PEMBAHASAN TO1 BATCH 1 2013

dr. Himawan, dr. Cemara, dr. Dini, dr. Yusuf, dr. Ratna, dr. Anshari

ILMU PENYAKIT DALAM

1. Komplikasi Kidney Failure
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Pasien ♂, 48 tahun Sulit BAK Kaki bengkak Mual muntah Riwayat kencing batu Kadar ureum 115, kreatinin 5,8, glukosa 168
Nilai Normal 7-25 mg/dL Deskripsi Urea dihasilkan dari metabolisme protein, difiltrasi di glomerulus. Jika GFR   urea direabsorbsi , kembali ke aliran darah Produk pemecahan keatinin fosfat dari otot rangka

Jenis Pemeriksaan Blood Urea Nitrogen (BUN)

Kreatinin Glukosa sewaktu

0,6-1,5 mg/dL 65-110 mg/dL

Uremia Symptoms

Chronic renal failure

Elevated concentration of urea nitrogen

Bacteria produce urease to disintegrate urea  high-concentration nitrogen
Stimulate gastrointestinal mucous membrane

Nausea & vomiting

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PF : TB 155 cm dan BB 39 kg (IMT = 16. nyeri sendi dan otot selama 5 minggu yang lalu. Sulit tidur. Luka-luka kecil yang menggaung yang pada awalnya terlihat seperti jerawat. Nafsu makan baik tetapi merasa BB .2  Underweight). Lab : CD4 575 .2. HIV    Laki-laki dewasa mudah merasa lemas.

Pathogenesis of HIV Infection .

How HIV Infection Become AIDS .

HIV Time Course http://www.com .microbiologybytes.

40 tahun Kuning seluruh tubuh sejak 2 minggu yll BAB dempul Bilirubin direk . Ikterik     ♂. bilirubin indirek normal Bilirubin direk = conjugated bilirubin Bilirubin indirek = unconjugated bilirubin .3.

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Type of Jaundice Wikipedia .

Color Atlas of Pathophysiology .

Color Atlas of Pathophysiology .

Table of Diagnostic Test Wikipedia .

muntah.4. bilirubin direct 6 . bilirubin total : 8. lemas Riwayat menggunakan suntik narkotika PF hepatomegali SGOT : 100. alkali fosfatase 720. mual. 35 thn Kuning 4 hari yang lalu. SGPT : 350. Serologi Hepatitis      ♂.

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Cirrhosis     ♂. 39 tahun Riwayat peminum alkohol PF: tampak tidur lelap. spider nevi (+) di dinding perut. kurus. terdapat bercak darah pada bibir dan bau amandel.5. ransang nyeri (-) Lab : ammonia darah meningkat .

wikimed.Color Atlas of Pathophysiology www.com .

Hemostasis    ♀. 61 tahun Perdarahan sejak 2 jam yll setelah cabut gigi Penderita jantung koroner dengan konsumsi aspirin 100mg selama beberapa tahun .6.

 Aspirin has an antiplatelet effect by inhibiting the production of thromboxane. which under normal circumstances binds platelet molecules together to create a patch over damaged walls of blood vessels .

Hemostasis („hemo”=blood. Following an injury to blood vessels several actions may help prevent blood loss. which is vitally important when blood vessels are damaged. sta=„remain”) is the stoppage of bleeding. including: Formation of a clot .

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TXA2.Formation of platelet aggregate  Injured blood vessel releases ADP. ADP. which accelerate vasoconstriction and causes PLT to swell and become more sticky  . which attracts platelets (PLT) PLT comming in contact with exposed collagen release: serotonin.

7. 40 tahun Badan lemas. tidak nafsu makan. Gambaran darah tepi: netrofil hipersegmen. demam(-) Lab : WBC: 4000 gr/dl. Hb: 8 gr/dl. makroovalosit . Anemia    ♂. Ht 34% MCV: 114 fl.

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• MCV less than lower limit of normal: microcytic anemia • MCV within normal range: normocytic anemia • MCV greater than upper limit of normal: macrocytic anemia • MCH less than lower limit of normal: hypochromic anemia • MCH within normal range: normochromic anemia • MCH greater than upper limit of normal: hyperchromic anemia .Anemias are defined based on cell size (MCV) and amount of Hgb (MCH).

Pernicious anemia (megaloblastic anemia due to vitamin B12 deficiency) Disturbance of proliferation and differentiation of stem cells Impaired RBC production Anemia of folic acid deficiency (megaloblastic anemia) Anemia of prematurity (premature infants at 2 to 6 weeks of age) Disturbance of proliferation and maturation of erythroblast ANEMIA Iron deficiency anemia (deficiency of heme synthesis) Intrinsic Thalassemia(deficiency of globin synthesis) Congenital dyserythropoietic anemias Increased RBC destruction (hemolytic anemias) Extrinsic Blood loss Anemia of renal failure Fluid overload .

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org/wiki/Megaloblastic_anemia .MEGALOBLASTIC ANEMIA   Anemia (of macrocytic classification) Laboratorium Findings: • Decreased red blood cell (RBC) count that results from inhibition of DNA synthesis in red blood cell production and hemoglobin levels[ • MCV >95 fl Pathopgenesis • Increased MCH  Folate and vitamin B12 • Normal MCHC. 32–36 g/dL deficienciesdefective RNA and • Decreased Reticulocyte count DNA syntheses destruction of fragile and  continuing cell growth without abnormal megaloblastic erythroid division precursor  Erythrogenic precursorslarger • Blood smear: • hypersegmented neutrophils than mature red blood cells • macroovalocytes macrocytes with oval (RBCs) shape RBC • Anisocytosis (increased variation in RBC size) and poikilocytosis (abnormally shaped RBCs). http://emedicine.medscape.com/article/ http://en.wikipedia.

png http://en.org/wiki/Glucose-6phosphate_dehydrogenase_deficiency .com/wpcontent/uploads/2009/05/g6pddeficiencyprocess.Glucose-6-phosphate dehydrogenase deficiency   an X-linked recessive hereditary disease characterised by abnormally low levels of glucose6-phosphate dehydrogenase Blood smear: Heinz body in RBC http://www.diseaseaday.wikipedia.

opening snap saat diastolik dengan nada rendah pada apikalis. hepatomegali (-) Opening Snap High-frequency early diastolic sound (occurs 50-100 msec after A2) associated with mitral stenosis. sound due to abrupt deceleration of mitral leaflets sound with associated murmur .8. 16 tahun Sesak napas saat beraktivitas sejak 3 bulan yll PF: Auskultasi P2 mengeras. Kelainan Katup Jantung    ♂.

• Loud P2 (pulmonic) component of the (S2) pulmonary hypertension secondary to severe mitral stenosis • An opening snap heard after the A2 (aortic) component of the (S2) • correlates to the forceful opening of the mitral valve • The mitral valve opens when the pressure in the left atrium is greater than the pressure in the left ventricle • This happens in ventricular diastole (after closure of the aortic valve). when the pressure in the ventricle precipitously drops .

