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ILMU PENYAKIT DALAM

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JenisPemeriksaan NilaiNormal Deskripsi

BloodUreaNitrogen(BUN) 7-25mg/dL Ureadihasilkandarimetabolismeprotein,difiltrasidiglomerulus.Jika

GFRureadireabsorbsi,kembali

kealirandarah

Kreatinin 0,6-1,5mg/dL Produkpemecahankeatininfosfatdari

ototrangka

Glukosasewaktu 65-110mg/dL

1. Komplikasi Kidney Failure

Pasien♂, 48 tahun

Sulit BAK

Kaki bengkak

Mual muntahRiwayat kencing batu

Kadar ureum 115, kreatinin 5,8, glukosa 168

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Uremia Symptoms

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Chronic renal failure

Elevated concentration of urea nitrogen

Bacteria produce urease to disintegrateurea high-concentration nitrogen

Stimulate gastrointestinal mucous

membrane

Nausea & vomiting

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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 = 16,2Underweight). Luka-luka kecil yang menggaungyang pada awalnya terlihat seperti jerawat.

Lab : CD4 575

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Pathogenesis of HIVInfection

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How HIVInfection

Become

AIDS

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HIV Time Course

http://www.microbiologybytes.com

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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

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Type of Jaundice

Wikipedia

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Color Atlas of Pathophysiology

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Color Atlas of Pathophysiology

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Table of Diagnostic Test

Wikipedia

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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

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5. Cirrhosis

♂, 39 tahun

Riwayat peminum alkohol

PF: tampak tidur lelap, kurus, spider nevi (+) didinding perut, terdapat bercak darah pada bibirdan bau amandel, ransang nyeri (-)

Lab : ammonia darah meningkat

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Color Atlas of Pathophysiologywww. wikimed.com

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6. Hemostasis

♀, 61 tahun

Perdarahan sejak 2 jam yll setelah cabut gigi

Penderita jantung koroner dengan konsumsi aspirin

100mg selama beberapa tahun

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Aspirin has anantiplatelet effect byinhibiting the productionof thromboxane, whichunder normalcircumstancesbinds platelet molecules

together to create apatch over damagedwalls of blood vessels

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Hemostasis („hemo”=blood; sta=„remain”) is the

stoppage of bleeding, which is vitally important whenblood vessels are damaged.

Following an injury to blood vessels several actions

may help prevent blood loss, including:

Formation of a clot

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Formation ofplatelet aggregate

Injured blood vesselreleases ADP, whichattracts platelets (PLT)

PLT comming in contactwith exposed collagenrelease: serotonin, ADP,TXA2, which accelerate

vasoconstriction andcauses PLT to swell andbecome more sticky

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7. Anemia

♂, 40 tahun

Badan lemas, tidak

nafsu makan, demam(-)

Lab : WBC: 4000gr/dl, Hb: 8 gr/dl, Ht34% MCV: 114 fl.Gambaran darah tepi:netrofil hipersegmen,

makroovalosit

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Anemias are defined based on cell size (MCV) andamount 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: normochromicanemia

• MCH greater than upper limit of normal:hyperchromic anemia

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A N E M I A

Perniciousanemia (megaloblastic

anemia due to vitamin B12

deficiency)

Anemia of folic aciddeficiency (megaloblastic

anemia)

Anemia of prematurity(premature infants at 2 to 6

weeks of age)

Iron deficiency anemia(deficiency of heme

synthesis)

Thalassemia(deficiencyof globin synthesis)

Congenitaldyserythropoietic anemias

Anemia of renal failure

Disturbance of proliferationand differentiation of stem

cells

Disturbance of proliferation

and maturationof erythroblast

Intrinsic

Extrinsic

Impaired RBC production

Increased RBC destruction(hemolytic anemias)

Blood loss

Fluid overload

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MEGALOBLASTIC

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• MCV >95 fl

• Normal MCHC, 32 – 36 g/dL

destruction of fragile andabnormal megaloblastic erythroid

precursor

MEGALOBLASTICANEMIA

Anemia (of macrocytic classification) Laboratorium Findings:that results from inhibition of DNA • Decreased red blood cell (RBC) countsynthesis in red blood cell production and hemoglobin levels[

