovaries, fallopian tubes, and uterus. Injury to these structures may be extraperitoneal in nature and therefore difficult to diagnose. The third is the retroperitoneal abdomen, which contains the kidneys, ureters, pancreas, aorta, and vena cava. Injuries to these structures are very difficult to diagnose based on physical examination findings. Evaluation of the structures in this region may require a CT scan, angiography, and an intravenous pyelogram. The fourth is the true abdomen, which contains the small and large intestines, the uterus (if gravid), and the bladder (when distended). Perforation of these organs is associated with significant physical findings and usually manifests with pain and tenderness from peritonitis. Plain x-ray films are helpful if free air is present. Additionally, DPL is a useful adjunct.

Contraindications While not a contraindication to surgical repair, the evaluation of a patient with blunt abdominal trauma must be prioritized based on the most urgent problems. This implies that injuries involving the head, the respiratory system, or the cardiovascular system may take precedence over an abdominal injury. Although a nasogastric tube is routine in order to decompress the stomach and assess for the presence of blood, it is contraindicated in patients with basilar skull fracture. An orogastric tube is preferred if the patient has evidence of a maxillofacial injury. Operative treatment is not indicated in every patient with positive FAST scan results. Hemodynamically stable patients with positive FAST findings may require a CT scan to better define the nature and extent of their injuries. Operating on every patient with positive FAST scan findings may result in an unacceptably high laparotomy rate. The only absolute contraindication to DPL is the obvious need for laparotomy. Relative contraindications include morbid obesity, a history of multiple abdominal surgeries, and pregnancy. Resuscitative thoracotomy is not recommended in patients with blunt thoracoabdominal trauma who have pulseless electrical activity upon arrival in the emergency department. The survival rate in this situation is virtually 0%. These patients may be allowed a thoracotomy in the emergency department only if they have signs of life upon arrival to the emergency department.

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MENINGITIS BAKTERIA

Filed under: Uncategorized — Tinggalkan komentar Februari 14, 2011 MENINGITIS BAKTERIAL Meningitis bakterial merupakan salah satu jenis penyakit infeksi pada selaput pembungkus otak atau meningen serta cairan yang mengisi ruang subarakhnoid. Meningitis bakterial merupakan penyakit yang serius atau penyakit kedaruratan medik apabila tidak ditangani dengan baik dan tepat. Penyebab Etiologi atau penyebab dari meningitis sebagian besar disebabkan oleh bakteri, dan selebihnya disebabkan oleh virus, parasit serta jamur. Dari hasil laporan kasus, bakteri penyebab meningitis terbanyak disebabkan oleh: Hemophilus influenzae, Streptococcus pneumoniae dan Neisseria meningitidis. Faktor Risiko Meningitis paling sering menyerang anak-anak usia 1 bulan- 2 tahun. Wabah meningitis meningokokus bisa terjadi dalam suatu lingkungan, misalnya perkemahan militer, asrama mahasiswa atau sekumpulan orang yang berhubungan dekat. Patofisiologi Patofisiologi terjadinya meningitis bakterialis, telah diperlihatkan pada percobaan binatang. Pada awalnya infeksi tersebut terjadi akibat dari masuknya bakteri patogen yang telah berkoloni di mukosa nasofaring pada selaput leptomeningeal (jaringan arakhnoid dan ruang subaraknoid) melalui darah. Bakteri patogen penyebab biasanya memiliki ciri berkapsul. Setelah membentuk koloni di rongga nasofaring, bakteri yang berkapsul itu memasuki lapisan epitel dan langsung menuju ke aliran darah. Kapsul pada bakteri itulah yang menghambat proses fagositosis oleh neutrofil dan antibodi yang dibentuk oleh tubuh. Dari proses penghambatan itulah bakteri patogen meningeal memperlihatkan kemampuan untuk mempertahankan proses bakteremianya. Pada tahap akhir, bakteri dalam darah akan mencapai selaput leptomening dan ruang subarakhnoid yang hingga saat ini belum diketahui secara jelas prosesnya. Gejala dan Tanda Akut, fulminan, dengan tanda-tanda khas “trias klasik” (3 tanda klasik) yang berupa: demam, kaku kuduk dan penurunan kesadaran. Tanda-tanda kaku kuduk biasanya sulit ditemukan pada keadaan tertentu seperti pada orang tua, neutropenia, gangguan imunologi serta pada neonatus. Selain tiga tanda diatas mual, muntah, kejang, fotofobia dan pada bayi sering ditemukan bulging (benjolan) pada fontanela bayi atau neonatus. Apabila ditemukan dalam keadaan koma, prognosinya akan buruk, dimana hal ini ditemukan pada 5-10 % kasus yang ada. Penatalaksanaan Penatalaksanaan yang paling efektif untuk terapi Meningitis bakterialis adalah dengan diberikan antimikroba segera setelah diagnosis ditegakkan. Beberapa prinsip penting yang harus diperhatikan dalam pemakaian antimikroba adalah faktor yang mempengaruhi bertambahnya kekuatan penetrasi dan konsentrasi dari antibiotik, yaitu dengan memperhatikan peningkatan permeabilitas dari sawar darah otak, karakteristik dari antibiotiknya sendiri. Untuk faktor pemilihan antibiotik yang harus diperhatikan adalah ukuran dari molekul antibiotik harus kecil, memiliki ikatan terhadap protein plasma lemah, pH fisiologi pada saat terjadi ionisasi juga harus lemah serta memiliki tingkat solubilitas yang tinggi terhadap lemak. Selain faktor diatas masih perlu juga memperhatikan faktor-faktor yang dapat mengurangi aktivitas antibiotik seperti rendahnya pH dalam cairan, tingginya konsentrasi protein dalam cairan serta tingginya temperatur cairan.

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BATU EMPEDU Filed under: Uncategorized — Tinggalkan komentar BATU EMPEDU Batu empedu adalah timbunan kristal di dalam kandung empedu atau di dalam saluran empedu. Batu yang ditemukan di dalam kandung empedu disebut kolelitiasis, sedangkan batu di dalam saluran empedu disebut koledokolitiasis. Penyebab Komponen utama dari batu empedu adalah kolesterol, sebagian kecil lainnya terbentuk dari garam kalsium. Cairan empedu mengandung sejumlah besar kolesterol yang biasanya tetap berbentuk cairan. Jika cairan empedu menjadi jenuh karena kolesterol, maka kolesterol bisa menjadi tidak larut dan membentuk endapan di luar empedu. Faktor Risiko Batu empedu lebih banyak ditemukan pada wanita dan faktor risikonya adalah : Usia lanjut. Kegemukan (obesitas). Diet tinggi lemak. Faktor keturunan. Patofisiologi Sebagian besar batu empedu terbentuk di dalam kandung empedu dan sebagian besar batu di dalam saluran empedu berasal dari kandung empedu. Batu empedu bisa terbentuk di dalam saluran empedu jika empedu mengalami aliran balik karena adanya penyempitan saluran atau setelah dilakukan pengangkatan kandung empedu. Batu empedu di dalam saluran empedu bisa mengakibatkan infeksi hebat saluran empedu (kolangitis), infeksi pankreas (pankreatitis) atau infeksi hati. Jika saluran empedu tersumbat, maka bakteri akan tumbuh dan dengan segera menimbulkan infeksi di dalam saluran. Bakteri bisa menyebar melalui aliran darah dan menyebabkan infeksi di bagian tubuh lainnya. Sebagian besar batu empedu dalam jangka waktu yang lama tidak menimbulkan gejala, terutama bila batu menetap di kandung empedu. Kadang-kadang batu yang besar secara bertahap akan mengikis dinding kandung empedu dan masuk ke usus halus atau usus besar, dan menyebabkan penyumbatan usus (ileus batu empedu). Yang lebih sering terjadi adalah batu empedu keluar dari kandung empedu dan masuk ke dalam saluran empedu. Dari saluran empedu, batu empedu bisa masuk ke usus halus atau tetap berada di dalam saluran empedu tanpa menimbulkan gangguan aliran empedu maupun gejala. Gejala dan Tanda Jika batu empedu secara tiba-tiba menyumbat saluran empedu, maka penderita akan merasakan nyeri. Nyeri cenderung hilang-timbul dan dikenal sebagai nyeri kolik. Timbul secara perlahan dan mencapai puncaknya, kemudian berkurang secara bertahap. Nyeri bersifat tajam dan hilang-timbul, bisa berlangsung sampai beberapa jam. Lokasi nyeri berlainan, tetapi paling banyak dirasakan di perut atas sebelah kanan dan bisa menjalar ke bahu kanan. Penderita seringkali merasakan mual dan muntah. Jika terjadi infeksi bersamaan dengan penyumbatan saluran, maka akan timbul demam, menggigil dan sakit kuning (jaundice). Biasanya penyumbatan bersifat sementara dan jarang terjadi infeksi. Nyeri akibat penyumbatan saluran tidak dapat dibedakan dengan nyeri akibat penyumbatan kandung empedu. Penyumbatan menetap pada duktus sistikus menyebabkan terjadinya peradangan kandung empedu (kolesistitis akut). Batu empedu yang menyumbat duktus pankreatikus menyebabkan terjadinya peradangan pankreas (pankreatitis), nyeri, jaundice dan mungkin juga infeksi. Kadang nyeri yang hilang-timbul kambuh kembali setelah kandung empedu diangkat, nyeri ini mungkin disebabkan oleh adanya batu empedu di dalam saluran empedu utama. Komplikasi Komplikasi yang mungkin segera terjadi adalah: Perdarahan Peradangan pankreas (pankreatitis). erforasi atau infeksi saluran empedu. Pada 2-6% penderita, saluran menciut kembali dan batu empedu muncul lagi. Pencegahan Karena komposisi terbesar batu empedu adalah kolesterol, sebaiknya menghindari makanan berkolesterol tinggi yang pada umumnya berasal dari lemak hewani. Penatalaksanaan Jika tidak ditemukan gejala, maka tidak perlu dilakukan pengobatan. Nyeri yang hilang-timbul bisa dihindari atau dikurangi dengan menghindari atau mengurangi makanan berlemak. Batu kandung empedu Jika batu kandung empedu menyebabkan serangan nyeri berulang meskipun telah dilakukan perubahan pola makan, maka dianjurkan untuk menjalani pengangkatan kandung empedu (kolesistektomi). Pengangkatan kandung empedu tidak menyebabkan kekurangan zat gizi dan setelah pembedahan tidak perlu dilakukan pembatasan makanan. Kolesistektomi laparoskopik mulai diperkenalkan pada tahun 1990 dan sekarang ini sekitar 90% kolesistektomi dilakukan secara laparoskopi. Kandung empedu diangkat melalui selang yang dimasukkan lewat sayatan kecil di dinding perut. Jenis pembedahan ini memiliki keuntungan sebagai berikut: Mengurangi rasa tidak nyaman pasca pembedahan. Memperpendek masa perawatan di rumah sakit. Teknik lainnya untuk menghilangkan batu kandung empedu adalah: Pelarutan dengan metil-butil-eter. Pemecahan dengan gelombang suara (litotripsi). Pelarutan dengan terapi asam empedu menahun (asam kenodiol dan asam ursodeoksikolik). Batu saluran empedu batu saluran empedu bisa menyebabkan masalah yang serius, karena itu harus dikeluarkan baik melalui pembedahan perut maupun melalui suatu prosedur yang disebut endoscopic retrograde cholangiopancreatography (ERCP). Pada ERCP, suatu endoskop dimasukkan melalui mulut, kerongkongan, lambung dan ke dalam usus halus. Zat kontras radioopak masuk ke dalam saluran empedu melalui sebuah selang di dalam sfingter oddi. Pada sfingterotomi, otot sfingter dibuka agak lebar sehingga batu empedu yang menyumbat saluran akan berpindah ke usus halus. ERCP dan sfingterotomi telah berhasil dilakukan pada 90% kasus. Kurang dari 4 dari setiap 1.000 penderita yang meninggal dan 3-7% mengalami komplikasi, sehingga prosedur ini lebih aman dibandingkan pembedahan perut. ERCP saja biasanya efektif dilakukan pada penderita batu saluran empedu yang lebih tua, yang kandung empedunya telah diangkat.

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Bakteri Legionella Wabah di Bali Filed under: Uncategorized — Tinggalkan komentar Bakteri Legionella Wabah di Bali Apa itu Bakteri Legionella yang Diduga Mewabah di Bali? Bakteri Legionella Dugaan wabah legionella di Bali setelah dilaporkan ada beberapa turis Australia terkena serangan bakteri tersebut. Bakteri ini menyerang saluran pernafasan. Bakteri Legionella biasanya berkembang di air, khususnya pada lingkungan yang hangat seperti pada bak mandi dengan air panas, tangki berisi air panas, sistem pipa dan sistem pendingin udara. Pengertian Menurut Situs kalbe.co.id Legionellosis adalah suatu penyakit infeksi bakteri akut yang bersifat new emerging diseases. Secara keseluruhan baru dikenal 20 spesies dan penyebab Legionellosis adalah Legionella pneumophila. Dimana Bakteri ini hidup Bakteri Legionella biasa hidup di air laut, air tawar, sungai, lumpur, danau, mata air panas, genangan air bersih, air menara sistem pendingin di gedung bertingkat, hotel, spa, pemandian air panas, air tampungan sistem air panas di rumah-rumah, air mancur buatan yang tidak terawat baik, endapan, lendir, ganggang, jamur, karat, kerak, debu, kotoran, atau benda asing lainnya. Bakteri ini juga terdapat di peralatan rumah sakit seperti alat bantu pernafasan.

