PEMBAHASAN TO1 BATCH 1 2013

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

ILMU PENYAKIT DALAM

1. Komplikasi Kidney Failure

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

2. HIV

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

Pathogenesis of HIV Infection

How HIV Infection Become AIDS

HIV Time Course

http://www.microbiologybytes.com

3. Ikterik

, 40 tahun Kuning seluruh tubuh sejak 2 minggu yll BAB dempul Bilirubin direk , bilirubin indirek normal

Bilirubin direk = conjugated bilirubin Bilirubin indirek = unconjugated bilirubin

Type of Jaundice

Wikipedia

Color Atlas of Pathophysiology

Color Atlas of Pathophysiology

Table of Diagnostic Test

Wikipedia

4. Serologi Hepatitis

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

5. Cirrhosis

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

Color Atlas of Pathophysiology www. wikimed.com

6. Hemostasis

, 61 tahun Perdarahan sejak 2 jam yll setelah cabut gigi Penderita jantung koroner dengan konsumsi aspirin 100mg selama beberapa tahun

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; sta=remain) is the stoppage of bleeding, which is vitally important when blood vessels are damaged. Following an injury to blood vessels several actions may help prevent blood loss, including:

Formation of a clot

Formation of platelet aggregate

Injured blood vessel releases ADP, which attracts platelets (PLT)

PLT comming in contact with exposed collagen release: serotonin, ADP, TXA2, which accelerate vasoconstriction and causes PLT to swell and become more sticky

7. Anemia

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

Anemias are defined based on cell size (MCV) and amount of Hgb (MCH). 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

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

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, 3236 g/dL deficienciesdefective RNA and Decreased Reticulocyte count DNA syntheses destruction of fragile and continuing cell growth without abnormal megaloblastic erythroid division precursor

Erythrogenic precursorslarger 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.org/wiki/Megaloblastic_anemia

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.com/wpcontent/uploads/2009/05/g6pddeficiencyprocess.png

http://en.wikipedia.org/wiki/Glucose-6phosphate_dehydrogenase_deficiency

8. Kelainan Katup Jantung

, 16 tahun Sesak napas saat beraktivitas sejak 3 bulan yll PF: Auskultasi P2 mengeras, 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

 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.

9. Heart Failure

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

Symptoms of heart failure

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 bodys 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

11. Syok Anafilaktik

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

Vasodilatation mucosaoedema

Oedem larynx

Stridor

Brochospasm

Wheezing

12. Acute coronary syndrome

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

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

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

13. Spirometri pada PPOK

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

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), lung recoil decreases (compliance increases) and the midposition of breathing is shifted toward inspiration (barrel chest) raises the functional residual capacity

14. Terapi Asma

Asma sudah 10 tahun

PF : RR 32x/ menit, 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 15 6-10 Oxygen Concentration 2844% 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%

GINA report 2011

15.Hipoaktivitas Kelenjar Adrenal

, 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

16. Sindrom Cushing

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

16. 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).

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

17. Komplikasi Akut DM

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

Acute Effect of Diabetes Mellitus (Diabetic Ketoacidosis)

Effect on Insufficiency of Insulin

18. Terapi Hipertiroid

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

Laboratorium Assesment for Thyroid Function

19. Disorder of Calcium Metabolism

, 35 tahun Pasca tiroidektomi sering mengalami kaku dan kejang

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

19. Disorder of Calcium Metabolism

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

20. Arthritis

Wanita, 30 tahun Nyeri dan bengkak pada sendi metakarpophalang dan interfalang kedua tangan, dan bengkak pada sendi lutut. Dirasakan saat bangun pagi LED 184 mm(), kadar urat serum 6,2 mg/dl

Rheumatoid Arthritis Definition:

Chronic inflammatory Autoimmune disorder, that affect the joints and may cause systemic manifestation

Reumatoid Arthritis
a score of 6 fulfilling the requirements for RA

RA Patophysiology

21. Malaria

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

Malaria Life Cycle

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.microbiol.unimelb.edu.au

22. Dengue Infection

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

Pathophysiology of Dengue Fever

Dengue Infection: Classification

ILMU BEDAH, ANESTESI DAN RADIOLOGI

23. Primary Survey

A. B.

C.