Pathopgenesis• Increased MCH

Folate and vitamin B12deficienciesdefective RNA and • Decreased Reticulocyte countDNA syntheses

continuing cell growth without

division

Erythrogenic precursorslarger • Blood smear:• hypersegmented neutrophils• macroovalocytesmacrocytes with oval

shape RBC• Anisocytosis (increased variation in RBC

size) and poikilocytosis (abnormallyshaped RBCs).

than mature red blood cells(RBCs)

http://emedicine.medscape.com/article/http://en.wikipedia.org/wiki/Megaloblastic_anemia

Gl 6 h h t

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Glucose-6-phosphate

dehydrogenase deficiency

an X-linked recessive hereditary diseasecharacterised by abnormally low levels of glucose-6-phosphate dehydrogenase

Blood smear: Heinz body in RBC

http://www.diseaseaday.com/wp-content/uploads/2009/05/g6pddeficiencyprocess.png

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

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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) associatedwith mitral stenosis; sound due to abrupt

deceleration of mitral leaflets sound with

associated murmur

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•

Loud P2 (pulmonic) component of the(S2) pulmonary hypertensionsecondary to severe mitral stenosis

• An opening snap heard after the A2(aortic) component of the (S2)

• correlates to the forceful openingof the mitral valve

• The mitral valve opens when thepressure in the left atrium is

greater than the pressure in the

left ventricle

• This happens in ventriculardiastole (after closure of theaortic valve), when the pressure

in the ventricle precipitouslydrops

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Pathophysiology of

Mitral Stenosis

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The sounds waves

responsible for heart soundsare generated by vibrationsinduced by:

valve closure,

abnormal valve opening, vibrations in the

ventricular chambers,

tensing of the chordae

tendineae, turbulent or abnormal

blood flow across valvesor between cardiacchambers

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• closure of theaortic andpulmonic valvesat the beginningof isovolumetricventricular

relaxation

• When audible, iscaused byvibration of theventricular wallduring atrial

contraction• Usuallyassociated witha stiffenedventricle.

• closure of themitral andtricuspid valvesat the beginningof isovolumetricventricularcontraction

• When audible,occurs early inventricular filling

• may representtensing of thechordaetendineae andthe AV ring,which is theconnective tissuesupporting theAV valve leaflet

Murmur:Abnormalmovement ofblood acrossvalves andbetween

cardiacchambersDivided into:-ventricularcontraction(systole)

-ventricularfilling(diastole)

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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

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Symptoms of heart failure

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

• Diastoleprocess by which

the heart returns to itsrelaxed state• the cardiac muscle is

perfused.• Diastolic dysfunction

• the heart is able to meetthe body‘s metabolicneeds,at a higher filling

pressure•

Transmission of higherend-diastolic pressure tothe pulmonary circulationpulmonary congestion

dyspnearight-sided

heart failure.

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10. Anti Hipertensi

Nyeri kepala hilang timbul selama 1 minggu, mualmuntah, riwayat hipertensi selama 10 tahun

PF : TD 180/110, GDS 375 dan proteinuria +1

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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

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Vasodilatation

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Vasodilatationmucosaoedema

Oedem

larynx

Stridor

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Brochospasm Wheezing

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12. Acute coronary syndrome

Keluhan 1 jam yang lalu nyeri dada seperti ditindihbeban berat

EKG irama sinus , ST Elevasi V1-V4, denyut jantung

72x/menit, peningkatan enzim jantung serial

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http://ceaccp.oxfordjournals.org/content/4/6/175.full

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Left coronary artery

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y ymensuplai area:

Anterior LVThe bulk of the

interventricular septum(anterior two thirds)The apex

Lateral and posterior LVwalls

Right coronary arterymensuplai area:

Right ventricle (RV)The posterior third of theinterventricular septum

The inferior wall(diaphragmatic surface) ofthe left ventricle (LV)A portion of the posteriorwall of the LV (by means ofthe posterior descendingbranch)

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EKG

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

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13. Spirometri pada PPOK

♂, 68 tahun

Sesak nafas + batuk sejak 3 minggu, dahak kentalkuning sampai kecoklatan. Riwayat batuk darah

disangkal. Perokok berat sejak usia 17thPF : hemithorax cembung dan perkusi hipersonor dikedua lapang paru

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Obstructive lung disease reduced ventilation the ratio of the

duration of expiration to that of inspiration is increased obstructedexpiration distends the alveolar ductules (centrilobular emphysema), lungrecoil decreases (compliance increases) and the midposition of breathingis shifted toward inspiration (barrel chest) raises the functional residual

capacity

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14. Terapi Asma

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p Asma sudah 10 tahun

PF : RR 32x/ menit, FN 110x/ menit

GINA Report 2011

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MANAGEMENTIN STABLE

CONDITION

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Pathophysiology of

Asthma

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http://www.eguidelines.co.uk