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KANKER OVARIUM DALAM KEHAMILAN Filed under: Uncategorized — Tinggalkan komentar Februari 13, 2011

KANKER OVARIUM DALAM KEHAMILAN Kanker adalah suatu masalah, terutama jika dialami oleh seorang wanita yang sementara hamil, apalagi jika kehamilan tersebut sangat diharapkan Walaupun kanker merupakan penyebab kedua terbanyak penyebab kematian pada usia reproduktif, namun angka kejadian kanker pada wanita hamil relatif jarang ditemukan. Penanganan diagnostik dan terapeutik terhadap wanita hamil sangat sulit dan diperlukan suatu kehati-hatian mengingat menyangkut dua jiwa, ibu dan janin yang dikandungnya. Kanker ovarium merupakan salah satu kasus keganasan ginekologik terbanyak yang ditemukan pada wanita hamil setelah kanker serviks dan kanker payudara. Kurang lebih 1 diantara 1000 kehamilan terdeteksi adanya tumor ovarium. Walaupun demikian, kebanyakan massa adneksa yang terdeteksi selama kehamilan bersifat jinak dan dapat mengecil dengan sendirinya pada trisemester kedua. Berdasarkan beberapa data yang ada, mungkin hanya berkisar 3-6% massa adneksa yang terdeteksi selama kehamilan menunjukkan tanda-tanda keganasan. Di Indonesia kanker ovarium sendiri menduduki urutan ke enam terbanyak dari keganasan pada wanita setelah karsinoma serviks uteri, payudara, kolorektal, kulit dan limfoma. Kanker ovarium merupakan tumor ganas ovarium yang dapat dikelompokkan atas 6 kelompok yaitu: epithelial, sel germinal, stromal and sex-cord, sel lipid, sarcoma dan metastasis karsinoma. Sampai saat ini faktor penyebab kanker ovarium belum diketahui secara pasti. Diduga adanya keterkaitan beberapa faktor antara lain: faktor lingkungan, diet, reproduksi, endokrin dan faktor herediter. Prinsip penanganan kanker ovarium pada wanita hamil sama halnya dengan wanita tidak hamil. Prognosisnya juga tampaknya tidak jauh berbeda pada wanita yang hamil maupun tidak hamil. Anatomi Ovarium Indung telur pada seorang wanita dewasa sebesar ibu jari tangan, terletak di kiri dan di kanan, dekat pada dinding pelvis di fossa ovarika. Ovarium berhubungan dengan uterus dengan ligamentum ovarii proprium. Pembuluh darah ke ovarium melalui ligamentum ovarii (ligamentum infundibulo pelvikum). Ovarium terletak pada lapisan belakang ligamentum latum. Sebagian besar ovarium berada intraperitoneal dan tidak dilapisi oleh peritoneum. Bagian ovarium kecil berada di dalam ligamentum latum (hilus ovarii). Di situ masuk pembuluh-pembuluh darah dan saraf ke ovarium. Lipatan yang menghubungkan lapisan belakang ligamentum latum dengan ovarium dinamakan mesovarium. Bagian ovarium yang berada dalam kavum peritonei dilapisi oleh epitel kubik-silindrik, disebut epithelium germinativum. Di bawah epitel ini terdapat tunika albuginea dan dibawahnya lagi baru ditemukan lapisan tempat folikel-folikel primordial. Pada wanita diperkirakan terdapat banyak folikel. tiap bulan satu folikel, kadang-kadang dua folikel, berkembang menjadi folikel de graaf. Folikel-folikel ini merupakan bagian ovarium yang terpenting dan dapat ditemukan di korteks ovarii dalam letak yang beraneka ragam, dan dapat pula dalam tingkat perkembangan dari satu sel telur yang dikelilingi oleh satu lapisan sel-sel saja sampai folikel de graaf yang matang ini terisi liquor follikuli yang mengandung estrogen dan siap untuk berovulasi. Menurut strukturnya ovarium terdiri dari : a. Kulit (korteks) atau zona parenkimatosa, terdiri dari : 1. Tunika albuginea, yaitu epitel berbentuk kubik 2. Jaringan ikat di sela-sela jaringan lain 3. Stroma, folikel primordial dan folikel de graaf 4. Sel-sel warthard b. Inti (medulla) atau zona vaskulosa, terdiri dari: 1. Stroma berisi pembuluh darah 2. Serabut saraf 3. Beberapa otot polos Pada waktu dilahirkan bayi mempunyai sekurang-kurangnya 750.000 oogonium. Jumlah ini berkurang akibat pertumbuhan dan degenerasi folikel-folikel. Pada umur 6-15 tahun ditemukan 439.000, pada 16-25 tahun 159.000, antara umur 26-35 tahun menurun sampai 59.000, dan antara 34-45 tahun hanya 34.000. Pada masa menopause semua folikel sudah menghilang.

Fisiologi Ovarium Ovarium memiliki dua fungsi utama yaitu : 1. Fungsi proliferatif (generatif) yaitu sebagai sumber ovum selama masa reproduksi. Di ovarium terjadi pembentukan folikel primer, folikel de graaf, peristiwa ovulasi dan pembentukan korpus luteum 2. Fungi sekretorik (vegetatif), yaitu tempat pembentukan dan pengeluaran hormon steroid (esterogen, progesteron dan androgen). Terkait dengan fungsinya, ovarium memiliki siklus yang turut serta dalam pengaturan haid. Siklus haid terjadi sebagai akibat pertumbuhan dan pengelupasan apisan endometrium uterus, sedangkan perubahan endometrium dikontrol oleh siklus ovarium. Rata-rata siklus 28 hari dan terdiri atas : 1. Fase folikular Hari ke 1-8 Pada awal siklus, kadar FSH dan LH relatif tinggi dan memacu perkembangan 0-20 folikel dengan satu folikel dominan. Folikel dominan tersebut tampak pada mid-folikuler dan sisa folikel mengalami atresia. Selama dan segera setelah haid kadar estrogen relatif rendah dan mulai meningkat karena terjadi perkembangan folikel. Hari ke 9-14 Sesuai peningkatan ukuran folikel, terjadi transformasi folikel primer menjadi folikel de graaf, dimana dikelilingi oleh 2-3 lapis sel granulose yang disebut kumulus ooforus. Sehubungan dengan pematangan folikel, terjadi kenaikan yang progresif dalam produksi esterogen (terutama estradiol) oleh sel granulose folikel. Mencapai puncak 18 jam sebelum ovulasi. Karena kadar esterogen meningkat, pelepasan gonadotropin FSH dan LH ditekan untuk mencegah hiperstimulasi ovarium dan pematangan banyak folikel. 2. Fase ovulasi Hari ke-14 Ovulasi adalah pembesaran folikel secara cepat yang diikuti oleh protusi dari permukaan korteks ovarium dan pecahnya folikel dengan ekskrusinya oosit yang ditempeli oleh cumulus ooforus. Perubahan hormon yang terjadi yaitu : estrogen meningkatkan sekresi LH (melalui hipotalamus) mengakibatkan meningkatnya produksi androgen dan estrogen (umpan balik positif), segera sebelum ovulasi terjadi penurunan kadar estradiol yang cepat dan peningkatan produksi progesteron. Ovulasi terjadi dalam 8 jam dan mid-cycle surge LH 3. Fase luteal Hari ke 15-28 Sisa folikel tertahan dalam ovarium dan dipenetrasi oleh kapilar dan fibroblast dari teka. Sel granulose mengalami luteinisasi menjadi korpus luteum. Korpus luteum merupakan sumber utama hormon steroid seks, estrogen dan progesterone disekrei oleh ovarium pada fase pasca ovulasi. Korpus luteum meningkatkan produksi progesteron dan estradiol. Kedua hormon tersebut diproduksi dari prekursor yang sama. Selama fase luteal kadar gonadotropin mencapai nadir dan tetap rendah sampai terjadi regresi korpus luteum yang terjadi pada hari ke 26-28. Jika terjadi konsepsi dan implantasi, korpus luteum tidak mengalami regresi karena dipertahankan oleh gonadotropin yang dihasilkan oleh trofoblas. Jika konsepsi dan implantasi tidak terjadi korpus luteum akan mengalami regresi dan terjadilah haid. Setelah kadar hormon steroid turun akan diikuti peningkatan gonadotropin untuk inisiasi siklus berikutnya. Terkait dengan fungsi sekretorik, ovarium membentuk hormon estrogen, progesteron dan sedikit andeogen. Estrogen secara umum berfungsi untuk peningkatan sintesis protein. Terhadap endometrium, esterogen berfungsi memicu proliferasi dan memperkuat kontraksi otot uterus. Terhadap serviks, esterogen meningkatkan sekresi getah serviks dan mengubah konsentrasinya pada saat ovulasi menjadi encer dan bening sehingga memudahkan penyesuaian dan memperlancar perjalanan spermatozoa. Terhadap vagina, estrogen menyebabkan perubahan selaput vagina, meningkatkan produksi getah dan meningkatkan kadar glikogen, sehingga terjadi peningkatan produksi asam laktat oleh bakteri Doderlein. Nilai pH yang rendah memperkecil kemungkinan terjadinya infeksi. Terhadap ovarium sendiri, estrogen berfungsi memicu sintesis reseptor FSH dan LH di sel-sel teka, mengatur kecepatan pengeluaran ovum dan mempersiapkan spermatozoa dalam genitalia wanita agar dapat menembus selubung ovum (proses kapisitasi). Progesteron secara umum berfungsi mempersiapkan tubuh untuk menerima kehamilan, sehingga merupakan syarat mutlak untuk konsepsi dan implantasi. Semua fungsi progesterone terjadi karena ada pengaruh estradiol sebelumnya, karena estradiol mensintesis reseptor untuk progesteron. Terhadap endometrium, progesteron menyebabkan perubahan sekretorik yang mencapai puncaknya pada hari ke-22 siklus haid normal. Bilamana progesteron terlalu lama memperngaruhi endometrium, maka akan terjadi degenerasi, sehingga tidak cocok lagi untuk menerima nidasi. Terhadap serviks pengaruh progesteron, jumlah getah serviks berkurang dan membentuk jala tebal sehingga merupakan sawar yang tidak dapat dilintasi oleh spermatozoa. Bersamaan dengan itu pula, porsio dan serviks menjadi sangat sempit, getahnya menjadi kental dan daya membenang menghilang. Terhadap miometrium progesteron menurunkan tonus, sehingga kontraksi berjalan lambat. Dalam kehamilan, fungsi ini sangat penting karena membuat uterus menjadi tenang. Progesterone juga menyebabkan peningkatan suhu badan basal segera setelah ovulasi. Hal tersebut terjadi melalui peningkatan sekresi norepinefrin yang timbul sekunder akibat meningkatnya kadar progesteron plasma terhadap pengaruh termogenik pusat pengaturan panas di hipotalamus. Insiden Pengunaan ultrasound (USG) dalam pemeriksaan kehamilan telah banyak membantu dalam mendeteksi adanya massa adneksa pada wanita-wanita hamil, namun kebanyakan massa adneksa yang terdeteksi selama kehamilan bersifat jinak. Estimasi insiden tumor ovarium itu sendiri kurang lebih 1 diantara 1000 kehamilan dan hanya sekitar 3%-6% dari massa adneksa tersebut yang bersifat ganas. Insiden kanker ovarium dalam kehamilan ditemukan kurang lebih 1 : 15.000 hingga 1: 32.000 kehamilan yang ada. Ueda dan Ueki melaporkan dari 106 kasus massa ovarium yang telah direseksi dari wanita hamil, 29% disebabkan oleh pembesaran fisiologis, 66%merupakan tumor jinak dan hanya 5% yang merupakan kanker ovarium. Menurut Burtness Barbara, insiden tumor jinak yang ditemukan 1 diantara 112 kasus,sedangkan tumor ganas ditemukan 1 diantara 1684 kasus. Penelitian yang dilakukan oleh Biomed Central, menemukan 603 kasuskanker ovarium selama periode tahun 1991 hingga 2002, 23 kasus diantara dalam 73,9% ditemukan pada stadium awal (stage 1), masa kehamilan. Rata-rata umur pasien tersebut dari 20-40 tahun. Gambaran histopatologi terbanyak yang ditemukan pada kelompok ini yaitu germ cell tumorsebanyak 11 dari 23 kasus. Kebanyakan kasus kanker ovarium dalam kehamilan didiagnosis pada stadium awal, hal ini sesuai dengan penelitian oleh BMC yaitu 73,9% ditemukan pada stadium awal (stage 1), dan hanya 17,3% yang ditemukan pada stadium lanjut yaitu stadium 3 dan 4.