Pathophysiology of Mitral Stenosis .

 The sounds waves responsible for heart sounds are generated by vibrations induced by:  valve closure.  abnormal valve opening.  vibrations in the ventricular chambers.  tensing of the chordae tendineae.  turbulent or abnormal blood flow across valves or between cardiac chambers .

.• closure of the mitral and tricuspid valves at the beginning of isovolumetric ventricular contraction • closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation Murmur: Abnormal movement of blood across valves and between cardiac chambers Divided into: -ventricular contraction (systole) -ventricular filling (diastole) • When audible. occurs early in ventricular filling • may represent tensing of the chordae tendineae and the AV ring. which is the connective tissue supporting the AV valve leaflet • When audible. is caused by vibration of the ventricular wall during atrial contraction • Usually associated with a stiffened ventricle.

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krepitasi pada kedua basal paru. dan edema pada extremitas . riwayat hipertensi dengan BP 150/90 PF : distensi vena leher.9. Heart Failure    Pasien 59 thn Sesak napas.

Symptoms of heart failure .

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http://www.aafp.org/afp/2006/0301/afp20060301p841-f1.gif

• Diastole process by which the heart returns to its relaxed state • the cardiac muscle is perfused. • Diastolic dysfunction • the heart is able to meet the body’s metabolic needs,at a higher filling pressure • Transmission of higher end-diastolic pressure to the pulmonary circulation pulmonary congestion dyspnea right-sided heart failure.

10. Anti Hipertensi

Nyeri kepala hilang timbul selama 1 minggu, mual muntah, riwayat hipertensi selama 10 tahun PF : TD 180/110, GDS 375 dan proteinuria +1

suhu 37 c.11. muka flushing. HR 84x/menit. RR 32x/menit. 25 thn Luka robek di kaki akibat kecelakaan  suntik lidocaine 1% infiltrasi untuk anestesi luka robeknya  5menit kemudian tjd gatal2 pada ekstremitas. kepala melayang dan sulit bernafas PF : BP 80/40. Syok Anafilaktik    ♂. auskultasi : stridor wheezing .

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Vasodilatation mucosaoedema Oedem larynx Stridor .

Brochospasm Wheezing .

12. ST Elevasi V1-V4. Acute coronary syndrome   Keluhan 1 jam yang lalu nyeri dada seperti ditindih beban berat EKG irama sinus . denyut jantung 72x/menit. peningkatan enzim jantung serial .

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full .http://ceaccp.org/c ontent/4/6/175.oxfordjournals.

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 Left coronary artery mensuplai area:      Anterior LV The bulk of the interventricular septum (anterior two thirds) The apex Lateral and posterior LV walls Right coronary artery mensuplai area:     Right ventricle (RV) The posterior third of the interventricular septum The inferior wall (diaphragmatic surface) of the left ventricle (LV) A portion of the posterior wall of the LV (by means of the posterior descending branch) .

EKG .

http://acutemed.co.uk/diseases/ACS+%28Acute+Coronary+Syndrome%29 .

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Perokok berat sejak usia 17th PF : hemithorax cembung dan perkusi hipersonor di kedua lapang paru . Riwayat batuk darah disangkal. Spirometri pada PPOK    ♂. dahak kental kuning sampai kecoklatan.13. 68 tahun Sesak nafas + batuk sejak 3 minggu.

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lung recoil decreases (compliance increases) and the midposition of breathing is shifted toward inspiration (barrel chest)  raises the functional residual capacity .Obstructive lung disease  reduced ventilation  the ratio of the duration of expiration to that of inspiration is increased  obstructed expiration distends the alveolar ductules (centrilobular emphysema).

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Terapi Asma   Asma sudah 10 tahun PF : RR 32x/ menit.14. FN 110x/ menit GINA Report 2011 .

MANAGEMENT IN STABLE CONDITION .

Pathophysiology of Asthma .

Algorithm of Asthma Diagnosis http://www.eguidelines.co.uk .

Terapi Oksigen Devices Nasal Cannula Rebreathing Mask/Simple Oxygen Mask Non Rebreathing Mask Flow Rate (L/min 1–5 6-10 Oxygen Concentration 28–44% 35-60% -First third of exhaled gases mix with reservoir -Exhaled gases from upper airway are oxygen rich Two valves added to prevents: -Entrainment of room air during inspiration -Retention of exhaled gases during expiration Description 10-12 95% Venturi Mask 4-8 25-60% Ventilator can be set 21-100% .

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GINA report 2011

15.Hipoaktivitas Kelenjar Adrenal
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♂, 40 th Letih lemah sejak 2 bulan yll, saat ini terapi TB, mengeluh bb turun, dibawah siku warna kulit tampak menjadi hitam PF : TD 80/50, nadi 72, tidak ada penyakit jantung

Adrenal Insufficiency

Adrenal tuberculosis is a manifestation of disseminated disease presenting rarely as adrenal insufficiency Addison's disease results from progressive destruction of the adrenals, which must involve >90% of the glands before adrenal insufficiency appears The adrenal is a frequent site for chronic granulomatous diseases, predominantly tuberculosis(70%-90% cases), but also histoplasmosis, coccidioidomycosis, and cryptococcosis

Effects and Symptoms of Adrenocortical Hormone Deficiency

5 C . PF:TB 158 cm. BB 65 kg (IMT = 26  Overweight). Sindrom Cushing      ♀. asupan makan tidak banyak bertambah meski cepat lapar.16. RR 18 x/menit dan suhu 36. Riwayat alergi makanan  membeli sendiri obat alergi atau jamu-jamuan. FN 80x/menit. TD 140/90 mmHg  Hipertensi. 25 tahun Kenaikan BB 10 kg dalam dua bulan.

Sindrom Cushing   Cushing's syndrome (hyperadrenocorticalism/hypercortisolism) The clinical condition resulting from chronic exposure to excessive circulating levels of glucocorticoids The most common cause: excess ACTH secretion from the anterior pituitary gland (Cushing's disease). McGraw-Hill. Thieme. . McPhee SJ. 2000. Silbernagl S. Color atlas of pathophysiology. et al. 5th ed.16. et al. 2006. Pathophysiology of disease: an introduction to clinical medicine.

Riwayat DM (+)  obat suntikan sejak 3 bulan yll. nafas kussmaul. 2 hari ini menghentikan obat. nadi 110x/menit.17. lidah kering. tensi 90/60 mmHg. 20 th Gaduh gelisah sejak 2 jam yll. RR 32x/menit. turgor kulit menurun . Komplikasi Akut DM    ♀. BB 45kg. PF TB 155cm. apatis.

Acute Effect of Diabetes Mellitus (Diabetic Ketoacidosis) .