Algorithm

of

Asthma

Diagnosis

T i Ok i

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Devices FlowRate

(L/min

Oxygen

Concentration

Description

NasalCannula 1 – 5 28 – 44%

Rebreathing

Mask/Simple

OxygenMask

6-10 35-60% -Firstthirdofexhaledgasesmixwith

reservoir

-Exhaledgasesfromupperairwayareoxygenrich

NonRebreathing

Mask

10-12 95% Twovalvesaddedtoprevents:

-Entrainmentofroomairduring

inspiration

-Retentionofexhaledgasesduringexpiration

VenturiMask 4-8 25-60%

Ventilator canbeset 21-100%

Terapi Oksigen

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GINA report 2011

15 Hi kti it K l j Ad l

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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 hitamPF : TD 80/50, nadi 72, tidak ada penyakit jantung

Ad l I ffi i

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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 glandsbefore adrenal insufficiency appears

The adrenal is a frequent site for chronic granulomatous

diseases, predominantly tuberculosis(70%-90% cases),

but also histoplasmosis, coccidioidomycosis, andcryptococcosis

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Effects and

Symptoms ofAdrenocortical

Hormone

Deficiency

16 Sindrom Cushing

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16. Sindrom Cushing

♀, 25 tahun

Kenaikan BB 10 kg dalam dua bulan. asupanmakan tidak banyak bertambah meski cepat lapar.

Riwayat alergi makanan membeli sendiri obatalergi atau jamu-jamuan.

PF:TB 158 cm, BB 65 kg (IMT = 26 Overweight),

TD 140/90 mmHg Hipertensi, FN 80x/menit, RR18 x/menit dan suhu 36,5 C

16. Sindrom CushingCushing's syndrome

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Cushing s syndrome

(hyperadrenocorticalism/hypercortisolism)

The clinical condition resulting from chronic exposureto excessive circulating levels of glucocorticoids

The most common cause: excess ACTH secretion fromthe 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

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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, tensi90/60 mmHg, nadi 110x/menit, nafas kussmaul,lidah kering, turgor kulit menurun

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Acute Effect of Diabetes

Mellitus

(Diabetic Ketoacidosis)

Effect on Insufficiency of Insulin

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Effect on Insufficiency of Insulin

18 Terapi Hipertiroid

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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

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Laboratorium Assesment for Thyroid Function

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Laboratorium Assesment for Thyroid Function

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19 Disorder of Calcium Metabolism

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19. Disorder of Calcium Metabolism

♀, 35 tahun

Pasca tiroidektomi sering mengalami kaku dankejang


McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5thed. McGraw-Hill; 2006.

19. Disorder of

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McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5th

ed. McGraw-Hill; 2006.

Calcium Metabolism

20 Arthritis

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20. Arthritis

Wanita, 30 tahun

Nyeri dan bengkak pada sendi metakarpophalangdan interfalang kedua tangan, dan bengkak pada

sendi lutut. Dirasakan saat bangun pagiLED 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

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Reumatoid Arthritis

a score of 6 fulfilling the requirements for RA

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21 Malaria

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21. Malaria

♂, 25 tahun

Penurunan kesadaran±2 jam yll, riwayat demamhilang timbul, demam tinggi, menggigil dan

keringat dinginPF: TD 100/70 mmHg, S 38,5oC, kulit tampakpucat, konjungtiva anemis.

Lab : ditemukan plasmodium sausage shape

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Malaria Life Cycle

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Malaria Life Cycle

Pathogenesis of Cerebral Malaria

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http://www.microbiol.unimelb.edu.au

Pathogenesis of Cerebral Malaria

• Possible cause:• Binding of

parasitized red cells

in cerebralcapillaries

• permeability of the

blood brain barrier

• Excessive induction

ofcytokines

22. Dengue Infection

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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 38,3°

C, Nadi98x/menit. Konjungtiva pucat (-). Thoraks: BJ I-IInormal, vesikuler. Abdomen : nyeri tekanepigastrium (+). Ext : petechiae pada lengan atas

kanan dan kiri.Lab: Hb 12 g/dL, hematokrit 36%, Leukosit 4700,Trombosit 98000

Pathophysiology of Dengue Fever

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Pathophysiology of Dengue Fever

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Dengue Infection: Classification

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g

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ILMU BEDAH, ANESTESIDAN RADIOLOGI

23 Primary Survey

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A.