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CPR ABC to ‘CAB’ New AHA guidlines for resuscitation Filed under: Uncategorized — Tinggalkan komentar

CPR ABC to ‘CAB’ New AHA guidlines for resuscitation Thursday, 11 November 2010 22:48 administrator American Heart Association (AHA) telah mengeluarkan panduan Resusitasi Jantung paru (RJP) secara periodik sejak tahun 1966 hingga sekarang. Publikasi panduan AHA tahun 2010 ini mengangkat banyak perhatian karena mengeluarkan sebuah perubahan standarisasi algoritma baru terutama untuk BLS yang cukup berbeda dari publikasi tahun 2005 yang telah dipakai secara universal dalam berbagai elemen. Basic Life Support (BLS) BLS adalah pilar dasar pertolongan pertama henti jantung. Aspek penting dalam BLS adalah pengenalan dini terhadap henti jantung dan mengaktivasi sistem respon darurat untuk memanggil bantuan, RJP dini yang berkualitas, penggunaan alat defibrilasi otomatis sesuai dengan indikasi.

Gambar 1. Chain of Survival3 Perubahan yang terlihat adalah pada algoritma Basic Life Support (BLS) umum untuk dewasa dan anak (terkecuali neonatus), yaitu urutan “A-B-C” (Airway, Breathing, Chest compression) yang telah lama digunakan kini berubah menjadi “C-A-B” (Chest compression, Airway, Breathing). Rekomendasi ini berdasarkan studi analisis komprehensif dari literatur mengenai resusitasi yang pernah dipublikasikan. Proses ini berlangsung selama 36 bulan, didalamnya terdapar 356 ahli resusitasi dari 29 negara yang telah menganalisa, mengevaluasi, mendebatkan dan mendiskusikan hal tersebut. Alasan untuk perubahan tersebut adalah : • Henti jantung terjadi sebagian besar pada dewasa. Angka keberhasilan kelangsungan hidup tertinggi dari pasien segala umur yang dilaporkan adalah henti jantung dan ritme Ventricular Fibrilation (VF) atau pulseless Ventrivular Tachycardia (VT). Pada pasien tersebut elemen RJP yang paling penting adalah kompresi dada (chest compression) dan defibrilasi otomatis segera (early defibrillation). • Pada langkah A-B-C yang terdahulu kompresi dada seringkali tertunda karena proses pembukaan jalan nafas (airway) untuk memberikan ventilasi mulut ke mulut atau mengambil alat pemisah atau alat pernafasan lainnya. Dengan mengganti langkah menjadi C-A-B maka kompresi dada akan dilakukan lebih awal dan ventilasi hanya sedikit tertunda satu siklus kompresi dada (30 kali kompresi dada secara ideal dilakukan sekitar 18 detik). • Kurang dari 50% orang yang mengalami henti jantung mendapatkan RJP dari orang sekitarnya. Ada banyak kemungkinan penyebab hal ini namun salah satu yang menjadi alasan adalah dalam algoritma A-B-C, pembebasan jalan nafas dan ventilasi mulut ke mulut dalam Airway adalah prosedur yang kebanyakan orang umum temukan paling sulit. Memulai dengan kompresi dada diharapkan dapat menyederhanakan prosedur sehingga semakin banyak korban yang bisa mendapatkan RJP. Untuk orang yang enggan melakukan ventilasi mulut ke mulut setidaknya dapat melakukan kompresi dada. AHA 2010 dalam panduannya memberikan 2 jenis algoritma BLS bagi korban dewasa yaitu sederhana untuk penolong non petugas kesehatan dan khusus untuk petugas kesehatan. Berikut algoritma terbaru dan penjelasannya.

Gambar 2. Algoritma BLS sederhana2 Algoritma sederhana ini diperuntukan untuk semua penolong untuk mempelajari, mengingat, dan mempraktekkan. Pengenalan dini. Jika seorang penolong menemukan korban dewasa yang tidak ada respon (tidak ada pergerakan atau respon terhadap stimulus luar) atau melihat korban tiba-tiba jatuh pingsan, maka penolong harus memastikan keamanan tempat kejadian lalu mengecek respon dengan menepuk bahu korban selagi meneriakkan nama korban. Jika penolong lebih dari satu orang maka langkah-langkah dalam algoritma ini dapat dilakukan bersamaan dan sinergis. Aktivasi sistem respon darurat. Penolong sebaiknya mengaktivasi sistem respon darurat yang dalam hal ini berarti menghubungi institusi yang mempunyai fasilitas/layanan gawat darurat, hal ini dapat beruba menghubungi rumah sakit, polisi, atau instansi terkait. Penolong non petugas kesehatan harus siap menerima instruksi dan melakukannya.2 Jika melihat korban tidak berespon dan dan tidak bernapas atau hanya sesak terengah-engah maka penolong dapat mengasumsikan bahwa korban mengalami henti jantung. Pemeriksaan denyut nadi. Riset menunjukkan bahwa terdapat kesulitan dalam pemeriksaan denyut nadi korban baik dilakukan oleh penolong non petugas ksesehatan ataupun petugas kesehatan sehingga dapat membuang waktu yang berharga. Karena hal tersebut maka terdapat dua rekomendasi baru yaitu : • Untuk penolong non petugas kesehatan tidak dianjurkan untuk memeriksa denyut nadi korban, penolong sebaiknya berasumsi bahwa korban mengalami henti jantung jika melihat gejala yang disebutkan diatas. • Untuk petugas kesehatan, pemeriksaan nadi korban sebaiknya tidak lebih dari 10 detik jika lebih dari waktu tersebut tidak didapatkan denyut nadi yang definitive maka petugas sebaiknya memulai RJP dengan kompresi dada. Resusitasi Jantung Paru dini. Berbeda dengan panduan BLS AHA 2005, kompresi dada dilakukan terlebih dahulu sebelum adanya dua kali ventilasi awal sehingga membentuk algoritma “CA-B”. Kompresi dada dilakukan sebanyak satu siklus (30 kompresi, sekitar 18 detik). Untuk mendapatkan kompresi dada yang efektif dalam algoritma tersebut terdapat dua kata kunci yaitu “push hard, push fast” yang berarti “tekan kuat, tekan cepat” hal ini memudahkan penolong non petugas kesehatan dalam melakukan kompresi seefektif mungkin. Dalam RJP yang efektif, kecepatan kompresi diharapkan mencapai sekitar 100 kompresi/menit dengan kedalaman sekitar 5 cm (2 inchi). Lokasi kompresi dilakukan pada tengah dada pasien. Setelah kompresi dada dilakukan sebanyak satu siklus dilanjutkan dengan ventilasi mulut ke mulut sebanyak dua kali ventilasi. Hal yang perlu diperhatikan adalah berikan jarak 1 detik antar ventilasi, perhatikan kenaikan dada korban untuk memastikan volume tidal yang masuk adekuat, dan perbandingan kompresi dan ventilasi untuk satu siklus adalah 30 : 2. Pengunaan alat defibrilasi otomatis. Algoritma diatas menunjukan adanya langkah terpisah untuk mendapatkan alat defibrilasi otomatis. Jika hanya terdapat satu penolong maka sebaiknya setelah mengaktivasi sistem darurat, penolong diharapkan mencari alat defibrilasi otomatis (jika tersedia dan dekat) lalu kembali ke korban untuk melakukan RJP. Jika ada lebih dari satu penolong maka langkah tersebut dilakukan bersamaan.2 Tipe strategi RJP. Terdapat 3 pola strategi RJP yang dapat diterapkan pada penolong sesuai dengan keadaannya. Pertama, untuk penolong non petugas kesehatan yang tidak terlatih, mereka dapat melakukan strategi “Hands only CPR” (hanya kompresi dada). Kompresi dada sebaiknya dilakukan hingga petugas kesehatan hadir atau alat defibrilasi otomatis tersedia. Kedua, untuk penolong non petugas kesehatan yang terlatih, mereka dapat melakukan strategi RJP kompresi dada dan dilanjutkan dengan ventilasi dengan perbandingan 30 : 2. RJP sebaiknya dilakukan hingga petugas kesehatan hadir atau alat defibrilasi otomatis tersedia. Ketiga, untuk petugas kesehatan, lakukan RJP kompresi dada sebanyak satu siklus yang dilanjutkan dengan ventilasi dengan perbandingan 30 : 2. Lakukan hal tersebut hingga advanced airway tersedia, kemudian lakukan kompresi dada tanpa terputus sebanyak 100 kali/menit dan ventilasi setiap 6-8 detik/kali (8-10 nafas/menit). Untuk petugas kesehatan penting untuk mengadaptasi urutan langkah sesuai dengan penyebab paling mungkin yang terjadi pada saat itu. Contohnya, jika melihat seseorang yang tiba-tiba jatuh, maka petugas kesehatan dapat berasumsi bahwa korban mengalami fibrilasi ventrikel, setelah petugas kesehatan mengkonfirmasi bahwa korban tidak merespon dan tidak bernapas atau hanya sesak terengah-engah, maka petugas sebaiknya mengaktifasi sistem respon darurat untuk memanggil bantuan, mencari dan menggunakan AED (Automated External Defibrilator), dan melakukan RJP. Namun jika petugas menemukan korban tenggelam atau henti nafas maka petugas sebaiknya melakukan RJP konvensional (A-B-C) sebanyak 5 siklus (sekitar 2 menit) sebelum mengaktivasi sistem respon darurat. Sama halnya dalam bayi baru lahir, penyebab arrestkebanyakan adalah pada sistem pernafasan maka RJP sebaiknya dilakukan dengan siklus A-B-C kecuali terdapat penyebab jantung yang diketahui.