Effect on Insufficiency of Insulin .

mata exopthalmus. TSH rendah . dan diare PF : TD 130/80 mmHg. HR 120x/mnt. akral hangat Laboratorium: peningkatan T3 dan T4. sulit tidur. RR 24x/mnt. gelisah. pembesara kelenjar tiroid difus. Terapi Hipertiroid     ♀.18. mudah lelah. 30 tahun Dada berdebar-debar sejak 1 minggu yll.

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Laboratorium Assesment for Thyroid Function .

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Color atlas of pathophysiology. 2000.19. Pathophysiology of disease: an introduction to clinical medicine. et al. McGraw-Hill. et al. 2006. Disorder of Calcium Metabolism   ♀. 35 tahun Pasca tiroidektomi sering mengalami kaku dan kejang Silbernagl S. McPhee SJ. 5th ed. . Thieme.

2000. Color atlas of pathophysiology. 5th ed. . Disorder of Calcium Metabolism Silbernagl S. Thieme. Pathophysiology of disease: an introduction to clinical medicine. 2006. et al.19. McGraw-Hill. et al. McPhee SJ.

kadar urat serum 6. 30 tahun Nyeri dan bengkak pada sendi metakarpophalang dan interfalang kedua tangan.20. that affect the joints and may cause systemic manifestation . Arthritis    Wanita. Dirasakan saat bangun pagi LED 184 mm(). dan bengkak pada sendi lutut.2 mg/dl Rheumatoid Arthritis • Definition: – Chronic inflammatory – Autoimmune disorder.

Reumatoid Arthritis a score of 6 fulfilling the requirements for RA .

RA Patophysiology .

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25 tahun Penurunan kesadaran ±2 jam yll.21. demam tinggi. S 38. Malaria     ♂. kulit tampak pucat. Lab : ditemukan plasmodium sausage shape . riwayat demam hilang timbul.5oC. menggigil dan keringat dingin PF: TD 100/70 mmHg. konjungtiva anemis.

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Malaria Life Cycle .

unimelb.microbiol.au .edu.Pathogenesis of Cerebral Malaria • Possible cause: • Binding of parasitized red cells in cerebral capillaries •  permeability of the blood brain barrier • Excessive induction ofcytokines http://www.

Suhu 38. vesikuler. Thoraks: BJ I-II normal. Abdomen : nyeri tekan epigastrium (+). Nadi 98x/menit. PF : TSS.22. Dengue Infection     ♂. mual. Lab: Hb 12 g/dL. hematokrit 36%. Leukosit 4700. Ext : petechiae pada lengan atas kanan dan kiri. 17 tahun Demam sejak 4 hari yang lalu disertai nyeri kepala.3°C. TD 120/80 mmHg. nyeri otot dan sendi. Trombosit 98000 . Konjungtiva pucat (-).

Pathophysiology of Dengue Fever .

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Dengue Infection: Classification .

ILMU BEDAH. ANESTESI DAN RADIOLOGI .

23. B. D. Airway Establish patent airway Breathing Assess and ensure adequate oxygenation Circulation • Level of consciousness • Skin color and temperature • Pulse rate and character Disability Baseline neurologic evaluation  GCS scoring  Pupillary response Environment Completely undress the patient and ventilation • Control hemorrhage • Restore volume • Reassess parameters ATLS . C. E. Primary Survey A.

optimized by optima .

Special diagnostic tests optimized by optima F. Complete Neurological examination E.Secondary Survey Componet: A. Re-evaluation . History namponade Allergic Medication Past illness Last meals Event B. Physical exam : head to toe C. Every orrifice examination D.

3. consisting of the placement of sutures. because of bacterial contamination or tissue loss. Often. Delayed primary closure. allowing the wound to stay open for a few days. this constitutes healing by secondary intention. Classification of Wounds 1. a wound will be left open to heal by granulation tissue formation and contraction. and the subsequent closure of the sutures 8th ed Schwartz's Principles of Surgery . 2. represents a combination of the first two. or healing by tertiary intention.24. An incised wound that is clean and sutured closed is said to heal by primary intention.

8th ed Schwartz's Principles of Surgery .

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25. Shock Definition
• A physiologic state characterized by – Inadequate tissue perfusion • Clinically manifested by – Hemodynamic disturbances – Organ dysfunction

optimized by optima

Hypovolemic Shock

Hemorrhagic Shock
Parameter I II III IV

Blood loss (ml)
Blood loss (%) Pulse rate (beats/min) Blood pressure Respiratory rate (bpm) Urine output (ml/hour) CNS symptoms
Crit Care. 2004; 8(5): 373–381.

<750
<15%

750–1500
15–30%

1500–2000
30–40%

>2000
>40%

<100
Normal 14–20 >30 Normal

>100
Normal 20–30 20–30 Anxious

>120
Decreased 30–40 5–15 Confused

>140
Decreased >35 Negligible Lethargic

optimized by optima

26. WHO Pain Management Stepladder

optimized by optima

Mekanisme kerja nsaid

optimized by optima

Mekanisme kerja opioid optimized by optima .

27.5 liters of blood . Hemothorax     Occurs when pleural space fills with blood Usually occurs due to lacerated blood vessel in thorax As blood increases. it puts pressure on heart and other vessels in chest cavity Each Lung can hold 1.

27-28 CHEST TRAUMA Hemothorax optimized by optima .

Hemothorax .

Hemothorax May put pressure on the heart .

Where does the blood come from. Lots of blood vessels .

Bloody Sputum Diminished Breath Sounds on Affected Side Tachycardia Flat Neck Veins .S/S of Hemothorax        Anxiety/Restlessness Tachypnea Signs of Shock Frothy.

Treatment for Hemothorax       ABC’s with c-spine control as indicated Secure Airway assist ventilation if necessary General Shock Care due to Blood loss Consider Left Lateral Recumbent position if not contraindicated RAPID TRANSPORT Contact Hospital and ALS Unit as soon as possible .

BLS Plus Care      Monitor Cardiac Rhythm Establish Large Bore IV preferably 2 and draw blood samples Airway management to include Intubation Rapid Transport If Development of Hemo/Pneumothorax needle decompression may be indicated .

Simple/Closed Pneumothorax     Opening in lung tissue that leaks air into chest cavity Blunt trauma is main cause May be spontaneous Usually self correcting .

Simple/Closed Pneumothorax S/S :  Chest Pain  Dyspnea  Tachypnea  Decreased Breath Sounds on Affected Side Th/ ABC’s with C-spine control Airway Assistance as needed If not contraindicated transport in semi-sitting position Provide supportive care Contact Hospital and/or ALS unit as soon as possible .

Open Pneumothorax    Opening in chest cavity that allows air to enter pleural cavity Causes the lung to collapse due to increased pressure in pleural cavity Can be life threatening and can deteriorate rapidly .

Open Pneumothorax .

Inhale Exhale Open Pneumothorax optimized by optima .

Inhale Exhale Open Pneumothorax .

Inhale Exhale Open Pneumothorax .