B.

C.

23. Primary Survey

AirwayEstablish patent airway

Breathing

Assess and ensure adequate oxygenation and ventilation

Circulation

•

•

•

Level of consciousnessSkin color and temperature

Pulse rate and character

D.

E.

Disability

Baseline neurologic evaluation

GCS scoringPupillary response

Environment

Completely undress the patient

• Control hemorrhage• Restore volume• Reassess parameters

ATLS

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optimized by optima

Secondary Survey

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F. Re-evaluation

Secondary Survey

optimized by optima

Componet:

A. History namponade

Allergic Medication Past illness

Last meals

Event

B. Physical exam : head to toe

C. Every orrifice examination

D. Complete Neurologicalexamination

E. Special diagnostic tests

24. Classification of Wounds

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1.

2.

3.

An incised wound that is clean and sutured closed is said toheal by primary intention.

Often, because of bacterial contamination or tissue loss, awound will be left open to heal by granulation tissue

formation and contraction; this constitutes healing bysecondary 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 afew days, and the subsequent closure of the sutures

8th ed Schwartz's Principles of Surgery

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8th ed Schwartz's Principlesof Surgery

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25. ShockDefinition• A physiologic state

characterized by – Inadequate tissue

perfusion

• Clinically manifested by

– Hemodynamicdisturbances

– Organ dysfunction

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optimized by optima

Hypovolemic Shock

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Parameter I II III IV

Bloodloss(ml) <750 750 – 1500 1500 – 2000 >2000

Bloodloss(%) <15% 15 – 30% 30 – 40% >40%

Pulserate(beats/min)

<100 >100 >120 >140

Bloodpressure Normal Normal Decreased Decreased

Respiratoryrate

(bpm) 14 – 20 20 – 30 30 – 40 >35

Urineoutput

(ml/hour) >30 20 – 30 5 – 15 Negligible

CNSsymptoms Normal Anxious Confused Lethargic

Hypovolemic Shock

Hemorrhagic Shock

optimized by optimaCrit Care. 2004; 8(5): 373 – 381.

6. WHO Pain Management Stepladder

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optimized by optima

Mekanisme kerja nsaid

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j

optimized by optima

Mekanisme kerja opioid

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j p

optimized by optima

27. Hemothorax

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Occurs when pleural space fills with blood

Usually occurs due to lacerated blood vessel inthorax

As blood increases, it puts pressure on heart andother vessels in chest cavity

Each Lung can hold 1.5 liters of blood

27-28 CHEST TRAUMA

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optimized by optima

Hemothorax

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Hemothorax

Hemothorax

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May put pressure on the heart

Hemothorax

Where does the blood come from.

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Lots of blood vessels

Where does the blood come from.

S/S of Hemothorax

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Anxiety/Restlessness

Tachypnea

Signs of Shock

Frothy, Bloody SputumDiminished Breath Sounds on Affected Side

Tachycardia

Flat Neck Veins

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BLS Plus Care

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Monitor Cardiac Rhythm

Establish Large Bore IV preferably 2 and drawblood samples

Airway management to include IntubationRapid Transport

If Development of Hemo/Pneumothorax needle

decompression may be indicated

Simple/Closed Pneumothorax

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Opening in lung tissue that

leaks air into chest cavity

Blunt trauma is main cause

May be spontaneous

Usually self correcting


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S/S :

Chest Pain

Dyspnea

Tachypnea Decreased Breath

Sounds on Affected

Side

Th/ABC‘s with C-spine controlAirway Assistance asneeded

If not contraindicatedtransport in semi-sittingpositionProvide supportive careContact Hospital and/or

ALS unit as soon as possible

Open Pneumothorax

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Open Pneumothorax

Opening in chest cavitythat allows air to enterpleural cavity

Causes the lung to

collapse due toincreased pressure inpleural cavity

Can be life threatening

and can deterioraterapidly

Open Pneumothorax

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Inhale

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Exhale

Open Pneumothoraxoptimized by optima

Inhale

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Inhale

Exhale

Open Pneumothorax

Inhale

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Inhale

Exhale

Open Pneumothorax

Open Pneumothorax

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S/S : Dyspnea

Sudden sharp pain

SubcutaneousEmphysema

Decreased lung soundson affected side

Red Bubbles onExhalation from wound(Sucking chest wound)