Gambar 3. Algoritma BLS untuk petugas kesehatan Untuk petugas kesehatan, prinsip dasar langkah-langkah algoritma tetap sama dengan yang sederhana. Pengenalan dini. Jika melihat seorang yang tiba-tiba jatuh atau tidak responsive maka petugas kesehatan harus mengamankan tempat kejadian dan memeriksa respon korban. Tepukan pada pundak dan teriakkan nama korban sembari melihat apakah korban tidak bernafas atau terengah-engah. Lihat apakah korban merespon dengan jawaban, erangan atau gerakan. Korban yang tidak responsif serta tidak ada nafas atau hanya terengah-engah maka petugas kesehatan dapat mengasumsi bahwa korban mengalami henti jantung. Aktivasi sistem darurat. Petugas sebaiknya mengaktivasi sistem respon darurat yang dalam hal ini berarti menghubungi institusi yang mempunyai fasilitas/layanan gawat darurat, contohnya menghubungi rumah sakit, polisi, atau instansi terkait. Hal yang perlu diperhatikan adalah pada AHA 2010 ini ada dua hal yang tidak dianjurkan setelah memeriksa korban tidak responsif yaitu : • Memeriksa ada tidaknya nafas pada korban dengan “look, feel, listen”. Sulitnya menilai nafas yang adekuat pada korban merupakan alasan dasar hal tersebut tidak dianjurkan. Nafas yang terengah dapat disalah artikan sebagai nafas yang adekuat oleh professional maupun bukan. Contohnya pada korban dengan sindroma koroner akut sering kali terdapat nafas terengah yang dapat disalah artikan sebagai pernafasan yang adekuat. Maka tidak dianjurkan memeriksa pernafasan dengan “look, feel, listen” dan direkomendasikan untuk menganggap pernafasan terengah sebagai tidak ada pernafasan. • Memeriksa denyut nadi pasien. Untuk petugas kesehatan, pemeriksaan nadi korban sebaiknya tidak lebih dari 10 detik jika lebih dari waktu tersebut tidak didapatkan denyut nadi yang definitive maka petugas sebaiknya memulai RJP. Kedua hal tersebut tidak lagi dianjurkan bertujuan untuk meminimalisir waktu untuk memulai RJP. Resusitasi Jantung Paru dini. Seperti yang telah disebutkan, mulai RJP dengan algoritma “C-A-B” . Lakukan kompresi dada sebanyak 30 kompresi (sekitar 18 detik). Kriteria penting untuk mendapatkan kompresi yang berkualitas adalah : • Frekuensi kompresi setidaknya 100 kali/menit. • Kedalaman kompresi untuk dewasa minimal 2 inchi (5 cm), sedangkan untuk bayi minimal sepertiga dari diameter anterior-posterior dada atau sekitar 1 ½ inchi (4 cm) dan untuk anak sekitar 2 inchi (5 cm). • Lokasi kompresi berada pada tengah dada korban (setengah bawah sternum). Petugas berlutut jika korban terbaring di bawah, atau berdiri disamping korban jika korban berada di tempat tidur (bila perlu dengan bantuan ganjalan kaki untuk mencapai tinggi yang diinginkan sehingga dan papan kayu untuk mendapatkan kompresi yang efektif selama tidak memakan waktu). • Menunggu recoil dada yang sempurna dalam sela kompresi. • Meminimalisir interupsi dalam sela kompresi. • Menghindari ventilasi berlebihan. • Jika ada 2 orang maka sebaiknya pemberi kompresi dada bergantian setiap 2 menit. Setelah itu melakukan langkah Airway dan Breathing. Kriteria peting pada Airway dan Breathing adalah : • Airway. Korban dengan tidak ada/tidak dicurgai cedera tulang belakang maka bebaskan jalan nafas melalui head tilt– chin lift. Namun jika korban dicurigai cedera tulang belakang maka bebaskan jalan nafas melalui jaw thrust. • Breathing. Berikan ventilasi sebanyak 2 kali. Pemberian ventilasi dengan jarak 1 detik diantara ventilasi. Perhatikan kenaikan dada korban untuk memastikan volume tidal yang masuk adekuat. Untuk pemberian mulut ke mulut langkahnya sebagai berikut : • Pastikan hidung korban terpencet rapat • Ambil nafas seperti biasa (jangan terelalu dalam) • Buat keadaan mulut ke mulut yang serapat mungkin • Berikan satu ventilasi tiap satu detik • Kembali ke langkah ambil nafas hingga berikan nafas kedua selama satu detik. Jika tidak memungkinkan untuk memberikan pernafasan melalui mulut korban dapat dilakukan pernafasan mulut ke hidung korban. Untuk pemberian melalui bag mask pastikan menggunakan bag mask dewasa dengan volume 1-2 L agar dapat memeberikan ventilasi yang memenuhi volume tidal sekitar 600 ml. Setelah terpasang advance airway maka ventilasi dilakukan dengan frekuensi 6 – 8 detik/ventilasi atau sekitar 8-10 nafas/menit dan kompresi dada dapat dilakukan tanpa interupsi. Jika pasien mempunyai denyut nadi namun membutuhkan pernapasan bantuan, ventilasi dilakukan dengan kecepatan 5-6 detik/nafas atau sekitar 10-12 nafas/menit dan memeriksa denyut nadi kembali setiap 2 menit. Untuk satu siklus perbandingan kompresi dan ventilasi adalah 30 : 2, setelah terdapat advance airway kompresi dilakukan terus menerus dengan kecepatan 100 kali/menit dan ventilasi tiap 68 detik/kali. RJP terus dilakukan hingga alat defibrilasi otomatis datang, pasien bangun, atau petugas ahli datang. Bila harus terjadi interupsi, petugas kesehatan sebaiknya tidak memakan lebih dari 10 detik, kecuali untuk pemasangan alat defirbilasi otomatis atau pemasangan advance airway. Alat defibrilasi otomatis. Penggunaanya sebaiknya segera dilakukan setelah alat tersedia/datang ke tempat kejadian. Pergunakan program/panduan yang telah ada, kenali apakah ritme tersebut dapat diterapi kejut atau tidak, jika iya lakukan terapi kejut sebanyak 1 kali dan lanjutkan RJP selama 2 menit dan periksa ritme kembali. Namun jika ritme tidak dapat diterapi kejut lanjutkan RJP selama 2 menit dan periksa kembali ritme. Lakukan terus langkah tersebut hingga petugas ACLS (Advanced Cardiac Life Support ) datang, atau korban mulai bergerak. Posisi mantap. Lebih dikenal dengan recovery posisition, dipergunakan pada korban tidak responsive yang memiliki pernafasan dan sirkulasi yang baik. Tidak ada posisi baku yang menjadi standar, namun posisi yang stabil dan hamper lateral menjadi prinsip ditambah menaruh tangan yang berada lebih bawah ke kepala sembari mengarahkan kepala menuju tangan dan menekuk kedua kaki menunjukan banyak manfaat.2 Referensi: • John M. Field, Part 1: Executive Summary: 2010 American Heart Association Guidelines forCardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122;S640-S656. • Robert A. Berg, et al. Part 5: Adult Basic Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation2010;122;S685-S705. • Andrew H. Travers, et al. Part 4: CPR Overview: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122;S676-S684 • Anggaditya Putra, MD.CPR ABC to ‘CAB’ New AHA guidlines for resuscitation.http://www.exomedindonesia.com /referensi-kedokteran/artikel-ilmiah-kedokteran/jantung-danpembuluh-darah-cardiovaskular/2010/11/06/cpr-abc-to-cba-new-aha-guidlines-for-resuscitation/

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Cedera Medula Spinalis Filed under: Uncategorized — Tinggalkan komentar

Cedera Medula Spinalis PENDAHULUAN Cedera pada medula spinalis dapat menyebabkan hilangnya fungsi-fungsi pada susunan saraf pusat yaitu fungsi motorik, fungsi sensorik dan fungsi otonom. KLASIFIKASI Menurut American Spinal Injury Association: 1. Grade A : Hilangnya seluruh fungsi motorik dan sensorik di bawah tingkat lesi. 2. Grade B : Hilangnya seluruh fungsi motorik dan sebagian fungsi sensorik di bawah tingkat lesi. 3. Grade C : Fungsi motorik intak tetapi dengan kekuatan di bawah 3. 4. Grade D : Fungsi motorik intak dengan kekuatan motorik di atas atau sama dengan 3. 5. Grade E : Fungsi motorik dan sensorik normal. DIAGNOSIS Apabila medula spinalis tiba-tiba mengalami kerusakan, maka akan ada 3 kelainan yang muncul, yaitu: 1. Semua pergerakan volunter di bawah lesi hilang secara mendadak dan bersifat permanen, sedangkan refleks fisiologis bisa menghilang atau meningkat. 2. Sensasi sensorik di bawah lesi juga menghilang, 3. Terjadi gangguan fungsi otonom. Cedera medula spinalis dapat menghasilkan satu atau lebih tanda-tanda klinis di bawah ini: 1. Nyeri menjalar. 2. Kelumpuhan/hilangnya pergerakan. 3. Hilangnya sensasi rasa. 4. Hilangnya kemampuan peristaltik usus. 5. Spasme otot atau bangkitan refleks yang meningkat. 6. Perubahan fungsi seksual. Pemeriksaan Fisik Untuk semua pasien trauma, pemeriksaan awal dimulai dengan penilaian kondisi jalan napas (airway), pernapasan (breathing) dan peredaran darah (circulation). Selain itu, adanya riwayat penyakit kardiopulmonal harus diketahui melalui anamnesis, karena memengaruhi fungsi paru. Pemeriksaan Penunjang – Foto Polos Vertebra. Merupakan langkah awal untuk mendeteksi kelainan-kelainan yang melibatkan medula spinalis, kolumna vertebralis dan jaringan di sekitarnya. Pada trauma servikal digunakan foto AP, lateral, dan odontoid. Pada cedera torakal dan lumbal, digunakan foto AP dan Lateral. – CT-scan Vertebra. Pemeriksaan ini dapat memperlihatkan jaringan lunak, struktur tulang, dan kanalis spinalis dalam potongan aksial. CT-Scan merupakan pilihan utama untuk mendeteksi cedera fraktur pada tulang belakang. – MRI Vertebra. MRI dapat memperlihatkan seluruh struktur internal medula spinalis dalam sekali pemeriksaan. PENATALAKSANAAN Tiga fokus utama penanganan awal pasien cedera medula spinalis yaitu: 1. mempertahankan usaha bernapas, 2. mencegah syok, dan 3. imobilisasi leher (neck collar dan long spine board). Selain itu, fokus selanjutnya adalah mempertahankan tekanan darah dan per napasan, stabilisasi leher, mencegah komplikasi (retensi urin atau alvi, komplikasi kardiovaskuler atau respiratorik, dan trombosis vena-vena profunda). Terapi utama: 1. Farmakoterapi. Metilprednisolon 30 mg/kg bolus selama 15 menit, lalu 45 menit setelah pemberian bolus pertama, lanjutkan dengan infus 5,4 mg/kg/jam selama 23 jam. 2. Imobilisasi. Traksi, untuk menstabilkan medula spinalis. 3. Bedah. Untuk mengeluarkan fragmen tulang, benda asing, reparasi hernia diskus atau fraktur vertebra yang mungkin menekan medula spinalis; juga diperlukan untuk menstabilisasi vertebra untuk mencegah nyeri kronis. PROGNOSIS Pasien dengan cedera medula spinalis komplet hanya mempunyai harapan untuk sembuh kurang dari 5%. Jika kelumpuhan total telah terjadi selama 72 jam, maka peluang untuk sembuh menjadi tidak ada. Jika sebagian fungsi sensorik masih ada, maka pasien mempunyai kesempatan untuk dapat berjalan kembali sebesar 50%. Secara umum, 90% penderita cedera medula spinalis dapat sembuh dan mandiri.

