CURRICULUM CONTENTS:
7. Omphalocele pecah dan Gastroschisis Omphalocele :
Defek dinding abdomen di daerah tali pusar karena gangguan penutupan secara kongenital pada janin usia 8 minggu di dalam kandungan, sehingga isi rongga abdomen seperti hepar dan usus halus berada diluar rongga abdomen, hanya di tutupi lapisan peritoneum, dengan besar defek berkisar antara 2-15 cm.
Gastroschisis :
Kegagalan penutupan dinding abdomen secara kongenital di sekitar umbilicus (umumnya di sebelah kanan umbilicus), sehingga usus halus dan atau sebagian kolon berada di luar rongga abdomen (jarang ditemukan hepar atau lien) tanpa ditutupi oleh peritoneum atau lapisan dinding abdomen lainnya, dengan lebar defek umumnya kurang dari 5 cm.
Secara bersamaan omphalocele dan gastoschisis dapat disertai kelainan lain seperti : 1. Exstrophy cloaca :
Omphalocele disertai agenesis hindgut, imperforasi anus, exstrophy vesika urinaria, dan vesikointestinal fistula.
2. Pentalogy Cantrell :
Omphalocele epigastrium, celah sternum, kelainan jantung kongenital, tidak terbentuknya diafragma sentral dan pericardium.
Pengelolaan penderita dengan gastrosciziz dan omphalokel pecah meliputi pemberian cairan intravena sesuai kebutuhan, pemasangan nasogastric tube 10-12, pemberian antibiotik spectrum luas sesuai kebutuhan, bungkus isi rongga abdomen yang berada di luar dengan kasa atau bahan steril dan dibasuhi dengan NaCl hangat (cairan fasiologis) dan tempatkan bayi dalam inkubator untuk mempertahankan suhu bayi optimal.
Terapi pembedahan pada penderita gastrosciziz dan omphalokel bisa melalui prosedur satu tahap (one stage) maupun bertahap (multistage repair) tergantung kondisi penderita dan kondisi usus saat pertama kali datang ke rumah sakit.
Daftar Pustaka
1. Chirdan LB, Ameh EA, Thomas AH. Infantile Hypertropic Pyloric Stenosis. J Pediatric Surgeon; 2008: 43: 1227-29
2. Gilchrist BF, Lessin MS,2010. chapter 29 : Lesion of the stomach, In Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 405- 414.
3. Holschneider A., Ure B.M., 2010. Chapter 35: Hirschsprung's Disease in: Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 456-67.
4. Hackam D.J., Newman K., Ford H.R. 2005. Chapter 38: Pediatric Surgery in: Schwartz's Principles of Surgery. 8th edition. McGraw-Hill. New York, p: 1496-8.
5. Ziegler M.M., Azizkhan R.G., Weber T.R. 2003. Chapter 56: Hirschsprung Disease In: Operative Pediatric Surgery. McGraw-Hill. New York, p: 617-40.
6. Puri P. 2009. Chapter 26: Hirschsprung's Disease in: Springer Pediatric Surgery 3rd edition. Saunders Company. Philadelphia, p: 275-83.
7. Leonidas J.C., Singh S.P., Slovis T.L. 2004. Chapter 4 Congenital Anomalies of The Gastrointestinal Tract In: Caffey's Pediatric Diagnostic Imaging 10l edition. Elsevier- Mosby. Philadelphia, p: 148-53.
8. Kartono D. Penyakit Hirschsprung. Sagung Seto. Jakarta. 2004.
9. Aresman R.M, Bambini D.A, 2010 . Congenital Diafragmatic Hernia and Eventeration. In: Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 304-319..
10. ElisabethM, Janine f, Annelies K, Dick T. Etiology of Esophageal Atresia and Tracheo esophageal fistula, Curr Gastroenterology Rep. 12 , 2010 : 215-222
11. Spitz L, 2010. Esophageal Atresia and tracheoesophageal Malformation, In Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 352-366.
12. Morrow SE, Newman KD, 2010. Appendicitis, In Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 577-584.
13. Weber TR, Tracy TF, Keller MS,2010. Groin Hernia and Hydroceles, In Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 697-714.