Th/ :ABC‘s with c-spine controlas indicatedHigh Flow oxygenListen for decreased

breath sounds on affectedsideApply occlusive dressingto woundNotify Hospital and ALS

unit as soon as possible

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Sucking Chest Wound Occlusive Dressing

28. Tension Pneumothorax

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Air builds in pleuralspace with no wherefor the air to escape

Results in collapse oflung on affected sidethat results in pressureon mediastium,the

other lung, and greatvessels

optimized by optima

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

Each time we inhale,

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the lung collapses further. Thereis no place for the air to

escape..

Heart is beingcompressed

The trachea ispushed to

the good side

S/S of Tension Pneumothorax

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Anxiety/Restlessness

Severe Dyspnea

Absent Breath sounds

on affected sideTachypnea

Tachycardia

Poor Color

Accessory Muscle Use

JVD

Narrowing Pulse

Pressures Hypotension

Tracheal Deviation

(late if seen at all)

Treatment of Tension Pneumothorax

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ABC‘s with c-spine as indicated

Needle Decompression of Affected Side

High Flow oxygen including BVM

Treat for S/S of ShockNotify Hospital and ALS unit as soon as possible

If Open Pneumothorax and occlusive dressing

present BURP occlusive dressing

Needle Decompression

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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 liealong bottom of rib)

Remove Stylette and listen for rush of air

Place Flutter valve over catheter

Reassess for Improvement

Needle Decompression

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30. Hirschsprung disease

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Congenital megacolon

the absence of myentericand submucosal ganglion

cells in the distal

alimentary tract

decreased motility in theaffected bowel segment

Results from the absence ofparasympathetic ganglion

cells in the myenteric andsubmucosal plexus of therectum and/or colon.

These ganglion cells arrive inthe proximal colon by 8

weeks of gestational ageand in the rectum by 12weeks of gestational age.

Arrest in migration leads toan aganglionic segment.

Definitions Pathophysiology

Hirschsprung disease

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approximately 1 per 5000 livebirths.

Sex: 4 times more common inmales than females.

Age:

Nearly all children withHirschsprung disease arediagnosed during the first 2years of life.

one half are diagnosed beforethey are aged 1 year.

Minority not recognized untillater in childhood or adulthood.

Mortality/Morbidity:

The overall mortality of

Hirschsprung enterocolitis is 25-30%,.

Classical HD (75% of cases):Rectosegmoid

Long segment HD (20% ofcases)

Total colonic aganglionosis (3-

12% of cases)rare variants include thefollowing:

Total intestinal aganglionosis

Ultra-short-segment HD

(involving the distal rectumbelow the pelvic floor and theanus)

Frequency Predilection

Clinical presentation

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Newborns :

Failure to pass meconium withinthe first 48 hours of life

Abdominal distension that isrelieved by rectal stimulation orenemas

Vomiting

Neonatal enterocolitisSymptoms in older children andadults include the following: Severe constipation Abdominal distension Bilious vomiting

Failure to thrive

Rontgen :

Plain abdominal radiography Dilated bowel

Air-fluid levels.

Empty rectum

Contrast enema Transition zone

Abnormal, irregular contractions ofaganglionic segment

Delayed evacuation of barium

Biopsy : absence of ganglion cells hypertrophy and hyperplasia of

nerve fibers,

HD-Assosciated enterocolitis

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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

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Surgical removal orbypass of theaganglionic bowel,

Rehydration,intravenous antibioticsand colonic irrigations.

Hirschsprung disease HD-Associated enterocolitis

31. Peritonitis

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PeritonitisInfection, 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

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Early or diffuse infection results in localized orgeneralized peritonitis.

Late and localized infections produces an intra-abdominal abscess.

2 Major Types

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Primary: Caused by thespread of an infection fromthe blood & lymph nodes tothe peritoneum. Very rare <1%

Usually occurs in people whohave an accumulation of fluidin their abdomens (ascites).

The fluid that accumulates

creates a good environmentfor the growth of bacteria.

Secondary: Caused by theentry of bacteria or enzymesinto the peritoneum from thegastrointestinal or biliary tract.

This can be caused due to anulcer eating its way throughstomach wall or intestinewhen there is a rupture of theappendix or a ruptureddiverticulum.

Also, it can occur due to anintestine to burst or injury to

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