D.

E.

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

optimized by optima

Secondary Survey
Componet: A. History namponade Allergic Medication Past illness Last meals Event B. Physical exam : head to toe C. Every orrifice examination

D. Complete Neurological
examination

E. Special diagnostic tests

optimized by optima

F. Re-evaluation

24. Classification of Wounds

1.

2.

3.

An incised wound that is clean and sutured closed is said to heal by primary intention. Often, because of bacterial contamination or tissue loss, a wound will be left open to heal by granulation tissue formation and contraction; this constitutes healing by secondary intention. Delayed primary closure, or healing by tertiary intention, represents a combination of the first two, consisting of the placement of sutures, allowing the wound to stay open for a few days, and the subsequent closure of the sutures

8th ed Schwartz's

Principles of Surgery

8th ed Schwartz's Principles of Surgery

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): 373381.

<750
<15%

7501500
1530%

15002000
3040%

>2000
>40%

<100
Normal 1420 >30 Normal

>100
Normal 2030 2030 Anxious

>120
Decreased 3040 515 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. 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 1.5 liters of blood

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

S/S of Hemothorax

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

Treatment for Hemothorax

ABCs 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/ ABCs 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/ : ABCs 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

28. 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, and great vessels
optimized by optima

Each time we inhale, the lung collapses further. There is no place for the air to escape..

Each time we inhale, the lung collapses further. There is no place for the air to escape.. 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

ABCs 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

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, artery, vein lie along bottom of rib) Remove Stylette and listen for rush of air Place Flutter valve over catheter Reassess for Improvement

Needle Decompression

29. Ureterolithiasis

Urinary tract stone disease Signs:

Flank pain Irritative voiding symptom Nausea microscopic hematuria

Urinary crystals of calcium oxalate, uric acid, or cystine may occasionally be found upon urinalysis Diagnosis: IVP

optimized by optima

30. 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.

Hirschsprung disease
Frequency

Predilection

approximately 1 per 5000 live births. Sex: 4 times more common in males than females. Age: Nearly all children with Hirschsprung disease are diagnosed during the first 2 years of life. one half are diagnosed before they are aged 1 year. Minority not recognized until later in childhood or adulthood. Mortality/Morbidity: The overall mortality of Hirschsprung enterocolitis is 2530%,.

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)

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, 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

HD-Assosciated enterocolitis

Abdominal distension, explosive diarrhea, vomiting, fever, lethargy, rectal bleeding, or shock The risk is greatest:
before

HD is diagnosed after the definitive pull-through operation. children with Down syndrome

Treatment
Hirschsprung disease

HD-Associated enterocolitis

Surgical removal or bypass of the aganglionic bowel,

Rehydration, intravenous antibiotics and colonic irrigations.

31. Peritonitis
Peritonitis Infection, or rarely some other type of inflammation, of the peritoneum.
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.

Intra-abdominal infections result in 2 major clinical manifestations

Early or diffuse infection results in localized or generalized peritonitis. Late and localized infections produces an intraabdominal abscess.

2 Major Types

Primary: Caused by the spread of an infection from the blood & lymph nodes to the peritoneum. Very rare < 1%
Usually occurs in people who have an accumulation of fluid in their abdomens (ascites). The fluid that accumulates creates a good environment for the growth of bacteria.

Secondary: Caused by the entry of bacteria or enzymes into the peritoneum from the gastrointestinal or biliary tract.
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. Also, it can occur due to an intestine to burst or injury to an internal organ which bleeds into the internal cavity.

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. Surgery is often necessary to remove the source of infection. Antibiotics are prescribed to control the infection & intravenous therapy (IV) is used to restore hydration.

Stomach/duodenum Perforation
Presentation :
abdominal
Pain

pain

on palpation Release pain

rigidity peritonism,

shock Air under diaphragm on X-ray Treatment

antibiotics, repair

resuscitate

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

32. Shock

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

Shock: Definitions

Kumar and Parrillo (1995) - The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury.