Open Pneumothorax S/S :  Dyspnea  Sudden sharp pain  Subcutaneous Emphysema  Decreased lung sounds on affected side  Red Bubbles on Exhalation from wound (Sucking chest wound) Th/ : ABC’s with c-spine control as indicated High Flow oxygen Listen for decreased breath sounds on affected side Apply occlusive dressing to wound Notify Hospital and ALS unit as soon as possible .

Sucking Chest Wound Occlusive Dressing .

and great vessels optimized by optima Each time we inhale.28. There is no place for the air to escape. the lung collapses further. Tension Pneumothorax   Air builds in pleural space with no where for the air to escape Results in collapse of lung on affected side that results in pressure on mediastium.the other lung. ..

There is no place for the air to escape..Each time we inhale. the lung collapses further. The trachea is pushed to the good side Heart is being compressed .

S/S of Tension Pneumothorax       Anxiety/Restlessness Severe Dyspnea Absent Breath sounds on affected side Tachypnea Tachycardia Poor Color Accessory Muscle Use  JVD  Narrowing Pulse Pressures  Hypotension  Tracheal Deviation (late if seen at all)  .

Treatment of Tension Pneumothorax       ABC’s with c-spine as indicated Needle Decompression of Affected Side High Flow oxygen including BVM Treat for S/S of Shock Notify Hospital and ALS unit as soon as possible If Open Pneumothorax and occlusive dressing present BURP occlusive dressing .

artery.Needle Decompression       Locate 2-3 Intercostal space midclavicular line Cleanse area using aseptic technique Insert catheter ( 14g or larger) at least 3‖ in length over the top of the 3rd rib( nerve. vein lie along bottom of rib) Remove Stylette and listen for rush of air Place Flutter valve over catheter Reassess for Improvement .

Needle Decompression .

or cystine may occasionally be found upon urinalysis Diagnosis: IVP optimized by optima . Ureterolithiasis   Urinary tract stone disease Signs:     Flank pain Irritative voiding symptom Nausea microscopic hematuria   Urinary crystals of calcium oxalate.29. uric acid.

. Hirschsprung disease Definitions   Pathophysiology   Congenital megacolon the absence of myenteric and submucosal ganglion cells in the distal alimentary tract decreased motility in the affected bowel segment   Results from the absence of parasympathetic ganglion cells in the myenteric and submucosal plexus of the rectum and/or colon. These ganglion cells arrive in the proximal colon by 8 weeks of gestational age and in the rectum by 12 weeks of gestational age. Arrest in migration leads to an aganglionic segment.30.

 one half are diagnosed before they are aged 1 year.Hirschsprung disease Frequency  Predilection     approximately 1 per 5000 live births. Age:  Nearly all children with Hirschsprung disease are diagnosed during the first 2 years of life.      Classical HD (75% of cases): Rectosegmoid Long segment HD (20% of cases) Total colonic aganglionosis (312% of cases) rare variants include the following: Total intestinal aganglionosis Ultra-short-segment HD (involving the distal rectum below the pelvic floor and the anus) . Sex: 4 times more common in males than females. Mortality/Morbidity:  The overall mortality of Hirschsprung enterocolitis is 2530%.  Minority not recognized until later in childhood or adulthood..

irregular contractions of Symptoms in older children and aganglionic segment adults include the following:  Delayed evacuation of barium  Severe constipation  Biopsy :  Abdominal distension  absence of ganglion cells  hypertrophy and hyperplasia of  Bilious vomiting nerve fibers.  Failure to thrive .Clinical presentation   Rontgen : Newborns :  Failure to pass meconium within  Plain abdominal radiography the first 48 hours of life  Dilated bowel  Abdominal distension that is  Air-fluid levels. relieved by rectal stimulation or  Empty rectum enemas  Contrast enema  Vomiting  Transition zone  Neonatal enterocolitis  Abnormal.

lethargy. fever.HD-Assosciated enterocolitis   Abdominal distension. explosive diarrhea. rectal bleeding.  children with Down syndrome . or shock The risk is greatest:  before HD is diagnosed  after the definitive pull-through operation. vomiting.

Rehydration. .Treatment Hirschsprung disease  HD-Associated enterocolitis  Surgical removal or bypass of the aganglionic bowel. intravenous antibiotics and colonic irrigations.

.31. or rarely some other type of inflammation. Peritoneum is a membrane that covers the surface of both the organs that lie in the abdominal cavity and the inner surface of the abdominal cavity itself. Peritonitis Peritonitis Infection. of the peritoneum.

 . Late and localized infections produces an intraabdominal abscess.Intra-abdominal infections result in 2 major clinical manifestations  Early or diffuse infection results in localized or generalized peritonitis.

The fluid that accumulates creates a good environment for the growth of bacteria.     . This can be caused due to an ulcer eating its way through stomach wall or intestine when there is a rupture of the appendix or a ruptured diverticulum. it can occur due to an intestine to burst or injury to an internal organ which bleeds into the internal cavity. Very rare < 1% Usually occurs in people who have an accumulation of fluid in their abdomens (ascites).  Secondary: Caused by the entry of bacteria or enzymes into the peritoneum from the gastrointestinal or biliary tract.2 Major Types  Primary: Caused by the spread of an infection from the blood & lymph nodes to the peritoneum. Also.

Signs & Symptoms          Swelling & tenderness in the abdomen Fever & Chills Loss of Appetite Nausea & Vomiting Increased breathing & Heart Rates Shallow Breaths Low BP Limited Urine Production Inability to pass gas or feces Exam :  The usual sounds made by the active intestine and heard during examination with a stethoscope will be absent. . because the intestine usually stops functioning.  The abdom may be rigid and boardlike  Accumulations of fluid will be notable in primary due to ascites.

Evaluation Lab :  Blood Test  Samples of fluid from the abdomen  CT Scan  Chest X-rays  Peritoneal lavage. . th/  Hospitalization is common.  Antibiotics are prescribed to control the infection & intravenous therapy (IV) is used to restore hydration.  Surgery is often necessary to remove the source of infection.

 repair resuscitate .Stomach/duodenum – Perforation Presentation :  abdominal  Pain pain on palpation  Release pain  rigidity  peritonism. shock  Air under diaphragm on X-ray  Treatment  antibiotics.

Mekanisme Sekresi Asam lambung optimized by optima .

Blunt Abdominal Trauma  The most commonly injured organs  Spleen  Liver  Retroperitoneum  small bowel  kidneys  Bladder  Colorectum  Diaphragm  pancreas .

the most common cause of death in American ICUs (the 13th leading cause of death overall in US) .the major contributor to early mortality from trauma (the #1 cause of death in those < 45 years of age) Septic shock . Shock    Cardiogenic shock .S.32. deaths) Hypovolemic shock .a major component of the the mortality associated with cardiovascular disease (the #1 cause of U.