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Wound Care Filed under: Uncategorized — 1 Komentar Wound Care This article discusses the management of chronic wounds. This topic is naturally diverse and far-reaching. Wound care in general and in terms of specific etiologies is considered. The images below depict a sacral pressure ulcer. Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture. Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture. Sacral pressure ulcer before and after flap closure. Sacral pressure ulcer before and after flap closure. Recent studies In a prospective study, Campbell et al determined the incidence of heel pressure ulcers in 150 orthopedic patients. The cohort consisted of patients who were admitted to an acute care hospital either for elective orthopedic surgery or for treatment of a fractured hip. The incidence of heel pressure ulcers in all patients was 13.3%, with the incidence in patients with hip fracture being higher than that in the elective surgery patients (16% vs 13%, respectively). However, patients with hip fracture in whom pillows and rolled sheets were used to relieve heel pressure had a significantly lower ulcer rate than did the other hip fracture patients. When all patients in the study were taken into account, the presence of respiratory disease was the only factor significantly associated with pressure ulcer development.1 Frequency Pressure ulcers occur in approximately 9% of hospitalized patients, usually during the first 2 weeks of hospitalization. A study found that even with the use of a pressure-reducing bed and early nutritional support, 3% of patients in a surgical intensive care unit who were employed in the study developed pressure ulcers.2 The annual risk of pressure ulceration in patients with neurologic impairment is 5-8%, with a lifetime risk of approximately 85% and a mortality rate of 8%. The prevalence of pressure ulcers among patients residing in long-term care facilities has been reported as 2.3-28% and has been an increasingly common reason for litigation.3,4,5,6,7 The presence of a pressure ulcer increases a nurse’s workload by 50% for the patient and adds approximately $20,000 to the hospital bill. The treatment of pressure ulcers in the United States is estimated to cost more than $1 billion annually. Venous ulcers make up 70% of chronic lower extremity ulcers.8 The incidence of venous ulcers in the United States is approximately 600,000 cases annually. The recurrence rate is up to 90%. According to the National Institute of Diabetes and Digestive and Kidney Diseases, an estimated 18 million Americans (6.3% of the population) are known to have diabetes, and millions more are considered to be at risk. Of those at risk, diabetes is undiagnosed in 5.2 million. Diabetic foot lesions are responsible for more hospitalizations than any other complication of diabetes. Among patients with diabetes, 15% will develop a foot ulcer, and 12-24% of those with a foot ulcer will require amputation. Indeed, diabetes is the leading cause of nontraumatic lower-extremity amputations in the United States, accounting for 60% of these amputations. Every year approximately 5% of persons with diabetes develop foot ulcers, and 1% require amputation.9 Diabetic peripheral neuropathy confers the greatest risk of foot ulceration; microvascular disease and suboptimal glycemic control contribute. Even with successful treatment resulting in ulcer healing, the recurrence rate in that patient population is 66%, and the amputation rate rises to 12%.10 For excellent patient education resources, visit eMedicine’s Diabetes Center. Also, see eMedicine’s patient education article Diabetic Foot Care. Etiology In general, factors that adversely affect wound healing can be remembered by using the mnemonic device DIDN’T HEAL, as follows: D = Diabetes: The long-term effects of diabetes impair wound healing by diminishing sensation and arterial inflow. In addition, even acute loss of diabetic control can affect wound healing by causing diminished cardiac output, poor peripheral perfusion, and impaired polymorphonuclear leukocyte phagocytosis. I = Infection: Infection potentiates collagen lysis. Bacterial contamination is a necessary condition but is not sufficient for wound infection. A susceptible host and wound environment are also required. Foreign bodies (including sutures) potentiate wound infection. D = Drugs: Steroids and antimetabolites impede proliferation of fibroblasts and collagen synthesis. N = Nutritional problems: Protein-calorie malnutrition and deficiencies of vitamins A, C, and zinc impair normal wound-healing mechanisms. T = Tissue necrosis, resulting from local or systemic ischemia or radiation injury, impairs wound healing. Wounds in characteristically well-perfused areas, such the face and neck, may heal surprisingly well despite unfavorable circumstances. Conversely, even a minor wound involving the foot, which has a borderline blood supply, may mark the onset of a long-term, nonhealing ulcer. Hypoxia and excessive tension on the wound edges also interfere with wound healing because of local oxygen deficits. See, for example, the pressure ulcers shown in the image below. Pressure ulcers of the lateral aspect of the right foot. Pressure ulcers of the lateral aspect of the right foot. H = Hypoxia: Inadequate tissue oxygenation due to local vasoconstriction resulting from sympathetic overactivity may occur because of blood volume deficit, unrelieved pain, or hypothermia, especially involving the distal extent of the extremities. E = Excessive tension on wound edges: This leads to local tissue ischemia and necrosis. A = Another wound: Competition between several healing areas for the substrates required for wound healing impairs wound healing at all sites. L = Low temperature: The relatively low tissue temperature in the distal aspects of the upper and lower extremities (a reduction of 1-1.5°C [2-3°F] from normal core body temperature) is responsible for slower healing of wounds at these sites. Specific etiologies Arterial insufficiency See Infrainguinal Occlusive Disease. Venous insufficiency Patients with varicose veins or nonfunctional venous valves after deep vein thrombosis develop ambulatory venous hypertension, that is, distal venous pressure remains elevated despite ambulation. This constant venous hypertension seems to cause white cell and fibrin buildup, which impairs capillary blood flow or traps growth factors. Macromolecules pass into the dermis and eventually cause the hemosiderin deposition and brawny induration in the distal leg (gaiter area) characteristic of chronic venous insufficiency. Lymphedema Although not typically a cause of ulceration, extremity ulcers may fail to heal because of untreated lymphedema. Nocturnal leg elevation and elastic wraps or support hose are appropriate adjuncts to the treatment of recalcitrant wounds in edematous extremities. For advanced and nonresponsive lymphedema, complex decongestive physiotherapy is a useful treatment option. Neuropathy Sensory neuropathy involving the feet may lead to unrecognized episodes of trauma caused by ill-fitting shoes. This is compounded by motor neuropathy causing intrinsic muscle weakness and spaying of the foot on weight bearing. The result is a convex foot with a rocker-bottom appearance. Multiple fractures go unnoticed, until bone and joint deformities become marked. This is termed a Charcot foot (ie, neuropathic osteoarthropathy) and is observed most commonly in people with diabetes mellitus, affecting approximately 2% of persons with diabetes. Pressure (decubitus) ulcers Pressure (decubitus) ulcers occur because of prolonged ischemia-producing external pressure, usually to a soft tissue region overlying a bony prominence. Tissue ischemia results when external pressure exceeds capillary closing pressure (ie, 25-32 mm Hg in healthy individuals), the minimum pressure that causes collapse of the capillary when applied to a capillary bed. Shearing forces, exposure to constant moisture, and heat buildup also are major contributing factors. For example, the stratum corneum, the outer layer of skin, becomes 25 times more fragile at a relative humidity of 100% than at a relative humidity of 25% and becomes 4 times more fragile at 95°F (35°C) than at 86°F (30°C). Neoplasms Neoplasms strongly suggest malignancy in any chronic nonhealing wound, particularly if the wound appears to have occurred spontaneously.11 Basal cell carcinoma appears smooth, pearly, and elevated above the skin surface, as illustrated in the image below, whereas squamous cell cancer is often somewhat erythematous and scaly and almost always occurs on sun-exposed areas. Particularly pertinent in wound care is the so-called Marjolin ulcer, a squamous cell carcinoma originating in a chronic wound, such as a burn scar or sinus tract.12 This implies that even a wound that is decades old is not necessarily benign. Patients with Kaposi sarcoma typically present with multifocal violaceous lower extremity lesions. Patients with cutaneous lymphoma present with a single nodule or a group of papules from one to several centimeters in diameter, and these almost always occurs above the waist. Basal cell cancer manifesting as a chronic leg ulcer. Basal cell cancer manifesting as a chronic leg ulcer. Perform a biopsy of every wound suggestive of neoplasm, but remember that biopsy findings are diagnostic only if an adequate representative specimen is obtained. Radiation damage The adverse effects of prolonged or excessive electromagnetic radiation vary with the wavelength. Wavelengths of electromagnetic radiation are as follows: Gamma rays – Less than 0.01 nm X-rays – 0.01-10 nm Ultraviolet C – 10-280 nm Ultraviolet B – 280-320 nm Ultraviolet A – 320-400 nm Visible light – 400-760 nm Infrared – 760 nm to 1 mm Microwave – 1 mm to 30 cm Radio waves – Centimeters to meters Gamma radiation and x-ray exposure cause a zone of stasis, in which local blood supply is impaired by coagulative necrosis due to thrombotic occlusion of smaller arteries. Gamma and x-ray radiation also spawn ionized oxygen that adversely affects DNA. The long-term result is inhibition of regeneration of skin cells from dividing basal cells. This may cause recalcitrant painful skin ulcers. The surrounding skin is atrophic, with atrophy of hair follicles and a paucity subcutaneous fat. Ultraviolet radiation exposure, particularly ultraviolet B, causes sunburn initially and subsequently conveys a continuing risk of skin malignancy (eg, basal cell carcinoma, squamous cell carcinoma, melanoma). Excessive exposure to infrared radiation, which induces repeated or persistent skin hyperthermia of 43-47°C, may cause erythema ab igne. Patients with this skin condition present with telangiectasia, erythematous patches, and hyperpigmentation. Atheroembolism syndrome Patchy areas of ischemia involving the feet, especially in the presence of palpable pedal pulses, suggest the possibility of atheroembolism of plaque fragments from ulcerated, although nonocclusive, proximal atherosclerotic plaques or from thrombi lining the wall of an infrarenal aortic aneurysm. Pyoderma gangrenosum Pyoderma gangrenosum usually starts as a small painful papule or nodule, which is often erroneously presumed to be the result of an insect bite. The lesion enlarges, becomes ulcerated, and develops overhanging, violaceous borders, as shown in the image below. Chronic ulcer of medial aspect of right leg due to pyoderma gangrenosum. Chronic ulcer of medial aspect of right leg due to pyoderma gangrenosum. The histologic findings often are nonspecific. Associated underlying systemic problems, which occur in one half of patients with pyoderma gangrenosum, are often the best clues to the diagnosis. Examples of such systemic diseases include various arthritides, inflammatory bowel disease, hepatitis, myeloproliferative disorders, myeloma, primary biliary cirrhosis, systemic lupus erythematosus, and Sjögren syndrome. An important clue is a paradoxical response in which debridement exacerbates the wound, particularly near the areas debrided. When myofascial and osseous tissues become involved, the only choice may be surgical debridement to try to save the extremity.13,14 Sickle cell

Patients with sickle cell–associated leg ulcers typically present with painful small ulcers that start as crusting nodules in the distal one third of the leg, often near the malleoli. The surrounding skin demonstrates absence of hair follicles, hyperpigmentation, and atrophy of subcutaneous fat. Radiograph findings may reveal periosteal thickening of underlying bone; true osteomyelitis is rare. Sickle cell ulcers are more common in males than in females and occur predominantly in persons aged 10-50 years. Patients with sickle cell anemia can also develop leg ulcers because of other etiologies; the physical examination should exclude arterial and venous insufficiency. Calciphylaxis Calciphylaxis is an unusual and often fatal syndrome of cutaneous necrosis that tends to develop in patients with chronic renal failure, particularly those with diabetes. The average time of onset is 3 years after the start of dialysis. The female-to-male ratio is 3:1. The initial finding of calciphylaxis may be that of livedo reticularis, followed by painful erythematous areas of thickening of the skin and subcutaneous tissues. The most common site is the thigh, though the condition may also occur in the legs or the upper extremities.15,16 Panniculitis signaling the onset of calciphylaxis may be precipitated by trauma, such as the site of an injection. Proximal painful myopathy, muscle weakness, and elevated serum creatine kinase (CK) levels may occur. Laboratory testing may demonstrate a high serum phosphate level and an elevated parathyroid hormone level. Skin biopsy reveals calcification of the arterial media and luminal stricture of small-to-medium blood vessels in the subcutaneous fat. Muscle biopsy shows patchy necrosis and atrophy.17 Necrobiosis lipoidica Necrobiosis lipoidica usually involves the anterior tibial areas, though it can also occur in the face, arms, and chest. Patients present with well-circumscribed, shiny, reddish-brown, oval, painless nodules or papules that have a thick shiny surface. Over several months or a year, the lesions may gradually expand and develop a waxy yellow color. Trauma may lead to infected ulcerations, and involvement of adjacent cutaneous nerves may precipitate considerable pain. Necrobiosis lipoidica is more common in women and in persons with diabetes than in others, but it may also occur in persons without diabetes and before the diagnosis of diabetes.18 Long-standing necrobiosis lipoidica may harbor a squamous cell carcinoma. Vasculitic wounds Vasculitic wounds tend to occur throughout the lower legs as multiple, small, painful, erythematous nodules. Scars resulting from previous vasculitic lesions may be a useful clue. Any of the disparate systemic manifestations of the diseases of cellular immunity associated with atypical skin lesions, including unexplained fevers, jaw claudication, malaise, Raynaud phenomenon, myalgias, neurologic abnormalities, and craniofacial pain syndromes, suggest the possibility of vasculitis. These lesions are rare. The differential diagnosis of wounds with these features includes other uncommon problems, such as anticoagulant-induced skin necrosis, atheroembolism syndrome (ie, trash foot), and Buerger disease. Leukocytoclastic vasculitides represent a disparate group of acquired connective tissue problems; patients present with palpable purpuric skin lesions, petechiae, and ecchymoses, usually involving the lower extremities. These syndromes include Wegener granulomatosis, Sjögren syndrome, cryoglobulinemia, systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis, and hepatitis B. The common factor among these syndromes is a hypersensitivity angiitis.19 Skin biopsy demonstrates cuffing of the dermal microcirculation by granulocytes, which are found in diverse stages of viability, including complete cellular disintegration (ie, nuclear dust). The various disorders in this group are differentiated by clinical and serologic criteria. The presence of asymptomatic palpable purpura without thrombocytopenia suggests a drug adverse effect, such as those caused by iodides, penicillin, aspirin, chlorothiazides, oxytetracycline, isoniazid, or benzoic acid. Anticoagulant-induced skin necrosis Anticoagulant-induced skin necrosis is an unusual complication of anticoagulant therapy.20 It may occur with heparin or warfarin, though it is more common with warfarin. Warfarin-induced skin necrosis manifests as painful hemorrhagic skin lesions, usually in an area having abundant adipose tissue, such as the thighs, abdomen, or breasts. The female-to-male ratio is 4:1. This complication is often attributable to hereditary coagulation abnormalities. Warfarin (Coumadin) depletes vitamin K–dependent coagulation factors, such as protein C. Therefore, during the first several days of warfarin therapy, a period of transient hypercoagulability may occur, particularly in patients with hereditary coagulation abnormalities, such as protein C deficiency or protein S deficiency, antithrombin 3 deficiency, or activated protein C resistance.20 Actinomycosis Actinomyces israelii is a fastidious anaerobic bacterium that is relatively common and usually nonpathogenic. In rare individuals, particularly hosts who are immunocompromised, the bacterium can become pathogenic and cause chronic, draining, painless skin ulcers and sinuses, usually in the head and neck. False-negative tissue cultures are common because the organism is often difficult to culture in vitro. However, microscopic examination of wound exudates may demonstrate characteristic sulfur granules. Actinomycosis is responsive to penicillin but requires long-term therapy. Yaws Yaws is a treponematosis caused by Treponema pertenue, which is endemic in humid regions near the equator. Approximately 3-4 weeks after exposure, a pruritic sore that resembles a raspberry (the mother yaw) develops at the site where the spirochete enters the skin. This lesion eventually opens to form an ulcer. Scratching spreads the organism and results in multiple tubercles and ulcerations elsewhere, including the hands, feet, and genitals. These ulcers may have a caseous crust. Results of serologic testing for syphilis may be positive. Treatment is with a single large dose of penicillin. Untreated yaws can erode to bone and joints and can become deforming and crippling. The lesions of pinta, caused by Treponema carateum, are similar to those of yaws, but, unlike yaws, no ulceration is present. Pinta typically begins as a papule on the dorsum of the foot or leg. The papule enlarges and becomes a pruritic plaque, which changes from a copper to gray to bluish color over time. Regional lymphadenopathy may occur. Pinta is also responsive to penicillin. Mucormycosis Mucormycosis is an acute and sometimes rapidly progressive, even fatal, fungal infection that may occur in patients who are immunocompromised, especially following a burn. The primary lesions are plaques, ulcerations and abscesses, or painful ecchymotic nodules, which may ulcerate and then become necrotic and form eschars. The diagnosis is confirmed by demonstrating fungal elements of the black discharge in KOH preparations and by culturing on standard laboratory media. Cutaneous anthrax Cutaneous anthrax results from skin exposure to Bacillus anthracis, a gram-positive bacillus. Cutaneous anthrax evolves from a pruritic papule to an ulcerated wound in 1 or 2 days and then into a black eschar over the next week or so. Associated regional lymphadenopathy may be present. Findings on special stains and cultures of the wound exudate are diagnostic. Anthrax is transmissible from specimens; therefore, so laboratory personnel should be warned in the event of clinical suspicion of this disease. Of course, appropriate public health authorities must be notified. See Anthrax for details. Pathophysiology The phases of normal wound healing can be described as follows: Hemostatic or inflammatory phase