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 - 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 - due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload Distributive shock - caused by loss of vasomotor control resulting in arteriolar/venular dilatation and characterized (after fluid resuscitation) by increased cardiac output and decreased SVR

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

DISTRIBUTIVE

Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic
Adrenal

crisis Thyroid storm

Toxic (e.g., nitroprusside, bretylium)

CLINICAL MARKERS OF SHOCK

Brachial systolic blood pressure: <110mmHg

Sinus tachycardia: >90 beats/min

Respiratory rate: <7 or >29 breaths/min Urine Output: <0.5cc/kg/hr Metabolic acidemia: [HCO3]<31mEq/L or base deficit>3mEq/L Hypoxemia: 0-50yr: <90mmHg; 51-70yr: <80mmHg; >71yo<70mmHg; K Cutaneous vasoconstriction vs. Mental Changes: anxiousness, agitation, indifference, lethargy, obtundation
l vasodilation. k j

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

HYPOVOLEMIC SHOCK
Decreased preload->small ventricular end-diastolic volumes -> inadequate cardiac generation of pressure and flow Causes:

bleeding: trauma, GI bleeding, ruptured aneurysms, hemorrhagic pancreatitis

protracted vomiting or diarrhea adrenal insufficiency; diabetes insipidus Dehydration

third spacing: intestinal obstruction, pancreatitis, cirrhosis

Hypovolemic Shock

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

SEPTIC/INFLAMMATORY SHOCK
Mechanism: release of inflammatory mediators leading to

1. Disruption of the microvascular endothelium

2. Cutaneous arteriolar dilation and sequestration of blood in cutaneous venules and small veins
Causes:

1. Anaphylaxis, drug, toxin reactions

2. Trauma: crush injuries, major fractures, major burns. 3. infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis, meningitis, cholangitis, pyelonephritis, necrotic tissue, pancreatitis, wet gangrene, toxic shock syndrome, etc.

Septic/Inflammatory Shock
Signs: Early warm w/ vasodilation, often adequate urine output, febrile, tachypneic. Late-- vasoconstriction, hypotension, oliguria, altered mental status.

Monitor/findings: Earlyhyperglycemia, respiratory alkylosis, hemoconcentration, WBC typically normal or low. Late Leukocytosis, lactic acidosis Very Late Disseminated Intravascular Coagulation & Multi-Organ System Failure.
Tx : ABCs, IVF, Blood cx, ABX, Drainage (ie abscess) pressors.

CARDIOGENIC SHOCK
Mechanism: Intrinsic abnormality of heart -> inability to deliver blood into the vasculature with adequate power
Causes: 1. Cardiomyopathies: myocardial ischemia, myocardial infarction, cardiomyopathy, myocardiditis, myocardial contusion

2. Mechanical: cardiac valvular insufficiency, papillary muscle rupture, septal defects, aortic stenosis
3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrial fibrillation, atrial flutter, ventricular fibrillation) 4. Obstructive disorders: PE, tension peneumothorax, pericardial tamponade, constrictive pericaditis, severe pulmonary hypertension

Cardiogenic Shock

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

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

Neurogenic Shock

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

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, dorsal displacement and angulation, radial displacement and angulation and avulsion of ulnar styloid process

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, loss of perianal sensation, paralysis of the bladder, and weakness of the anal sphincter Surgical intervention in these cases is urgent

Spondylolisthesis

Gradation of spondylolisthesis

Meyerdings 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)

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, with or without leg pain, may be present Other possible symptoms Tired legs, dysthesias, anesthesias Partial pain relief by leaning forward or sitting

Spondylolisthesis

Diagnosis

Plain radiographs CT, in some cases with leg symptoms Rest NSAID medication Physical therapy Steroid injections

Nonoperative Care

Spondylolisthesis

Surgical care

Failure of nonoperative treatment Decompression and fusion

Instrumented Posterior approach With interbody fusion

Spondylolysis

Spondylolysis

Also known as pars defect Also known as pars fracture With or without spondylolisthesis A fracture or defect in the vertebra, usually in the posterior elementsmost frequently in the pars interarticularis