Shock: Definitions  Kumar and Parrillo (1995) . to irreversible cellular injury.‖ .―The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible. and then if prolonged.

due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/ mechanical failure of the cardiac anatomy an characterized by elevations of diastolic filling pressures and volumes Extra-cardiac obstructive shock .Shock: Classification     Hypovolemic shock .due to decreased circulating blood volume in relation to the total vascular capacity and characterized by a reduction of diastolic filling pressures Cardiogenic shock .caused by loss of vasomotor control resulting in arteriolar/venular dilatation and characterized (after fluid resuscitation) by increased cardiac output and decreased SVR .due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload Distributive shock .

Hypovolemic  Hemorrhagic  Trauma  Gastrointestinal  Retroperitoneal Fluid depletion (nonhemorrhagic) External fluid loss  Dehydration  Vomiting  Diarrhea  Polyuria  Interstitial fluid redistribution  Thermal injury  Trauma  Anaphylaxis Increased vascular capacitance (venodilatation)  Sepsis  Anaphylaxis  Toxins/drugs    .

CARDIOGENIC    Myopathic Blunt Cardiac Injury (trauma) Myocarditis  Pharmacologic : Calcium channel blockers Mechanical     Cardiomyopathy Post-ischemic myocardial stunning Valvular failure (stenotic or regurgitant) Hypertropic cardiomyopathy Ventricular septal defect Arrhythmic Bradycardia       Septic myocardial depression Tachycardia .

EXTRACARDIAC OBSTRUCTIVE  Impaired diastolic filling (decreased ventricular preload)  Direct venous obstruction (vena cava)  intrathoracic obstructive tumors  Increased intrathoracic pressure  Tension pneumothorax  Mechanical ventilation (with excessive pressure or volume depletion)  Asthma  Decreased cardiac compliance  Constrictive pericarditis  Cardiac tamponade  Impaired systolic contraction (increased ventricular afterload)  Right ventricle  Pulmonary embolus (massive)  Acute pulmonary hypertension  Left ventricle  embolus  Aortic dissection .

rickettsial) Toxic shock syndrome Anaphylactic. nitroprusside.DISTRIBUTIVE      Septic (bacterial. bretylium) . viral. anaphylactoid Neurogenic (spinal shock) Endocrinologic  Adrenal crisis  Thyroid storm  Toxic (e.g. fungal..

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agitation. lethargy. obtundation l vasodilation. 51-70yr: <80mmHg. >71yo<70mmHg. K • Cutaneous vasoconstriction vs. • Mental Changes: anxiousness. k j .CLINICAL MARKERS OF SHOCK • Brachial systolic blood pressure: <110mmHg • Sinus tachycardia: >90 beats/min • Respiratory rate: <7 or >29 breaths/min • Urine Output: <0. indifference.5cc/kg/hr • Metabolic acidemia: [HCO3]<31mEq/L or base deficit>3mEq/L • Hypoxemia: 0-50yr: <90mmHg.

Etiology & Hemodynamic Changes in Shock Etiology of shock example CVP CO SVR VO2 sat preload hypovolemic low low high low contractility afterload cardiogenic distributive high low high low .

Etiology & Hemodynamic Changes in Shock (Afterload) ETIOLOGY OF SHOCK AFTERLOAD EXAMPLE DISTRIBUTIVE Hyperdynamic Septic CVP CO SVR VO2 SAT Low/High Low/High Low Low High Low Low Low Low High Low Low High Low/High Low Low Hypodynamic Septic Neurogenic Anaphylactic .

pancreatitis. ruptured aneurysms.HYPOVOLEMIC SHOCK • Decreased preload->small ventricular end-diastolic volumes -> inadequate cardiac generation of pressure and flow • Causes: • bleeding: trauma. cirrhosis . hemorrhagic pancreatitis • protracted vomiting or diarrhea • adrenal insufficiency. diabetes insipidus • Dehydration • third spacing: intestinal obstruction. GI bleeding.

Tachycardia. MS. CO. BP.CVP. MS change. lactic acid and PCWP Treatment: ABCs. HR.Hypovolemic Shock    Signs & Symptoms: Hypotension. Hct. Trasfusion Stem ongoing Blood Loss . IVF (crystalloid). Deminished Pulses. Oliguria. Markers: monitor UOP.

pancreatitis. Anaphylaxis. toxin reactions 2. drug. .SEPTIC/INFLAMMATORY SHOCK Mechanism: release of inflammatory mediators leading to 1. infection/sepsis: G(-/+ ) speticemia. cholangitis. toxic shock syndrome. 3. major burns. Disruption of the microvascular endothelium 2. necrotic tissue. Cutaneous arteriolar dilation and sequestration of blood in cutaneous venules and small veins Causes: 1. etc. pneumonia. meningitis. pyelonephritis. major fractures. Trauma: crush injuries. wet gangrene. peritonitis.

IVF. altered mental status. Late – Leukocytosis. Monitor/findings: Early—hyperglycemia. Late-. often adequate urine output. tachypneic. oliguria. febrile. respiratory alkylosis. Tx : ABCs.Septic/Inflammatory Shock Signs: Early– warm w/ vasodilation. Drainage (ie abscess) pressors. lactic acidosis Very Late– Disseminated Intravascular Coagulation & Multi-Organ System Failure. ABX. WBC typically normal or low. hemoconcentration. Blood cx.vasoconstriction. hypotension. .

cardiomyopathy. constrictive pericaditis. severe pulmonary hypertension . pericardial tamponade. Obstructive disorders: PE. myocardial contusion 2. myocardiditis. ventricular fibrillation) 4. septal defects. myocardial infarction. Arrythmias: bradyarrythmias (heart block). tension peneumothorax. Cardiomyopathies: myocardial ischemia. papillary muscle rupture. atrial flutter. tachyarrythmias (atrial fibrillation. Mechanical: cardiac valvular insufficiency. aortic stenosis 3.CARDIOGENIC SHOCK Mechanism: Intrinsic abnormality of heart -> inability to deliver blood into the vasculature with adequate power Causes: 1.

intraaortic ballon pump & ventricular assist device. elevated CVP.pressors. LV failure – pressors.Cardiogenic Shock     Characterized by high preload (CVP) with low CO Signs/SXS: Dyspnea. rales. Tx: CHF– diuretics & vasodilators +/. loud P2 gallop. low BP. oliguria Monitor/findings: CXR pulm venous congestion. decrease afterload. Low CO. .

Drugs 4. venules. Spinal cord injury 2.NEUROGENIC SHOCK Mechanism: Loss of autonomic innervation of the cardiovascular system (arterioles. Neurological disorders . Regional anesthesia 3. including the heart) Causes: 1. small veins.

Neurogenic Shock     Characterized by loss of vascular tone & reflexes. Bradycardia. vasoactive medications if refractory . test bulbo-carvernous reflex Tx: IVF. Signs: Hypotension. Accompanying Neurological deficits. Monitor/findings: hemodynamic instability.