This phase starts immediately and lasts 2-5 days. Tissue damage releases chemical mediators called cytokines (eg, transforming growth factor [TGF]-beta [interleukin-1beta]), which initiate a complex interrelated process that causes hemostasis and begins the healing process. Platelets aggregate to stem bleeding. They also release serotonin and other vasoconstrictors and activate the coagulation cascade. The result is conversion of fibrinogen into fibrin, which stabilizes the platelet plug. At that point, prostaglandins and activated complement cause vasodilation and increase capillary permeability. This allows plasma to leak into the tissue surrounding the wounded area. This is the inflammatory exudate. Monocytes and neutrophils are attracted to the site of injury. Neutrophils trap and kill bacteria immediately, while monocytes become activated macrophages, which produce growth factors and cytokines and scavenge nonviable tissue and bacteria. Angiogenic growth factors stimulate neovascularization of the wound bed. Proliferative phase This phase lasts from 2 days to 3 weeks. Macrophages recruit fibroblasts. These cells create a network of collagen fibers. When adequate oxygen and vitamin C are present, granulation tissue forms. Oxygen is incorporated by 2 amino acids, proline and lysine, which are both required for collagen chain synthesis. Vitamin C is required for the hydroxylation of proline to hydroxyproline, an amino acid found in collagen. During granulation, fibroblasts create a collagen bed to fill the defect and grow new capillaries. During contraction, myofibroblasts pull the wound edges closer together to decrease the size of the wound. During epithelialization, new epithelium migrates from the intact epidermis around the wound and can grow up to 3 cm over the granulation tissue. This process requires a moist surface. Remodeling phase This phase lasts from 3 weeks to 2 years.21 An organized form of collagen gradually replaces the immature, soft, gelatinous collagen. The effect is to increase the tensile strength of the healed wound, but it is less than 80% as strong as the original tissue. Types of wound healing First intention, also termed primary healing, is the healing that occurs when a clean laceration or a surgical incision is closed primarily with sutures, Steri-Strips, or skin adhesive. Second intention, also termed secondary healing, is the healing that occurs when a wound is left open to heal by granulation, contraction, and epithelialization. Delayed primary closure is a combination of the other 2 types of wound healing. It is often intentionally applied to lacerations that are not considered clean enough for primary closure. The wound is left open for 5-10 days; then, it is sutured closed to decrease the risk of wound infection. For excellent patient education resources, visit eMedicine’s Procedures Center. Also, see eMedicine’s patient education article Suture Care. Presentation See Etiology. Indications All chronic wounds require assessment.22 Many heal with topical wound care; some require surgical intervention. The details vary widely with the nature of the wound. This article provides information regarding wound care in general and specific wound etiologies in particular. Relevant Anatomy Life is a constant battle against entropy (ie, disorder). The skin provides the primary barrier between the human protoplasm and the entropy of the external environment. Histologically, the skin is divided into the epidermis and the dermis. The epidermis consists of 5 histologic strata. From superficial to deep these layers are the (1) stratum corneum, (2) stratum lucidum, (3) stratum granulosum, (4) stratum spinosum, and (5) stratum germinativum. The keratinocyte, the preponderant epidermal cell, is generated in the stratum germinativum and eventually desquamates (sloughs) when it reaches the stratum corneum. The dermis underlies the epidermis. A dermal vascular network functions in thermoregulation and provides metabolic support for the avascular epidermis. Fibroblasts synthesize supportive and structural polymers, including ground substance, collagen, and elastin. Skin appendages include sebaceous glands, hair follicles, and sweat glands. Wound Care: Treatment Treatment Medical Therapy General treatment of nonhealing wounds can be described as follows: See Treatment of specific types of wounds. Assess the entire patient Successful treatment of difficult wounds requires assessment of the entire patient and not just the wound. Systemic problems often impair wound healing; conversely, nonhealing wounds may herald systemic pathology. Consider the negative effects of endocrine diseases (eg, diabetes, hypothyroidism), hematologic conditions (eg, anemia, polycythemia, myeloproliferative disorders), cardiopulmonary problems (eg, chronic obstructive pulmonary disease, congestive heart failure), GI problems that cause malnutrition and vitamin deficiencies, obesity, and peripheral vascular pathology (eg, atherosclerotic disease, chronic venous insufficiency, lymphedema). Characterize the wound Assess the following: (1) size and depth of involvement and the extent of undermining; (2) the appearance of the wound surface, that is, necrotic or viable; (3) amount and characteristics of wound exudate; and (4) status of the periwound tissues (eg, pigmented, scarred, atrophic, cellulitic). Ensure adequate oxygenation The usual reason for inadequate tissue oxygenation is local vasoconstriction as a result of sympathetic overactivity. This may occur because of blood volume deficit, unrelieved pain, or hypothermia, especially involving the distal extent of the extremities. Ensure adequate nutrition Adequate nutrition is an often-overlooked requirement for normal wound healing.23 Address protein-calorie malnutrition and deficiencies of vitamins and minerals. Inadequate protein-calorie nutrition, even after just a few days of starvation, can impair normal wound-healing mechanisms. For healthy adults, daily nutritional requirements are approximately 1.25-1.5 g of protein per kilogram of body weight and 30-35 calories/kg. Increase these requirements for those with sizable wounds. Suspect malnutrition in patients with chronic illnesses, inadequate societal support, multisystemic trauma, or GI or neurologic problems that may impair oral intake. Protein deficiency occurs in approximately 25% of all hospitalized patients. Chronic malnutrition can be diagnosed by using anthropometric data to compare actual and ideal body weights and by observing low serum albumin levels. Serum prealbumin is sensitive for relatively acute malnutrition because its half-life is 2-3 days (vs 21 d for albumin). A serum prealbumin level of less than 7 g/dL suggests severe protein-calorie malnutrition. Vitamin and mineral deficiencies also require correction. Vitamin A deficiency reduces fibronectin on the wound surface, reducing cell chemotaxis, adhesion, and tissue repair. Vitamin C is required for the hydroxylation of proline and subsequent collagen synthesis. Vitamin E, a fat-soluble antioxidant, accumulates in cell membranes, where it protects polyunsaturated fatty acids from oxidation by free radicals, stabilizes lysosomes, and inhibits collagen synthesis. Vitamin E inhibits prostaglandin synthesis by interfering with phospholipase-A2 activity and is therefore anti-inflammatory. Vitamin E supplementation may decrease scar formation. Zinc is a component of approximately 200 enzymes in the human body, including DNA polymerase, which is required for cell proliferation, and superoxide dismutase, which scavenges superoxide radicals produced by leukocytes during debridement. Treat infection Issues to consider are wound infection versus colonization and osteomyelitis.24 A positive wound culture does not confirm a wound infection. Opportunistic microorganisms may colonize any wound. Wound exudate, which is naturally bactericidal, inhibits the spread of surface contamination from becoming a deep wound infection. However, when wound ischemia or systemic immune compromise supervenes, pathogenic microorganisms propagate until an excessive concentration of bacteria in the wound precludes healing. This heralds a true wound infection. Multidrug resistant organisms are becoming increasingly common. Foul-smelling drainage, a spontaneously bleeding wound bed, flimsy friable tissue, increased levels of wound exudate, increasing pain, surrounding cellulitis, crepitus, necrosis, fasciitis, and regional lymphadenopathy characterize the infected wound. Fever, chills, malaise, leukocytosis, and an elevated erythrocyte sedimentation rate are common systemic manifestations of wound infection. Wound infection requires surgical debridement and appropriate systemic antibiotic therapy. Topical antiseptics are usually avoided because they interfere with wound healing because of cytotoxicity to healing cells. Proving the absence of osteomyelitis is often as onerous as establishing its presence. Although osteomyelitis may be associated with fevers, malaise, chronic fatigue, and limited range of motion of the affected extremity, patients often present with only a nonhealing wound or a chronic draining sinus tract overlying a bone or joint. Plain radiographs, CT scans, radionuclide bone scans, and MRIs have a role in the workup of osteomyelitis. All too often, even a comprehensive imaging evaluation is nondiagnostic. Therefore, negative findings on radiologic workup should not deter the clinician from performing curettage of suspicious bone underlying a chronic draining wound. Osteomyelitis is treated with surgical curettage and appropriate systemic antibiotics. Provide a wound bed that is conducive to wound healing. Surgically debride nonvitalized tissue and with appropriate irrigation. Significant amounts of nonviable and fibropurulent tissue must be removed surgically. Initial aggressive debridement in the operating room with the patient under local anesthesia with sedation or under regional or general anesthesia is often wise. Subsequent debridement in an outpatient setting can be performed by using topical lidocaine gel or spray anesthesia and by gentle excision using iris scissors and forceps or by scraping using a curette. Dressing changes require clean but not necessarily sterile technique. Remove foreign bodies Be attentive to the possibility of foreign bodies, which may prevent healing of traumatic wounds, including road debris and retained fragments of dressing materials or suture material. Irrigate Gently irrigate the wound with a physiologic saline solution. If cost is a major consideration, the patient can prepare a saline solution at home by using 1 gallon of distilled water and 8 teaspoons of table salt. The solution is boiled and then cooled to room temperature before use. If surface exudate is present, consider irrigation under pressure. An irrigation pressure of approximately 8 psi can be achieved with saline forced through a 19-gauge angiocatheter with a 35mL syringe. Pat the wound surface with soft moist gauze; do not disrupt viable granulation tissue. Whirlpool treatment is reserved for large and infected wounds. Provide a moist (not wet) wound bed

After debridement, apply a moist saline dressing, an isotonic sodium chloride gel (eg, Normlgel [Scott Health Care], IntraSite gel), or a hydroactive paste (eg, DuoDerm [ConvaTec]). Optimal wound coverage requires wet-to-damp dressings, which support autolytic debridement, absorb exudate, and protect surrounding normal skin. A polyvinyl film dressing (eg, OpSite [Smith & Nephew], Tegaderm [3M]), which is semipermeable to oxygen and moisture and impermeable to bacteria, is a good choice for wounds that are neither dry nor highly exudative.

For dry wounds, hydrocolloid dressings, such as DuoDerm or IntraSite hydrocolloid, are impermeable to oxygen, moisture, and bacteria. They maintain a moist environment, and they support autolytic debridement. They are a good choice for relatively desiccated wounds. For exudative wounds, absorptive dressings, such as calcium alginates (eg, Kaltostat [Calgon Vestal], Curasorb [Kendall]) and hydrofiber dressings (eg, Aquacel and Aquacel-AG [Convatec]), are highly absorptive and are appropriate for exudative wounds. Alginates are available in rope form, which is useful for packing deep wounds. For very exudative wounds, impregnated gauze dressings, such as Mesalt (Scott), are useful. Twice-daily dressing changes may be needed. For infected wounds, use silver sulfadiazine (Silvadene) if the patient is not allergic to sulfa drugs. If the patient is allergic to sulfa, bacitracin-zinc ointment is a good alternative. An ionicsilver hydrofiber dressing (Aquacel-AG) is also a good choice.25,26,27,28,29 Bandaging a challenging anatomic area (eg, around a heel ulcer) requires a highly conformable dressing, such as an extra-thin hydrocolloid. Securing a dressing in a highly moist challenging site (eg, around a sacrococcygeal ulcer) requires a conformable and highly adherent dressing, such as a wafer hydrocolloid. Hydrogel sheets and nonadhesive forms are useful for securing a wound dressing when the surrounding skin is fragile. Table 1. Characteristics and Uses of Wound-Dressing Materials Table Category

Examples

Description

Applications

Alginate

AlgiSite, Comfeel, Curasorb, Kaltogel, Kaltostat, Sorbsan, Tegagel

Alginate dressings are made of seaweed extract contains guluronic and mannuronic acids that provide tensile strength and calcium and sodium alginates, which confer an absorptive capacity. Some can leave fibers in the wound if they are not thoroughly irrigated. These dressings are secured with secondary coverage.

These dressings are highly absorbent and useful for wounds have copious exudate. Alginate rope is particularly useful to pack exudative wound cavities or sinus tracts.

Hydrofiber

Aquacel, Aquacel-Ag, Versiva

An absorptive textile fiber pad, hydrofiber is also available as a ribbon for packing of deep wounds. This material is covered with a secondary dressing. The hydrofiber combines with wound exudate to produce a hydrophilic gel. Aquacel-Ag contains 1.2% ionic silver that has strong antimicrobial properties against many organisms, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci.

Hydrofiber absorbent dressings used for exudative wounds.

Debriding agents

Hypergel (hypertonic saline gel), Santyl (collagenase), Accuzyme (papain urea)

Various products provide some chemical or enzymatic debridement.

Debriding agents are useful for necrotic wounds as an adjunct to surgical debridement.

Foam

LYOfoam, Spyrosorb, Allevyn

Polyurethane foam has absorptive capacity.

These dressings are useful for cleaning granulating wounds with minimal exudate.

Hydrocolloid

CombiDERM, Comfeel, DuoDerm CGF Extra Thin, Granuflex, Tegasorb

Hydrocolloid dressings are made of microgranular suspension of natural or synthetic polymers, such as gelatin or pectin, in an adhesive matrix. The granules change from a semihydrated state to a gel as the wound exudate is absorbed.