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

Spondylolysis

Diagnosis

Plain oblique radiographs CT, in some cases Limit athletic activities Physical therapy

Nonoperative care

Most fractures heal without other medical intervention

Spondylolysis

Surgical care
Failure

of nonoperative treatment Posterior fusion

Instrumented
May

require decompression

Ankylosing spondilitis

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35. ABDOMINAL INJURIES

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 and Solid Organs

The type of injury will depend on whether the organ injured is solid or hollow.

hollow organs include: stomach intestines gallbladder bladder

solid organs include: liver spleen kidneys

Abdominal Injuries
Hollow Organ Injuries

Solid Organ Injuries

when hollow organs rupture, their highly irritating and infectious contents spill into the peritoneal cavity, 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, the symptoms of shock may overshadow those from peritonitis

Abdominal Injuries

Abdominal injuries can be obvious, such as an open wound, or subtle, such as a blow to the flank that initially causes little pain, 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

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. Avulsion of pedicle is fatal

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, flank, or upper left abdomen

Kehrs sign
Left

upper quadrant pain radiates to left shoulder Common complaint with splenic injury

Management : Resuscitation. Laparotomy (repair, partial excision or splenectomy) Observation in hospital for patients with sub-capsular haematoma

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

Stomach/duodenum
Perforation

Bleeding

Presentation :
abdominal pain rigidity peritonism, 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

36. ILEUS

Introduction and Definitions

Accounts for 5% of all acute surgical admissions Patients are often extremely ill requiring prompt assessment, 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. Paralytic Ileus is a paralytic or functional variety of obstruction
Obstruction is: Partial or complete Simple or strangulated

Pathophysiology I

8L of isotonic fluid received by the small intestines (saliva, stomach, duodenum, 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, Methane & CO2), 600 ml of flatus is released Enteric bacteria consist of coliforms, anaerobes and strep.faecalis. Normal intestinal mucosa has a significant immune role
Distension results from gas and/ or fluid and can exert hydrostatic pressure. 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, septaecemia and toxaemia.

Pathophysiology II
Obstruction results in:
1.
2. 3. 4. 5. 6. 7. 8.

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 3,4,5 result in hypovolaemia and electrolyte imbalance Further: localised anoxia, mucosal depletion necrosis and perforation and peritonitis. Bacterial over growth with translocation of bacteria and its toxins causing bacteraemia and septicaemia.

Decompress with NGT Replace lost fluid Correct electrolyte abnormalities Recognise strangulation and perforation Systemic antibiotics.

1. History
The Universal Features
Colicky abdominal pain, vomiting, constipation (absolute), abdominal distension. Complete HX ( PMH, PSH, ROS, Medication, 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

Causes- Small Bowel

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

Congenital adhesions
Hernia Volvulus

2. Examination
General Vital signs: P, BP, RR, T, Sat dehydration Anaemia, jaundice, LN Assessment of vomitus if possible Full lung and heart examination Abdominal
Abdominal distension and its pattern Hernial orifices Visible peristalsis Cecal distension Tenderness, guarding and rebound Organomegaly Bowel sounds
High pitched Absent

Others
Systemic examination If deemed necessary. CNS Vascular Gynaecological muscuoloskeltal

Rectal examination

Initial Management in the ER

Resuscitate:

Air way (O2 60-100%) Insert 2 lines if necessary IVF : Crytloids at least 120 ml/h. (determined by estimated fluid loss and cardiac function). Add K+ at 1mmmol/kg

Draw blood for lab investigations Inform a senior member in the team. 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.

Indications for Surgery

Immediate intervention: Evidence of strangulation (hernia.etc) Signs of peritonitis resulting from perforation or ischemia

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, tricyclic antidepressants

Clinical Findings
Clinical features

Is there an under lying cause? Is the abdomen distended but tenderness is not marked. Is the bowel sounds diffusely hypoactive.

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.