33. FOREHAND FRACTURE .

Montegia Fracture Dislocation    It is a fracture of the proximal 1/3rd of the Ulna with dislocation of head of radius anteriorly. Posteriorly or laterally Head of Radius dislocates same direction as fracture It requires ORIF or it will redisplace .

Montegia : Lateral displacement optimized by optima .

Galliazi Fracture  It is a fracture of distal Radius and dislocation of inferior Radio.Ulnar joint Like Montegia fracture if treated conservatively it will redisplace This fracture appeared in acceptable position after reduction and POP   .

Greenstick Fractures .

Colles’ Fracture      Most common fracture in Osteoporotic bones Extra-Articular : 1 inch of distal Radius Results from a fall on dorsi flexed wrist Typical deformity : Dinner Fork Deformity is : Impaction. radial displacement and angulation and avulsion of ulnar styloid process . dorsal displacement and angulation.

Colles’ Fracture optimized by optima .

# distal 1’’ Impaction .Dorsal displacement and dorsal tilt .

Colles’ Fracture optimized by optima .

Smith Fracture .

Smith Fracture      Almost the opposite of Colles’ fracture Much less common compared to colles’ Results from a fall on palmer flexed wrist Typical deformity : Garden Spade Management is conservative : MUA and Above Elbow POP .

34. LOW BACK PAIN .

Herniated Nucleus Pulposus   The progressive degeneration of a disc. or traumatic event. can lead to a failure of the annulus to adequately contain the nucleus pulposus This is known as herniated nucleus pulposus (HNP) or a herniated disc .

Herniated Nucleus Pulposus  Symptoms  Back pain  Leg pain  Dysthesias  Anesthesias .

Herniated Nucleus Pulposus   Varying degrees Disc bulge  Mild symptoms  Usually go away with nonoperative treatment  Rarely an indication for surgery Moderate/severe symptoms   Extrusion (herniation)  Nonoperative treatment .

Herniated Nucleus Pulposus  Diagnosis  Magnetic resonance imaging (MRI)/patient exam Initial bed rest Nonsteroidal antiinflammatory (NSAID) medication Physical therapy   Nonoperative Care    Exercise/walking  Steroid injections .

Herniated Nucleus Pulposus  Surgical care  Failure of nonoperative treatment  Minimum of 6 weeks in duration  Can be months Discectomy   Removal of the herniated portion of the disc  Usually through a small incision  High success rate .

Herniated Nucleus Pulposus  Cauda Equina Syndrome    Caused by a central disc herniation Symptoms include bilateral leg pain. paralysis of the bladder. loss of perianal sensation. and weakness of the anal sphincter Surgical intervention in these cases is urgent .

Spondylolisthesis  Gradation of spondylolisthesis  Meyerding’s Scale  Grade 1 = up to 25%  Grade 2 = up to 50%  Grade 3 = up to 75%  Grade 4 = up to 100%  Grade 5 >100% (complete dislocation. spondyloloptosis) .

with or without leg pain. anesthesias  Partial pain relief by leaning forward or sitting .Spondylolisthesis  Symptoms  Low back pain  With or without buttock or thigh pain  Pain aggravated by standing or walking  Pain relieved by lying down  Concomitant spinal stenosis. may be present  Other possible symptoms  Tired legs. dysthesias.

in some cases with leg symptoms Rest NSAID medication Physical therapy Steroid injections  Nonoperative Care     .Spondylolisthesis  Diagnosis   Plain radiographs CT.

Spondylolisthesis  Surgical care   Failure of nonoperative treatment Decompression and fusion    Instrumented Posterior approach With interbody fusion .

usually in the posterior elements—most frequently in the pars interarticularis .Spondylolysis  Spondylolysis     Also known as pars defect Also known as pars fracture With or without spondylolisthesis A fracture or defect in the vertebra.

Spondylolysis  Symptoms      Low back pain/stiffness Forward bending increases pain Symptoms get worse with activity May include a stenotic component resulting in leg symptoms Seen most often in athletes   Gymnasts at risk Caused by repeated strain .

in some cases Limit athletic activities Physical therapy   Nonoperative care   Most fractures heal without other medical intervention .Spondylolysis  Diagnosis   Plain oblique radiographs CT.

Spondylolysis  Surgical care  Failure of nonoperative treatment  Posterior fusion  Instrumented  May require decompression .

Ankylosing spondilitis optimized by optima .

ABDOMINAL INJURIES .35.

Causes  injuries to the abdomen. pelvis and genitalia are generally caused by accidents involving high kinetic energy and acceleration or deceleration forces .

Open vs. Closed Injuries   Abdominal injuries can be either open or closed Open injuries are caused by sharp or high velocity objects that create an opening between the peritoneal cavity and the outside of the body  Closed injuries are caused by compression trauma associated with deceleration forces and include:  contusions  ruptures  lacerations  shear injuries .

 hollow organs include:  stomach  intestines  gallbladder  bladder  solid organs include:  liver  spleen  kidneys .Hollow and Solid Organs The type of injury will depend on whether the organ injured is solid or hollow.

the symptoms of shock may overshadow those from peritonitis . producing a painful inflammatory reaction called peritonitis   damage to solid organs such as the liver can cause severe internal bleeding blood in the peritoneal cavity causes peritonitis when patients injure solid organs. their highly irritating and infectious contents spill into the peritoneal cavity.Abdominal Injuries Hollow Organ Injuries  Solid Organ Injuries  when hollow organs rupture.

such as a blow to the flank that initially causes little pain.Abdominal Injuries  Abdominal injuries can be obvious. such as an open wound. or subtle. but damages the liver or spleen  Suspect abdominal internal injury in any patient who has a penetrating abdominal wound or has suffered compression trauma to the abdomen .

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 Avulsion of pedicle is fatal  .Liver    Largest organ in abdominal cavity Right upper quadrant Injured from trauma to:  After injury. blood and bile leak into peritoneal cavity Shock  Peritoneal irritation   Eighth through twelfth ribs on right side of body  Upper central part of abdomen   Management: Suspect liver injury when: Steering wheel injury  Lap belt injury  Epigastric trauma  Resuscitation  Laparotomy and repair or resection.

partial excision or splenectomy)  Observation in hospital for patients with sub-capsular haematoma . flank.Spleen     Upper left quadrant Rich blood supply Slightly protected by organs surrounding it and by lower rib cage  Most commonly injured organ from blunt trauma  Associated intraabdominal injuries common Suspect splenic injury in:  Motor vehicle crashes  Falls or sports injuries involving was an impact to the lower left chest.  Laparotomy (repair. or upper left abdomen  Kehr’s sign  Left upper quadrant pain radiates to left shoulder  Common complaint with splenic injury  Management :  Resuscitation.