Hydrocolloid dressings are useful for dry necrotic wounds, wounds with minimal exudate and for clean granulating wounds.

Hydrogel

Aquasorb, DuoDerm, Intrasite Gel, Granugel, Normlgel, NuGel, Purilon Gel, KY Jelly

Hydrogel dressings are water-based or glycerin-based semipermeable hydrophilic polymers; cooling properties may decrease wound pain. These gels can lose or absorb water depending upon the state of hydration of the wound. They are secured with secondary covering.

These dressings are useful for dry, sloughy, necrotic wounds (eschar).

Lowadherence dressing

Mepore, Skintact, Release

Low-adherence dressings are made of various materials designed to remove easily without damaging underlying skin.

These dressings are useful for acute minor wounds, such as skin tears, or as a final dressing for chronic wounds that have nearly healed.

Transparent film

OpSite, Skintact, Release, Tegaderm, Bioclusive

Transparent films are highly conformable acrylic adhesive films with no absorptive capacity and little hydrating ability. They may be vapor permeable or perforated.

These dressings are useful for clean, dry wounds with minimal exudate. They also are used to secure an underlying absorptive material, to protect high-friction areas and areas that are difficult to bandage (eg, heels) and to secure intravenous catheters.

Category

Examples

Description

Applications

Alginate

AlgiSite, Comfeel, Curasorb, Kaltogel, Kaltostat, Sorbsan, Tegagel

Alginate dressings are made of seaweed extract contains guluronic and mannuronic acids that provide tensile strength and calcium and sodium alginates, which confer an absorptive capacity. Some can leave fibers in the wound if they are not thoroughly irrigated. These dressings are secured with secondary coverage.

These dressings are highly absorbent and useful for wounds have copious exudate. Alginate rope is particularly useful to pack exudative wound cavities or sinus tracts.

Hydrofiber

Aquacel, Aquacel-Ag, Versiva

An absorptive textile fiber pad, hydrofiber is also available as a ribbon for packing of deep wounds. This material is covered with a secondary dressing. The hydrofiber combines with wound exudate to produce a hydrophilic gel. Aquacel-Ag contains 1.2% ionic silver that has strong antimicrobial properties against many organisms, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci.

Hydrofiber absorbent dressings used for exudative wounds.

Debriding agents

Hypergel (hypertonic saline gel), Santyl (collagenase), Accuzyme (papain urea)

Various products provide some chemical or enzymatic debridement.

Debriding agents are useful for necrotic wounds as an adjunct to surgical debridement.

Foam

LYOfoam, Spyrosorb, Allevyn

Polyurethane foam has absorptive capacity.

These dressings are useful for cleaning granulating wounds with minimal exudate.

Hydrocolloid

CombiDERM, Comfeel, DuoDerm CGF Extra Thin, Granuflex, Tegasorb

Hydrocolloid dressings are made of microgranular suspension of natural or synthetic polymers, such as gelatin or pectin, in an adhesive matrix. The granules change from a semihydrated state to a gel as the wound exudate is absorbed.

Hydrocolloid dressings are useful for dry necrotic wounds, wounds with minimal exudate and for clean granulating wounds.

Hydrogel

Aquasorb, DuoDerm, Intrasite Gel, Granugel, Normlgel, NuGel, Purilon Gel, KY Jelly

Hydrogel dressings are water-based or glycerin-based semipermeable hydrophilic polymers; cooling properties may decrease wound pain. These gels can lose or absorb water depending upon the state of hydration of the wound. They are secured with secondary covering.

These dressings are useful for dry, sloughy, necrotic wounds (eschar).

Lowadherence dressing

Mepore, Skintact, Release

Low-adherence dressings are made of various materials designed to remove easily without damaging underlying skin.

These dressings are useful for acute minor wounds, such as skin tears, or as a final dressing for chronic wounds that have nearly healed.

Transparent film

OpSite, Skintact, Release, Tegaderm, Bioclusive

Transparent films are highly conformable acrylic adhesive films with no absorptive capacity and little hydrating ability. They may be vapor permeable or perforated.

These dressings are useful for clean, dry wounds with minimal exudate. They also are used to secure an underlying absorptive material, to protect high-friction areas and areas that are difficult to bandage (eg, heels) and to secure intravenous catheters.

Consider other topical agents Topically applied platelet-derived growth factors have a modestly beneficial effect in promoting wound healing. Becaplermin gel 0.01% (Regranex), recombinant human platelet-derived growth factor (PDGF) that is produced through genetic engineering, is approved by the US Food and Drug Administration (FDA) to promote healing of diabetic foot ulcers. Regranex is contraindicated in persons with known skin cancers at the site of application. Freeze-dried, platelet-rich plasma showed promise in an animal study.30 Collagen comprises a significant fraction of the necrotic soft tissues in chronic wounds. The enzyme collagenase, which is derived form fermentation of Clostridium histolyticum, helps remove nonviable tissue from the surface of wounds. However, collagenase is not a substitute for an initial surgical excision of a grossly necrotic wound. Other topical agents that have been used for wound treatment are sugar, antacids, and vitamin A&D ointment. Avoid cytotoxic agents, such as hydrogen peroxide, povidone iodine, acetic acid, and Dakin solution (sodium hypochlorite). Consider compression therapy Consider the advisability of compression therapy. Compression is appropriate for ulcers caused or exacerbated by extremity edema. Compression may have to be avoided entirely in the presence of significant arterial inflow compromise. Use support hose or elastic wraps with approximately 40-60 mm Hg of pressure in the absence of arterial disease and 20-30 mm Hg in the presence or suspicion of mild arterial insufficiency. Manage pain Manage wound pain by moistening dressings before removal. Consider using 2% topical lidocaine gel during wound care. (Anecdotal reports describe the use of topical morphine and diamorphine-infused gel for palliation of pressure ulcer pain in patients who are terminally ill,31 but this use is not FDA approved.) Treatment of specific types of wounds can be described as follows: See General treatment of nonhealing wounds. Pressure ulcers Treatment of decubitus ulcers requires prolonged surgical and nursing care.32,33,34,35 During the extended period of treatment required, the patient remains at risk for the development of new pressure ulcers at other sites.36,37,38 Treatment, particularly indications for support surfaces, is based on appropriate staging of the pressure ulcer.39,40 Milne et al reported the outcome of a long-term acute care hospital’s program to reduce the incidence of pressure ulcers.41 The facility used a failure mode and effects analysis to determine where improvements in care were most needed. The hospital determined that its ulcer prevalence rates, which were believed to be above average, were associated with such problems as “a lack of 1) wound care professionals, 2) methods to consistently document prevention and wound data, and 3) an interdisciplinary wound care team approach.” After the hospital addressed these issues, it saw the incidence of facility-acquired pressure ulcers drop from 41% (the baseline figure) to an average of 4.2%, over a 12-month period. Table 2. Staging Pressure Ulcers Table

Stage

Definition

Appearance

Appropriate topical treatment

Average healing time (d)

I

Nonblanchable erythema of intact skin

Pink skin that does not resolve when pressure is relieved; discoloration; warmth; induration

DuoDerm q2-3d

14

II

Partial-thickness skin loss involving epidermis and/or dermis

Cracking, blistering, shallow crater, abrasion

Cleanse with saline; DuoDerm/Tegaderm dressing

45

III

Full-thickness skin loss into subcutaneous fatty tissues or fascia

Distinct ulcer margin; deep crater (in general, 2.075 mm or deeper [the thickness of a nickel])

Debride; irrigate with saline; apply DuoDerm/Tegaderm

90

IV

Full-thickness skin loss with extensive tissue involvement of underlying tissues

Extensive necrosis; damage to underlying supporting structures, such as muscle, bone, tendon, or joint capsule

Surgically debride; irrigate with saline (possibly under pressure); apply advanced topical dressings; consider antibiotics

120

*When the overlying skin is necrotic, the staging cannot be accurate until debridement is performed. Stage

Definition

Appearance

Appropriate topical treatment

Average healing time (d)

I

Nonblanchable erythema of intact skin

Pink skin that does not resolve when pressure is relieved; discoloration; warmth; induration

DuoDerm q2-3d

14

II

Partial-thickness skin loss involving epidermis and/or dermis

Cracking, blistering, shallow crater, abrasion

Cleanse with saline; DuoDerm/Tegaderm dressing

45

III

Full-thickness skin loss into subcutaneous fatty tissues or fascia

Distinct ulcer margin; deep crater (in general, 2.075 mm or deeper [the thickness of a nickel])

Debride; irrigate with saline; apply DuoDerm/Tegaderm

90

IV

Full-thickness skin loss with extensive tissue involvement of underlying tissues

Extensive necrosis; damage to underlying supporting structures, such as muscle, bone, tendon, or joint capsule

Surgically debride; irrigate with saline (possibly under pressure); apply advanced topical dressings; consider antibiotics

120

*When the overlying skin is necrotic, the staging cannot be accurate until debridement is performed. Pressure ulcers often require the following steps: Debridement: The ulcer often requires surgical excision, usually down to underlying bone. In the absence of erythema, edema, fluctuance, or drainage, clean dry eschar does not need to be debrided surgically but may be softened and allowed to separate using dressings (eg, colloids, hydrogels) that provide a moist environment to encourage autolysis. Topical wound care: Weeks or months of daily dressing changes are required before the wound begins granulating and appears clean enough for myocutaneous flap closure. Treatment of infection: Debridement is a clean, not sterile, procedure. Frequent debridements maintain superficial colonization at acceptable levels. Swab cultures are often meaningless because they reflect only surface colonization of local infection, which does not require antibiotic treatment. In general, systemic antibiotics are not useful unless signs of progressive infection, such as bacteremia, septicemia, progressive cellulitis, or intractable osteomyelitis, are present. Control of chronic wound contamination: Chronic wound contamination because of fecal incontinence can be a vexing problem in typical bedridden patients, who tend to develop sacral and ischial pressure ulcers. These types of ulcers are depicted in the images below. Initial treatment is dietary management. Foods that thicken the stool include applesauce, bananas, boiled milk, bread, cheese, creamy peanut butter, grits, oat bran, oatmeal, pasta, pretzels, rice, tapioca, and yogurt. In rare cases, fecal diversion by means of colostomy is required. Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture. Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.

Sacral pressure ulcer before and after flap closure. Sacral pressure ulcer before and after flap closure.

Sacral ulcer. Sacral ulcer. Positioning: Patients with pressure ulcers or those at risk for a pressure ulcer should be turned in bed every 2 hours. Patients who are immobile should not be positioned directly on the trochanters; foam wedges and pillows are useful to pad pressure points, to prevent direct contact between bony prominences, and to raise their heels off the bed surface. Pressure ulcers can also be induced by shear forces if patients slide down the bed; therefore, try to use the lowest degree of elevation of the head of the bed that the patient’s medical conditions allow. Use of support surfaces Support surfaces are further discussed as follows: Federal regulations (Medicare Bulletin 405) dictate that patients with bedsores or those who are at risk for bedsores must be placed on an appropriate support surface. Federally mandated standards of care dictate what support surfaces are allowable and provide for both civil and criminal penalties for health care entities that fail to comply. Proper prevention and management of pressure ulcers in health care facilities is mandated by federal regulations (Ch IV § 483.25 (c)(1)&(2), 10/1/95), which state, “Based on the comprehensive assessment of a resident, the facility must ensure that (1) a resident who enters the facility without pressure sores does not develop pressure sores unless the individual’s clinical condition demonstrates that they were unavoidable, and (2) a resident having pressure sores receives necessary treatment and services to promote healing, prevent infection and prevent new sores from developing.” A class I support surface is a simple pressure pad device that is required as follows: For patients who cannot independently change their body position to effectively alleviate pressure For patients who have any stage of pressure ulcer on the trunk or pelvis, plus impaired nutritional status, fecal or urinary incontinence, altered sensory perception, or compromised circulatory status A class II support surface is a pressure-relieving device that reduces pressure over bony prominences to less than 32 mm Hg and that does so for a sustained period. A class II support surface is required as follows: For patients who have multiple pressure ulcers on the trunk or pelvis that has not improved despite a comprehensive treatment, including a class I support surface for a stage II, III, or IV pressure ulcer for at least 1 month For patients who have large or multiple stage III or IV pressure ulcers on the trunk or pelvis For patients who have had a myocutaneous flap or skin graft procedure for a pressure ulcer on the trunk or pelvis within the past 60 days and have been on a class II or III support surface immediately before a recent discharge from a hospital or nursing facility within the past 30 days A class III support surface is an advanced pressure-relieving device. A class III support surface, that is, an air-fluidized bed, may be used only for failure of a comprehensive conservative treatment plan after 30 days. (Note that an air-fluidized bed is contraindicated for any patient with associated severe pulmonary compromise because the absence of firm back support makes coughing ineffective, and the dry air thickens pulmonary secretions.) Such a conservative treatment program includes the following: Education of the patient and the caregiver. A patient information page regarding pressure ulcers is available.34 Assessment by a licensed health care practitioner, at least weekly Appropriate turning and positioning Use of a class II support surface Appropriate wound care Appropriate management of incontinence Appropriate nutritional management Table 3. Support Surfaces Table Class

