RS*T Hebring

Cerita lagi yuuk....

Kali ini tentang seputar kehidupan praktikan di RSUP Soer*dj* T*rtoneg*ro (hehe, sensor.... teeeet). Rumah Sakit terhebat yang pernah kutemui (iyalah, secara baru praktek 3x). Tapi tetep aja habat. Sekali hebat tetep hebat.... MERDEKA...... lhoh...... -.-a

Kisahku dan kawan-kawan dimulai pas hari minggu sore, tanggal berapa aku lupa (penyakitnya lupa yang kumatan. Ampun dahh). Eh eh... sik sik... tapi seminggu sebelum hari minggu itu aku duluan yang memulai ceritanya. Diawali dari ekspedisi pencarian rumah kost. Dapet di depan RS pas (tapi mahal boo), akhirnya batal. Truz cari di belakang RS. Hii, ternyata ngeriiii. Tak bayangin kalo bener-bener kost di belakang RS yang gak usah pake nyebrang jalan sol-ja (solo-jogja.red), mau pulang aja musti lewat ruang jenazah, abiz itu lewat sawah-sawah, kuburan, baru dah nyampe kost. Ya ampuuuunnn, emooooh.....

Dan jadilah saia dapet kos di desa seberang. Alias ndadak nyebrang jalan sol-ja. Tapi yaudah lah mumpung murah. Dapet kamar VIP pula (haha, belom tau aja ada apa didalamnya).

Nahh, minggu sore mulai pindahan. Hadeeh, benar-benar terdampar saia. Inget waktu praktek di Banyudono aja perjuangannya setengah mati, direwangi nangis pula gara-gara kangen mama (hehehehe, buka aib sendirii ^^,). Nah ini jauh bangett dari rumah. Bisa sih pulang, jalannya tinggal lurus aja. Tapi lurusnya itu yang bikin males, gak ada seninya... wkwkwkwk.

Malam pertama menempati kost VIP. Melihat keadaan kost yang bervasilitas lengkap dengan kamar mandi didalamnya, huftt.. kayaknya bakalan betah dahh :D

Tak kenalin penghuni kost ini yahh. Kami sekamar bertiga. Ada aku (anak mama yang simple dan tidak ribet), ana (ternyata anak mama juga nih, tetep overload barang bawaan) sama niken (yang gak bisa pisah sama radio jadulnya. Haha, maap ken saia mencantumkan radiomu di note ini). Kalo bertiga ini ngumpul udah kebayang gimana ributnya suasana kamar.

Omegott, malam pertama saia mimpi buruk uey.... kalo kata ibuk sih aku masuk kost pertama belum salam. Haha... tapi namanya mimpi kan datang tak diundang. Adaada saja ah....
Truz juga pas malem ke berapa gitu (lupa), tengah malem aku liat niken sama ana tukeran tempat tidur. Pas paginya tak liat udah tukeran lagi. Tapi katanya mereka gak tukeran tuhh. Nah lohhh, siapa yang mindahin kaliannnnn?????hiiiiii.......

Kesan pertama masuk RSUP Soer*dj* T*rtoneg*ro, horor...... bangunan tua tuh, peninggalan belanda kali. Kalo pas malem suasananya kayak gimana yha?? Embuh lah... tapi kayaknya asik. Hehe...

Okee.... my 1st ward, Dahlia. Sekelompok sama Eri plus Niken (hadeee, jodoh nih kita) :P

Disana ada pak Agung dengan kumis tebalnya (hehe), truz pak Sardjiman yang akrab dipanggil pak Ardji (CI-ku ituhhh). Ada juga mbak Vero yang cantikk dan kalo rodok galak malah bikin ngakak. Mbak Nunung (lucu nih mbaknya), mz Fajar yang pintar ber-jantung ria, mz Zaii yang ternyata kakaknya temen kostku di soloo (lagek nyadar pas udah keluar. Payahh). Ada mz Yudii yang gokill dan ibuk ibuk perawat yang aku lupa namanya. Hehe....

Bayanganku kalo aku dapet CI pasti kayak biasanya, agak susah diajak kompromi. Tapi ini enggak..... malah aku seneng bangett tiap hari dibimbing, diarahkan, dikasih masukan, diajarin cara ngaskep yang bener, responsi juga santai (biasanya kalo udah madep CI sama LP bawaannya parno mulu. Tapi ini beda).

Beruntung aku dapet CI yang mau meluangkan waktu buat mahasiswa praktikannya. Walopun cuma setengah jam, pasti bimbingan di ruang konverensi.