Stomach/duodenum    Not commonly injured by blunt trauma Protected location in abdomen Penetrating trauma may cause gastric transection or laceration  Signs of peritonitis from leakage of gastric contents Unless nasogastric drainage returns blood  Diagnosis confirmed during surgery  .

shock  Air under diaphragm on X-ray  Presentation : Haematemesis +/ Melaena  Severity   Treatment Antibiotics  resuscitate  repair  Increased PR>90  Fall BP<100   Treatment : transfusion  inject DU  .Stomach/duodenum Perforation  Bleeding  Presentation : abdominal pain  rigidity  peritonism.

ILEUS .36.

resuscitation and intensive monitoring Obstructive ileus A mechanical blockage arising from a structural abnormality that presents a physical barrier to the progression of gut contents.Introduction and Definitions Accounts for 5% of all acute surgical admissions Patients are often extremely ill requiring prompt assessment. Paralytic Ileus is a paralytic or functional variety of obstruction Obstruction is: Partial or complete Simple or strangulated .

   . stomach. anaerobes and strep. septaecemia and toxaemia. Normal intestinal mucosa has a significant immune role Distension results from gas and/ or fluid and can exert hydrostatic pressure. pancreas and hepatobiliary ) 7L absorbed 2L enter the large intestine and 200 ml excreted in the faeces Air in the bowel results from swallowed air ( O2 & N2) and bacterial fermentation in the colon ( H2.Pathophysiology I       8L of isotonic fluid received by the small intestines (saliva. In case of BO Bacterial overgrowth can be rapid If mucosal barrier is breached it may result in translocation of bacteria and toxins resulting in bactaeremia. Methane & CO2). 600 ml of flatus is released Enteric bacteria consist of coliforms. duodenum.faecalis.

4. 5. Bacterial over growth with translocation of bacteria and it’s toxins causing bacteraemia and septicaemia. mucosal depletion necrosis and perforation and peritonitis.      Decompress with NGT Replace lost fluid Correct electrolyte abnormalities Recognise strangulation and perforation Systemic antibiotics. Initial overcoming of the obstruction by increased paristalsis Increased intraluminal pressure by fluid and gas Vomiting sequestration of fluid into the lumen from the surrounding circulation Lymphatic and venous congestion resulting in oedematous tissues Factors 3. 3. 2. 7.Pathophysiology II Obstruction results in: 1. 8. 4.5 result in hypovolaemia and electrolyte imbalance Further: localised anoxia. . 6.

ROS. PSH. FH. SH) High •Pain is rapid •Vomiting copious and contains bile jejunal content •Abdominal distension is limited or localized •Rapid dehydration Distal small bowel •Pain: central and colicky •Vomitus is feculunt •Distension is severe •Visible peristalsis •May continue to pass flatus and feacus before absolute constipation Colonic • Preexisting change in bowel habit •Colicky in the lower abdomin •Vomiting is late •Distension prominent •Cecum ? distended Persistent pain may be a sign of strangulation Relative and absolute constipation .1. Complete HX ( PMH. History The Universal Features Colicky abdominal pain. vomiting. Medication. abdominal distension. constipation (absolute).

Causes. lumbricoides Mural Neoplasms lipoma polyps leiyomayoma hematoma lymphoma carcinoid carinoma secondary Tumors Crohns TB Stricture Intussusception Congenital Extraluminal Postoperative adhesions Congenital adhesions Hernia Volvulus . Body Bezoars Gall stone Food Particles A.Small Bowel Luminal F.

2. guarding and rebound •Organomegaly •Bowel sounds –High pitched –Absent Others Systemic examination If deemed necessary. •CNS •Vascular •Gynaecological •muscuoloskeltal •Rectal examination . T. LN •Assessment of vomitus if possible •Full lung and heart examination Abdominal •Abdominal distension and it’s pattern •Hernial orifices •Visible peristalsis •Cecal distension •Tenderness. Sat •dehydration •Anaemia. BP. Examination General •Vital signs: P. RR. jaundice.

NPO. Decompress with Naso-gastric tube and secure in position Insert a urinary catheter (hourly urinary measurements) and start a fluid input / output chart Intravenous antibiotics (no clear evidence) If concerns exist about fluid overloading a central line should be inserted Follow-up lab results and correction of electrolyte imbalance The patient should be nursed in intermediate care Rectal tubes should only be used in Sigmoid volvulus. (determined by estimated fluid loss and cardiac function). .Initial Management in the ER  Resuscitate:    Air way (O2 60-100%) Insert 2 lines if necessary IVF : Crytloids at least 120 ml/h. Add K+ at 1mmmol/kg           Draw blood for lab investigations Inform a senior member in the team.

Indications for Surgery    Immediate intervention: Evidence of strangulation (hernia….etc) Signs of peritonitis resulting from perforation or ischemia .

tricyclic antidepressants .Paralytic Ileus  Associated with the following conditions:  Postoperative and bowel resection  Intraperitoneal infection or inflammation  Ischemia  Extra-abdominal: Chest infection. Myocardia infarction  Endocrine: hypothyroidism. diabetes  Spinal and pelvic fractures  Retro-peritoneal haematoma  Metabolic abnormalities:  Hypokalaemia  Hyponatremia  Uraemia  Hypomagnesemia  Bed ridden  Drug induced: morphine.

Does the patient improve on conservative measures . Radiological features:   Is the bowel diffusely distended Is there gas in the rectum  Are further investigasions (CT or Gastrografin studies) helpful in showing an obstruction. Is the bowel sounds diffusely hypoactive.Clinical Findings Clinical features    Is there an under lying cause? Is the abdomen distended but tenderness is not marked.

BURN INJURY .37.

vasoconstriction  Renal or hepatic failure  Formation of eschar  Complications of circumferential burn . Infection.Burn Injuries  Potential complications  Fluid and Electrolyte loss  Hypovolemia  Hypothermia. Acidosis   catecholamine release.

Burn Injuries   An important step in management is to determine depth and extent of damage to determine where and how the patient should be treated Depth Classification  Superficial  Partial thickness  Full thickness  Thermal burn Skin injury  Inhalation injury   Chemical burn Skin injury  Inhalation injury  Mucous membrane injury   Electrical burn  Lightning  Radiation burn .

sunburn  Usually heal in ~ 7 days  . but no blistering  Burn blanches under pressure  Example .Burn Classifications  1st degree (Superficial burn) Involves the epidermis  Characterized by reddening  Tenderness and Pain  Increased warmth  Edema may occur.

shiny appearance  Salmon pink to red color  Painful  Does not have to blister to be 2nd degree  Usually heal in ~7-21 days .Burn Classifications  2nd degree  Damage extends through the epidermis and involves the dermis.  Not enough to interfere with regeneration of the epithelium  Moist.

nerve endings are destroyed  Pain is due to intermixing of 2nd degree  May be minor bleeding  Cannot heal and require grafting .Burn Classifications  3rd degree  Both epidermis and dermis are destroyed with burning into SC fat  Thick. dry appearance  Pearly gray or charred black color  Painless .

Burn Injuries  Often it is not possible to predict the exact depth of a burn in the acute phase. Some 2nd degree burns will convert to 3rd when infection sets in. . When in doubt call it 3rd degree.