Type

Principle

Examples

I

Simple

Pressure-relieving pad or mat

3- to 5-inch foam mattress, gel overlay, egg-crate mattress

II

Advanced

Powered air* overlay for mattress with low air loss feature; nonpowered advanced pressure-reducing mattress replacement or powered air* floatation bed with or without low air loss feature

Roho dry floatation mattress system, Pegasus Renaissance mattress

III

Air fluidized

Floatation by filtered air* flow pumped through porcelain beads

Clinitron bed

*Long-term use of powered air devices is relatively contraindicated for patients with chronic obstructive lung disease, such as chronic bronchitis, emphysema, and asthma. Class

Type

Principle

Examples

I

Simple

Pressure-relieving pad or mat

3- to 5-inch foam mattress, gel overlay, egg-crate mattress

II

Advanced

Powered air* overlay for mattress with low air loss feature; nonpowered advanced pressure-reducing mattress replacement or powered air* floatation bed with or without low air loss feature

Roho dry floatation mattress system, Pegasus Renaissance mattress

III

Air fluidized

Floatation by filtered air* flow pumped through porcelain beads

Clinitron bed

*Long-term use of powered air devices is relatively contraindicated for patients with chronic obstructive lung disease, such as chronic bronchitis, emphysema, and asthma. Additional protection is described as follows: Proper off-loading for ischial ulcers: Sacral ulcers usually result from prolonged supine bed rest or from shearing forces, particularly because of the patient sliding down the bed when the head is elevated. On the other hand, ischial ulcers often result from prolonged sitting either in the head-up position in the bed or in a wheelchair. Hence, off-loading for ischial ulcer prevention and treatment requires support surfaces for sitting as well as mattress support surfaces. Sitting time must also be limited. Heel protection: Pressure ulcers involving the heel regions commonly occur in patients who are bedridden, even if they are immobilized for just a few days, such as after hip surgery. A heel pressure ulcer is illustrated in the image below. Prevention and treatment of heel pressure ulcers requires off-loading. Off-loading devices are usually selected based on availability and include the following: Heel pressure ulcer. Heel pressure ulcer. Booties are simple pressure pads that surround the heel with polyester fibers, iconized fibers, or foam material. Boots are made from a firm outer shell lined with pressure-relief padding. They can also provide positioning capability to help treat contractures and foot drop. Pillows made from polyester and sheepskin fleece or special rubber or plastic interpose a conformable soft overlay between the heel and the mattress. Suspension devices isolate the heel and transfer the weight to the lower leg. These devices also have positioning capabilities that are useful in treating contractures and foot drop. Inflatable devices made from plastic sheets surround the heel and adjacent tissues. Venous ulcers Treatment of venous ulcers includes compression therapy, providing a moist wound environment and debridement of necrotic tissue.42,43 Most venous ulcers heal with these measures alone. Some require split-thickness skin grafting or application of bioengineered skin (eg, Apligraf, Dermagraft).44 Pentoxifylline (Trental) and horse chestnut seed (available in supermarkets and health food specialty stores) have been shown to expedite healing of venous stasis ulcers. In some cases, compression therapy is inadequate to maintain healing of venous ulcers, and surgical vein stripping or ligation of venous perforators may be helpful. A study of 98 limbs with active chronic venous ulcers revealed that all but one had venous reflux; the study also suggested that most of these patients would benefit from surgical or endovascular intervention.45 Other studies suggested a more modest level of benefit from corrective venous surgery.46 Table 4. Compression Bandages for Venous Ulcers* Table Type

Description

Examples

Single layer

Single-layer simple tubular woven nylon/elastic bandages may be imprinted with rectangles that stretch to squares when appropriate wrapping tension (30-40 mm Hg) is applied.

ACE bandage, Comperm (Conco Medical), Setopress (Seton Healthcare Group)

Three layer

The layers include a padding absorption layer, a compression bandage layer, and a cohesive compression bandage. Bandages may be left in place for up to 1 week depending on wound exudate.

Dyna-Flex (Johnson & Johnson)

Four layer

The layers include a nonwoven wound contact layer that is permeable to wound exudate and 4 overlying bandages. Bandages may be left in place for up to 1 week depending on exudate volume.

Profore (Smith & Nephew)

Impregnated wrap

The porous flexible occlusive dressing is composed of stretchable gauze and a nonhardening zinc oxide paste.

Unna boot (ConvaTec)

*Compression wraps are contraindicated in severe arterial compromise. Some of these products are contraindicated in patients who are allergic to latex. Type

Description

Examples

Single layer

Single-layer simple tubular woven nylon/elastic bandages may be imprinted with rectangles that stretch to squares when appropriate wrapping tension (30-40 mm Hg) is applied.

ACE bandage, Comperm (Conco Medical), Setopress (Seton Healthcare Group)

Three layer

The layers include a padding absorption layer, a compression bandage layer, and a cohesive compression bandage. Bandages may be left in place for up to 1 week depending on wound exudate.

Dyna-Flex (Johnson & Johnson)

Four layer

The layers include a nonwoven wound contact layer that is permeable to wound exudate and 4 overlying bandages. Bandages may be left in place for up to 1 week depending on exudate volume.

Profore (Smith & Nephew)

Impregnated wrap

The porous flexible occlusive dressing is composed of stretchable gauze and a nonhardening zinc oxide paste.

Unna boot (ConvaTec)

*Compression wraps are contraindicated in severe arterial compromise. Some of these products are contraindicated in patients who are allergic to latex. Diabetic foot ulcers The treatment of diabetic foot ulcers requires the following: (1) appropriate therapeutic footwear, (2) daily saline or similar dressings to provide a moist wound environment, (3) debridement when necessary, (4) antibiotic therapy if osteomyelitis is present, (5) optimal control of blood glucose, and (6) evaluation and correction of peripheral arterial insufficiency.47,48,49,50,51 See also Diabetic Ulcers. Wound coverage with cultured human cells or heterogeneic dressings and/or grafts, application of recombinant growth factors, negative pressure wound therapy, and hyperbaric oxygen treatments may also be beneficial.17,52,53,54 Lymphedema Although lymphedema is not typically a cause of ulceration, ulcers on the extremities may fail to heal because of untreated lymphedema. Nocturnal leg elevation and elastic wraps or support hose are appropriate adjuncts to the treatment of the recalcitrant wound in an edematous extremity. For advanced and nonresponsive lymphedema, complex decongestive physiotherapy is a useful treatment option. Surgical Therapy Methods are available to expedite healing of the clean wound. After a wound is in a steady clean state, a decision must be made about allowing it to heal by natural processes or expediting healing with a surgical procedure. Clinical experience and observation of the healing progress in the individual case dictate the appropriate treatment. Surgical options include skin grafting, application of bioengineered skin substitutes, and use of flap closures.55

Skin grafting: Autologous skin grafting is the criterion standard for viable coverage of partial-thickness wounds. The graft can be harvested with the patient under local anesthesia in an outpatient procedure. Meshing the graft allows wider coverage and promotes drainage of serum and blood. Cadaveric allografting: A cadaveric skin allograft is a useful covering for relatively deep wounds after surgical excision when the wound bed does not appear appropriate for application of an autologous skin graft. The allograft is only a temporary solution. Application of bioengineered skin substitutes50,56,57 Apligraf (Organogenesis; Novartis) is a bilayered skin substitute produced by combining bovine collagen and living cells derived from tissue-cultured human infant foreskins. One study of diabetic foot ulcers demonstrated 12-week healing rates of 39% for patients who received only standard wound care versus 56% for those who were treated by application of an Apligraf after a period of standard wound care. Dermagraft (Smith & Nephew, Inc) is human fibroblast-derived dermal substitute manufactured by seeding dermal fibroblasts onto a 3-dimensional bioabsorbable scaffold. It has been marketed for use in the treatment of diabetic foot ulcers, venous ulcers, and pressure sores. A clinical trial showed improved healing rates in diabetic foot ulcers. Oasis (Healthpoint, Ltd), a relatively new product, is a xenogeneic acellular collagen matrix derived from porcine small intestinal submucosa in such a way that an extracellular matrix and natural growth factors remain intact. This provides a scaffold for inducing wound healing.58 Do not use this in patients with allergies to porcine materials. Cultured epithelial autograft (Epicel; Genzyme Tissue Repair, Cambridge, Mass) is an epidermal replacement that is grown in a tissue culture from a skin biopsy taken from the recipient and is cocultured with mouse cells. Preparation of the graft requires about 2 weeks of culture time. Use of flap closures: Delayed primary closure of a chronic wound, as shown below, requires well-vascularized clean tissues and tension-free apposition. This usually requires undermining and mobilization of adjacent tissue planes by creating skin flaps or myocutaneous flaps.59 Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture. Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.

Sacral pressure ulcer before and after flap closure. Sacral pressure ulcer before and after flap closure. Complications Complications of nonhealing wounds include the following: Amyloidosis – See Amyloidosis, Macular. Bacteremia – See Shock, Septic. Cellulitis Endocarditis Heterotopic bone formation Maggot infestation Meningitis Osteomyelitis Perineal-urethral fistula Pseudoaneurysm – See Peripheral Vascular Injuries. Septic arthritis Sinus tract or abscess Squamous Cell Carcinoma

Komentar

Steroid Injection, Carpal Tunnel Filed under: Uncategorized — Tinggalkan komentar

Steroid Injection, Carpal Tunnel Introduction Carpal tunnel syndrome (CTS) is a compressive focal mononeuropathy that is brought on by compression of the median nerve as it travels through the carpal tunnel. Patients commonly experience pain, paresthesias, and weakness in the median nerve distribution. Carpal tunnel steroid injection at the wrist is used to treat the symptoms of carpal tunnel syndrome by injecting a steroid solution into the ulnar bursa surrounding the median nerve. For mild to moderate carpal tunnel syndrome, carpal tunnel steroid injection can be used in conjunction with other conservative measures such as splinting, physical therapy, ergonomic modifications, rest, and regular exercise.1,2,3,4,5 Conservative modalities, including median nerve steroid injections, should generally be attempted prior to pursuing surgical options.6 Historically, carpal tunnel steroid injections were typically used for only mild median nerve entrapment (as documented by electroneurography) as well as for temporary pain relief in anticipation of definitive flexor retinaculum surgical release. In general, injected corticosteroids appear effective in reducing subjective symptoms for 1-3 months when compared to placebo.7 While short-term relief of symptoms after injection appears superior to relief after carpal tunnel release surgery, the advantage is lost over the course of a year.8 Electrodiagnostic studies such as nerve conduction studies and electromyography are typically obtained to determine the severity of nerve damage prior to performing the procedure.9,10 Steroid injections should be avoided prior to planned electrodiagnostic testing, as the presence of steroids may alter test results. Several clinical tests can be used to diagnose carpal tunnel syndrome. One is Tinel’s sign, which is done by over the median nerve at the volar crease at the wrist to reproduce the paresthesia. The Phalen test involves holding the flexed wrists against each other for several minutes to provoke the symptoms in the median nerve distribution. Manual carpal compression testing is done by applying pressure over the transverse carpal ligament and evaluating for paresthesia within 30 seconds of applying pressure.11 Carpal tunnel anatomy The carpal tunnel of the wrist is defined anatomically by the transverse carpal ligament on the volar surface and the carpal bones on the dorsal surface. The transverse carpal ligament, also known as the flexor retinaculum, attaches radially to the trapezium and scaphoid tuberosity and ulnarly to the hamate and pisiform. The contents of the carpal tunnel include the 4 flexor digitorum profundus tendons, the 4 flexor digitorum superficialis tendons, the flexor pollicis longus tendon, and the median nerve. See images below.

Carpal tunnel anatomy. [ CLOSE WINDOW ]

Carpal tunnel anatomy.

Carpel tunnel anatomy, cross-section. [ CLOSE WINDOW ]

Carpel tunnel anatomy, cross-section. There are 2 bursae in the wrist. The radial bursa contains the flexor pollicis longus tendon. The ulnar bursa, also known as the common flexor sheath, holds the flexor digitorum superficialis and profundus tendons. When the hand is supinated, the 4 superficialis tendons lay on top of the 4 profundus tendons, forming a U-shaped structure referred to as the ulnar bursa. On top of the ulnar bursa, and below the transverse carpal ligament, lies the median nerve. Although the median nerve itself has 2 sensory branches and 1 motor branch, only 1 sensory branch and the motor branch traverse through the carpal tunnel and are affected by carpal tunnel syndrome. This sensory branch is responsible for sensory innervation of the thumb, index finger, middle finger, and radial half of the ring finger.

Indications Carpal tunnel syndrome not relieved by conservative measures Electrodiagnostic changes consistent with mild-to-moderate median nerve entrapment

Contraindications Adverse reaction to injectable steroid or anesthetic Uncontrolled diabetes mellitus Active systemic or local infection Compromised skin integrity over the area Immunosuppression Planned electrodiagnostic study

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