14. Fallat ME, 2010. Intussusception, In Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 533-542.
15. Klein MD,2010. Congenital Abdominal Wall Defects, In Ashcraft Pediatric Surgery 5th edition. Saunders Company. Philadelphia, p: 659-668.
Lecture 11
Traumatic Brain Injury Resuscitation
I Pt Pramana Suarjaya/ IB Krisna Jaya Sutawan
Learning Obyektif
1. To describe Traumatic Brain Injury (TBI)
2. To implement Glasgow Coma Scale to classiflying severity of TBI 3. To implement initial brain recucitation
a. Primary survey i. Airway
ii. Breathing/Ventilation iii. Circulation
iv. Disability v. Exposure b. Secondary survey
4. To describe management of elevated ICP
Abstract
Traumatic Brain Injury (TBI)
TBI is a nondegenerative, noncongenital insults to the brain from external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness. TBI from trauma results from two distinct processes: primary injury and secondary injury. Primary injury is the damage produced by the direct mechanical impact and the acceleration- deceleration stress onto the skull and the brain tissue, which results in skull fractures and intracranial lesions. The intracranial lesions are further classified into two types: diffuse injury and focal injury.
1. Diffuse brain injury
a. Brain concussion : loss of consciousness lasting < 6 hours b. Diffuse axonal injury : traumatic coma lasting > 6 hours 2. Focal brain injury
a. Brain contusion
b. Epidural hematoma (EDH) c. Subdural hematoma (SDH) d. Intracerebral hematoma (ICH)
Secondary injury develop within minutes, hours or days of the initial injury and cause further damage to nervous tissue. The common denominators of secondary injury are cerebral hypoxia and ischemia. Secondary injuries are caused by the following disorders:
1. Respiratory dysfunction: hypoxemia, hypercapnia
2. Cardiovascular instability: hypotension, low cardiac output (CO) 3. Elevation of ICP
4. Metabolic derangements
Glasgow Coma Scale (GCS) to classifying severity of TBI
GCS is composed of three components: eye opening (1 to 4 points), verbal response (1 to 5 points) and motor response (1 to 6 points). The sum of these components defines the TBI severity classification into :
1. Severe : GCS score of 3 to 8 2. Moderate : GCS score 9 to 13 3. Mild : GCS score 14 and 15
Glasgow Coma Scale for all age group
4 years to Adult Child < 4 years Infant Eye Opening
4 Spontaneous Spontaneous Spontaneous
3 To speech To speech To speech
2 To pain To Pain To Pain
1 No respon No respon No respon
5 Alert and oriented Oriented, social, speaks, interacts
coos, babbles
4 Disoriented Confused speech,
disoriented, consolable, aware
Irritable cry
3 speaking but nonsensical Inappropriate words,inconsolable, unaware cries to pain 2 Moan or unintelligible sounds Incomprehensible, agitated, restless, unaware Moans to pain
1 No response No response No response
Motor response
6 Follows commands Normal, spontaneous movements
Normal, spontaneous movements
5 Localizes pain Localizes pain withdraws to touch
4 Moves or withdraws to pain
Withdraws to pain withdraws to pain
3 Decorticate flexion Decoritcate flexion Decorticate flexion 2 Decerebrate extension Decerebrate extension decerbrate extension
1 No response No response No response
Initial Brain Resuscitation
Patients who have TBI should be either treated at a designated trauma center that has neurosurgical coverage or transferred to such a center after initial stabilization. The prompt assessment and management of TBI begin with the treatment of associated injuries that may cause hypoxia, hypoventilation and shock. This is best accomplished using a systematic approach such as the Advanced Trauma Life Support (ATLS) Algorithm, which consists of primary and secondary surveys.