Does the patient improve on conservative measures

37. BURN INJURY

Burn Injuries

Potential complications Fluid and Electrolyte loss Hypovolemia Hypothermia, Infection, Acidosis catecholamine release, vasoconstriction Renal or hepatic failure Formation of eschar Complications of circumferential burn

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

Burn Classifications

1st degree (Superficial burn)

Involves the epidermis Characterized by reddening Tenderness and Pain Increased warmth Edema may occur, but no blistering Burn blanches under pressure Example - sunburn Usually heal in ~ 7 days

Burn Classifications

2nd degree Damage extends through the epidermis and involves the dermis. Not enough to interfere with regeneration of the epithelium Moist, 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

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

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

Body Surface Area Estimation

Rule of Nines
Peds
For

each yr over 1 yoa, subtract 1% from head and add equally to legs

Palm Rule

38. ARTERIAL DISEASE

Arterial Disease

Raynaud phenomenon is a vasospastic disease of the digital arteries; occurs in susceptible people when exposed to cool temperatures or during emotional stress. Symptoms: numbness, paresthesias, or Pain Raynaud's syndrome is used to encompass both the primary & secondary conditions causing Raynaud phenomenon.

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, related to local accumulation of desaturated hemoglobin

ruddy color as blood flow resumes

Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011. Brunicardi FC. Schwartz principles of surgery. 8th ed. McGraw-Hill; 2004.

Arterial Disease
Raynaud disease:

Raynaud phenomenon:

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

39. Urine Incontinence

40. Urethral Trauma

Anterior Urethral Trauma

Position : Distal from urogenital diagphram Etiology :

Straddle Injury Instrumentation Blood from urethral meatus Hematom, perineal pain Urinary retenstion

Clinical Signs :

Radiology : urethrogram Therapy : Sistostomy

immediate repair
Tanagho EA, et al. Smiths general urology. 17th ed. McGraw-Hill; 2008.

Urethral Trauma
Posterior Urethral Trauma

Etiology

Pelvic bone fracture Blood from meatus Urinary retention Pain, hematom on pubic region Pelvic Photo Urethrogram Sistostomy Repair 3-4 days later.

Clinical Symptoms

Radiology

Therapy

Tanagho EA, et al. Smiths general urology. 17th ed. McGraw-Hill; 2008.

41. Pericardial Disease

Etiology of cardiac tamponade: neoplastic, postviral, & uremic pericarditis.

Acute hemorrhage into pericardium: blunt/penetrating chest trauma, rupture of the left ventricular free wall following MI, dissecting aortic aneurysm

Pulsus Paradoxus
decreased of SBP 10 mmHg during inspiration
Thorax expansion during inspiration

Intrathoracic pressure become more negative

In cardiac tamponade, the normal situation (left diagram) is exaggerated because both ventricles share a reduced, 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, including severe asthma & COPD.

Facilitates venous return & right ventricle filling

Increase in RV size diminishes LV filling

LV stroke volume & systolic blood pressure decline slightly

McPhee SJ, et al. Pathophysiology of disease. 5th ed. McGraw-Hill; 2006. Silbernagl S. Color atlas of pathophysiology. 1st ed. Thieme; 2000. Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

Cardiac Tamponade
Management: ABCs 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

Compartment Syndrome
A condition in which increased pressure within a limited space compromises the circulation and function of the tissues within that space.

Elevated tissue pressure within a closed fascial space Reduces tissue perfusion - ischemia Results in cell death necrosis

True Orthopaedic Emergency

Compartment Syndrome Etiology

Compartment Size
tight

dressing; Bandage/Cast localised external pressure; lying on limb Closure of fascial defects

Compartment Content
Bleeding;

Fx, vas inj, bleeding disorders Capillary Permeability;

Ischemia / Trauma / Burns / Exercise / Snake Bite / Drug Injection / IVF

optimized by optima

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. 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, pulselessness, paralysis, paraesthesia etc. appear very late and we should not wait for these things.

Willis &Rorabeck OCNA 1990

Compartment Syndrome
Pressure Measurements

Infusion
manometer saline

Arterial line
16

3-way

stopcock (Whitesides, CORR 1975)

- 18 ga. Needle (5-19 mm Hg higher) transducer monitor

Catheter
wick slit

Stryker device
Side

wick

port needle

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 !!!

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