Body Surface Area Estimation  Rule of Nines  Adult  Palm Rule .

subtract 1% from head and add equally to legs  Palm Rule .Body Surface Area Estimation  Rule of Nines  Peds  For each yr over 1 yoa.

38. ARTERIAL DISEASE .

Schwartz principles of surgery. Vasospasm of digital arteries  obliterates the lumen Inhibited blood flow  triphasic color response fingers blanch to a distinct white as blood flow is interrupted cyanosis. Symptoms:  numbness. McGraw-Hill. occurs in susceptible people when exposed to cool temperatures or during emotional stress. Pathophysiology of heart disease. 2004. 5th ed. Lipincott William & Wilkins.  paresthesias. related to local accumulation of desaturated hemoglobin   ruddy color as blood flow resumes Lilly LS. Brunicardi FC. 8th ed. . or  Pain Raynaud's syndrome is used to encompass both the primary & secondary conditions causing Raynaud phenomenon.Arterial Disease  Raynaud phenomenon is a vasospastic disease of the digital arteries. 2011.

or  thermal or vibration injury.   vascular sensitivity to adrenergic  carpal tunnel syndrome. Lipincott William & Wilkins. 2011. Pathophysiology of heart disease.  In patients with connective tissue   vasoconstrictor stimuli diseases/arterial occlusive disease: the (serotonin. Lilly LS.Arterial Disease Raynaud disease:  Raynaud phenomenon:  may appear as a component of other conditions. 5th ed. stimuli.  arterial occlusive disorders. thromboxane. dressing in warm pressure & greater susceptibility to sympathetically mediated clothes. & wearing insulated gloves or vasoconstriction. footwear.  Mechanism:  Causes:  connective tissue diseases   sympathetic discharge in (scleroderma & SLE) response to cold. Predominantly woman ages 20-40 . • Preventing vasospasm with CCB or alpha blocker. & digital vascular lumen is largely endothelin) obliterated by sclerosis or inflammation  lower intraluminal Treatment: • avoiding cold environments.

39. Urine Incontinence .

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perineal pain Urinary retenstion  Clinical Signs :      Radiology : urethrogram Therapy :  Sistostomy  immediate repair Tanagho EA. . 17th ed. Urethral Trauma Anterior Urethral Trauma   Position : Distal from urogenital diagphram Etiology :   Straddle Injury Instrumentation Blood from urethral meatus Hematom. et al.40. Smith’s general urology. 2008. McGraw-Hill.

hematom on pubic region  Pelvic Photo  Urethrogram  Sistostomy  Repair 3-4 days later. 2008.Urethral Trauma Posterior Urethral Trauma   Etiology  Pelvic bone fracture  Blood from meatus  Urinary retention  Pain. Clinical Symptoms  Radiology  Therapy Tanagho EA. . et al. McGraw-Hill. Smith’s general urology. 17th ed.

postviral. Pericardial Disease Etiology of cardiac tamponade:  neoplastic.  Acute hemorrhage into pericardium:  blunt/penetrating chest trauma.  dissecting aortic aneurysm .41.  rupture of the left ventricular free wall following MI. & uremic pericarditis.

the normal situation (left diagram) is exaggerated because both ventricles share a reduced. et al. fixed volume as a result of external compression by the tense pericardial fluid. Pulsus paradoxus may also be manifested by other conditions in which inspiration is exaggerated. Lipincott William & Wilkins. Silbernagl S. including severe asthma & COPD. Lilly LS. 2011. Pathophysiology of disease. . 2006. McGraw-Hill.Pulsus Paradoxus decreased of SBP ≥10 mmHg during inspiration Thorax expansion during inspiration Intrathoracic pressure become more negative In cardiac tamponade. 5th ed. Pathophysiology of heart disease. Color atlas of pathophysiology. 5th ed. Thieme. 2000. 1st ed. Facilitates venous return & right ventricle filling Increase in RV size  diminishes LV filling LV stroke volume & systolic blood pressure decline slightly McPhee SJ.

Cardiac Tamponade Management:  ABC’s with c-spine control as indicated  High Flow oxygen  Cardiac Monitor  Large Bore IV access  Rapid Transport  What patient needs is pericardiocentesis Pericardiosentesis  Using aseptic technique. Insert at least 3‖ needle at the angle of the Xiphoid Cartilage at the 7th rib  Advance needle at 45 degree towards the clavicle while aspirating syringe till blood return is seen Continue to Aspirate till syringe is full then discard blood and attempt again till signs of no more blood   Closely monitor patient due to small about of blood aspirated can cause a rapid change in blood pressure .

42. COMPARTMENT SYNDROME .

 Elevated tissue pressure within a closed fascial space Reduces tissue perfusion .Compartment Syndrome A condition in which increased pressure within a limited space compromises the circulation and function of the tissues within that space.ischemia Results in cell death necrosis   True Orthopaedic Emergency .

 Fx. bleeding disorders  Capillary Permeability. Bandage/Cast  localised external pressure. lying on limb  Closure of fascial defects Compartment Content  Bleeding. vas inj. Ischemia / Trauma / Burns / Exercise / Snake Bite / Drug Injection / IVF optimized by optima .Compartment Syndrome Etiology Compartment Size  tight dressing.

optimized by optima .

optimized by optima .

Compartment Syndrome Etiology       Fractures-closed and open Blunt trauma Temp vascular occlusion Cast/dressing Closure of fascial defects Burns/electrical      Exertional states IV/A-lines Intraosseous IV(infant) Snake bite Arterial injury .

Compartment Syndrome Diagnosis Pain out of proportion Palpably tense compartment Pain with passive stretch Paresthesia/hypoesthesia Paralysis Pulselessness/pallor       .

‖ .Clinical Evaluation ―Pain and the aggravation of pain by passive stretching of the muscles in the compartment in question are the most sensitive (and generally the only) clinical finding before the onset of ischemic dysfunction in the nerves and muscles.

Clinical Evaluation    Pain – most important. Willis &Rorabeck OCNA 1990 . paraesthesia etc. paralysis. pulselessness. Especially pain out of proportion to the injury (child becoming more and more restless /needing more analgesia) Most reliable signs are pain on passive stretching and pain on palpation of the involved compartment Other features like pallor. appear very late and we should not wait for these things.

18 ga. CORR 1975)  . Needle (5-19 mm Hg higher)  transducer  monitor  Catheter  wick  slit Stryker device  Side wick port needle .Compartment Syndrome Pressure Measurements  Infusion  manometer  saline  Arterial line  16  3-way stopcock (Whitesides.

Compartment Syndrome Emergent Treatment      Remove cast or dressing Place at level of heart (DO NOT ELEVATE to optimize perfusion) Alert OR and Anesthesia Bedside procedure Medical treatment .

Surgical Treatment   Fasciotomy remove Casts and tight bandages or loosen any constricting bandages All compartments !!! optimized by optima .