1. Primary Survey
A brief history is obatained according to the AMPLE mnemonic (Allergies, Medications, Past medical history, Last meal, Event). Examination and immediate resuscitation are performed according to ABCDE mnemonic (Airway, Breathing, Circulation, Disability, Exposure). Plans for initial operative or non- operativemanagements are based on the results of the primary and the secondary surveys.
a. Airway : in the setting of TBI, airway management is performed with particular attention to changes in mean arterial pressure (MAP), ICP, arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2) and cervical
stability.
i. Indications for intubation include inability to protect the airway, difficulty with oxygenation or ventilation, shock, a GCS score < 9, and rapid neurologic deterioritation
ii. Manual inline stabilization (MILS) iii. Rapid squence induction (RSI)
iv. Induction agent that can be used are propofol, thiopental and etomidate.
v. Several neuromuscular blocking drugs are appropriate for TBI such as succinylcholine, rocuronium and mivacurium.
vi. As with all intubations, airway manager should consider awake- topical intubation if they are uncertain about their ability to establish an airway quickly and safely.
vii. Lidocaine IV
viii. Laryngeal mask airway (LMA) devices are useful backup tools for ventilation and intubation. Surgical airway techniques, such as cricothyroidotomy and tracheostomy are also backup methods for intubation.
ix. Endotracheal intubation must be confirmed by physical examinaton plus a method for CO2 detection such as colorimetric or continous capnography.
x. Chest x-ray are useful for verification of endotracheal tube positionas well as identificationof associated chest pathology such as pneumothorax, lung contusion, and pulmonary edema.
b. Breathing/ventilation
i. High-flow oxygen is provided as supplement to all patients before intubation to prevent hypoxia and provide sufficient apneic time in case further RSI is needed.
ii. Oxygen saturation should be maintained above level now concidered acceptable for patients who have acute respiratory distress syndome. iii. Positive-pressure ventilation is provided as needed to maintain
adequate ventilation and oxygenation. iv. The PaCO2 should be kept at normocarbia
v. Sedation : The ideal sedative drug in TBI should have rapid onset and offset, anticonvulsant properties, and favorable effects on CPP.
vi. Analgesia and blunting of stimulation associated with the endotracheal tube can be achieved with opioids
c. Circulation: Systemic hypotension is one of the major contributor to poor outcome after TBI. When necessary, fluid resuscitation is initiated immediately, inotropic and vasopressor drugs are administered as required to stabilize the blood pressure (BP) at or above 90 mmHg.
i. Life-threatening cardiogenic shock as from tension pneumothorax and cardiac tamponade is identified and either controlled or treated definitively.
ii. Hypovolemic shock should be resuscitated.
iii. Total osmolality is the most important factor in determining brain edema formation.
iv. Patient who have a low hematocrit may require a tranfusion. v. Glucose-containing solutions are avoided.
vi. Inotropes and vasopressors. If the BP and cardiac output (CO) cannot be restored through fluid resuscitation, the administration of intravenous inotropic and vasopressor drugs may be necessary. An infusion of either phenylephrine or dopamine is recommended to maintain the CPP above 60 mmHg.
d. Disability : When not absolutely contraindicated by the need for immediate endotracheal intubation, the initial neurological assessment should be performed before the administration of sedative or neuromuscular-blocking drugs. Neurological status is assessed by using GCS with attention to the signs and symptoms of increased ICP and brain herniation. In addition, the examiner notes the pupillary response and diameter, presence of lateral
deficits, and level of spinal motor and sensory deficits. Emergency therapy for brain herniation includes reassessment and treatment of extracranial insults such as hypoxia and shock, head elevation to 30o, mannitol infusion, brief hyperventilation, and surgical decompression.
e. Exposure : The patient is fully undressed and examination for any associated injuries while precautions are taken to avoid hypothermia.
2. Secondary survey
a. The secondary survey includes a more complete history and physical examination as well as laboratory and ancillary testing to diagnose the extent of TBI and associated injuries.
b. Commonly requested investigation include x-ray examination of the chest and pelvis, complete metabolic panel, complete blood count, clotting parameters, serum osmolarity, urinalysis, ethanol blood level.
c. Unless contraindicated by need for immediate laparotomy or other procedure to prevent death from shock, all TBI patients should have a non-contrast computed tomographic (CT) scan of the head and cervical spine as soon as possible.
Management of elevated ICP
The reduction of elevated ICP and the maintenance of BP are crucial in the management of intracranial hypertension because CPP is directly related to both MAP and ICP. ICP monitoring is recommended in patient who have CT evidence of elevated ICP including midline shift, effaced ventricles, compressed basal cisterns, or the presence of an intracranial space-occupying lesion.
1. Hyperventilation: when evidence of transtentorial herniation in patients who have severe TBI exist, hyperventilation should be instituted because hyperventilation can reduce ICP rapidly and effectively.
2. Diuretic therapy: manitol is administered to patients in whom transtentorial herniation is suspected. The serum osmolality is monitor frequently.
3. Posture: a head-up tilt to 10o to 30o facilitates cerebral venous and CSF drainage and lower ICP.
4. Barbiturate: are known to exert cerebral protective and ICP-lowering effects. High dose barbiturate therapy may considered in severely head injuries patients whose intracranial hypertension is refractory to maximal medical and surgical ICP-lowering therapy. However the prophylactic use of barbiturate come is not indicated.
5. Decompressive craniectomy: is an surgical advanced treatment option for ICP control in severe TBI.
Enviromental injury
Agus Roy Rusly Hariantana Hamid
a. Definisi Luka bakar
Suatu trauma panas yang disebabkan oleh air / uap panas, arus listrik, bahan kimia, radiasi dan petir yang terutama mengenai jaringan permukaan yang menyebabkan kerusakan atau kehilangan jaringan.
Fase Luka BakarFase Akut / Fase Syok Saat di tempat kejadian sampai saat penanganan di Instalasi Gawat Darurat. Masalah yang ada pada fase ini adalah masalah penyelamatan hidup terutama untuk pernafasan dan cairan. Disamping itu masalah perawatan luka juga penting karena sangat mempengaruhi kondisi umum pasien dan juga penyembuhan luka.
b. Penilaian Luka Bakar
Berdasarkan :
1. Kedalaman luka bakar • Derajat I : Epidermis • Derajat II : Dermis A. Superfisial/ permukaan B. Dalam
• Derajat III : Seluruh tebal kulit/ lebih dalam sampai otot, tulang Kedalaman luka bakar tergantung:
• Tingginya panas
• Penyebab
• Lamanya kontak • Ketebalan kulit • Suplai darah
Derajat Kedalaman Klinis Rasa nyeri
Derajat I Hyperemis Hyper estesia
Derajat II A Bulla, merah Hyper estesia Derajat II B Bulla, pucat Hypo estesia Derajat III Hitam, kering An estesia
2. Luas luka bakar
Berdasarkan Rule of Nine dari Wallace
9 14 9 9 18 18 18 18 9 9 18 18 16 16 9 18 18 14 10 14 18
Untuk luka bakar yang tersebar dalam bentuk pulau-pulau dapat dihitung dengan telapak tangan penderita dianggap 1%.
c. Keparahan Luka Bakar
1. Luka bakar ringan
• Luka bakar derajat II < 15%
• Luka bakar derajat II < 10% pada anak-anak • Luka bakar derajat III < 1%
2. Luka bakar sedang
• Luka bakar derajat II 15-25% pada orang dewasa • Luka bakar derajat II 10-20% pada anak-anak • Luka bakar derajat III < 10%
3. Luka bakar berat
• Luka bakar derajat II 25% atau lebih pada orang dewasa • Luka bakar derajat II 20% atau lebih pada anak-anak • Luka bakar derajat III 10% atau lebih
• Luka bakar mengenai tangan, wajah, telinga, mata, kaki dan genetalia/perineum.
• Luka bakar dengan cedera inhalasi, listrik, disertai trauma lain
d. Indikasi Rawat
▪ Luka bakar sedang ▪ Luka bakar Grade II a. Dewasa >20%
b. Anak / Orang tua > 15% ▪ Luka Bakar Grade III
▪ Luka Bakar dengan komplikasi jantung, otak dll
e. Komplikasi
• Gagal pernafasan • Syok hipovolemik • Gagal ginjal
Lecture 12
UROLOGYC CONCERN IN CRITICAL CARE FOR NON TRAUMA CASE