Nah yang menarik dari responsi ala Dahlia adalah........ aku tanya sebelum ditanya. Gak jadi responsi ini namanya. Malah pak Ardji yang jelasin, kasih pengertian banyaaaaaak banget (hmm, seperti perpustakaan hidup –pikirku-). Tapi okelah, menyenangkan sekaliii. Dan akhirnya saia tidak jadi ditanya. Wkwkwkwkwk...... tapi aku mikirnya kan lebih baik aku tanyain apa yang belum mudheng. Daripada ditanya gak bisa jawab, sekalian aja jujur kalo belum mudheng. Hoho.....

Hari pertama dinas, jujur aku stress. Teoritis banget.... apapun harus sesuai SOP. Dari persiapan alat, APD dan prosedur. Kalo biasanya injeksi gak usah pake perlak pengalas, disini WAJIB. Ngomong soal injeksi jadi inget skin test sm mbak vero. Ada rumusnya nih kalo ngoplos obat. Jadi obat vial itu musti dioplos dulu sama aquabides 5cc. Truz diambil 0,1 cc baru ditambah aquabides lagi 0,9 cc. Hoho.... ribet kan, tapi katanya ini yang bener.

Di Dahlia yang bikin heboh adalah balance cairan. 6 praktikan diajari ngitung balance cairan susah nyangkut di otak. Kalo satu mudheng yang laen belom, dijelasin pake cara lain. Nah yang udah mudheng itu malah jadi mubeng. Haha.... ruwet dahh.... setelah dua hari dinas baru bener-mener mantep sama ‘matematika’ ala Dahlia. (-.-)v

Kasus pertama aku ambil CC. Baru tau ada istilah CC juga pas praktek di Dahlia. Setelah bimbingan baru tau juga kalo CC itu ada 2 jenis, Contusio dan Commotio Cerebri. Intinya.... Cidera Kepala...... ahihihi......

Paling sebell pas dapet setengah pengkajian truz pak Agung datang sambil berkata,”Ririn, i’m sorry... your patient is APS.” Waaaaaaaa........ kapok dah ambil pasien Umum buat askep tugas. Finally ganti kasus Anemia pake embel-embel Grafis. Gara-gara ini juga aku jadi dapet mbah kakung baru. Hehe....

Hmm, anemia grafis? Apa bedanya sama anemia biasa? Ini tak tanyain juga sama pak Ardji. Dijawab gini nih,”setau saya anemia grafis itu adalah anemia yang kadar hemoglobinnya kurang dari 4 mg/dl.” Ooooooo begituuu.....

Abiz itu ditanyain nih sama pak Agung pas laporan pagi, “Rin, what’s anemia grafis?”. Ahihihi...udah dijelasin kemaren. PD nih jawabnya,”anemia which its hemoglobin rate less than 4 mg/dl.” Pak Agung ngangguk2, pak Ardji senyum2. Whaha.... luccuu dah jadinya....

Hari ke-2 pengkajian kasus anemia grafisku, haduh... Hb udah 9,7. Gimana kalo askepku gagal T.T (tapi wotever, seperti ditampar.. diingatkan biar gak melulu mikirin askep. Tujuanku udah nyaris berhasil walopun askepku gagal. Ternyata melihat pasien dan keluarga bahagia atas kemajuan kondisinya ituuu, lebih menyenangkan daripada lengkap di askep tapi pasien gitu-gitu aja kondisinya. Alhamdulillah :D)

Di RSUP Soer*dj* T*rtoneg*ro, aku menemukan tempat favorit. Masjid Baitusy Syafi’i, letaknya di semping bansal Dahlia pass. Kalo abiz balance cairan jam 13.00, pasti langsung ke masjid. Sholatnya di lantai atas. Di sebuah ruangan luas tanpa jendela. Begitu tengok kanan pemandangannya adalah indahnya hamparan sawah luas dan gunung Merapi yang samar tertutup awan dibumbui dengan susana hitam putih jalan aspal yang baru dibangun di kompleks RS. Sepii, adem, damai dan menyenangkan. Huhuuu, aku merindukan tempat itu. Tempat dimana aku bisa merasakan sejuknya air wudhu yang khas, tempat dimana aku bisa menghirup udara persawahan dan pesona alam yang menakjubkan. Betah disana >,<

Ada banyak hal lucu juga nih di Dahlia. Salah satunya tentang mister...... ehm.... yang ini Niken sama Pina paling paham. Hoho... gara-gara jam tangan dan infus jadi runyam urusannya. Gak usah dicritain lah yaaaa, pasti udah pada tau.

Truz pas evaluasi klinik, dapet pasien bapak-bapak. Seharian ngrawat si bapak jadi apal dah. Besoknya......... simak dialog ini........
Bapak : Mbak ini pegawai apa masih sekolah?
Aku : Masih sekolah pak. Hehe... kenapa pak?
Bapak : Kok semangat banget. Padahal gak digaji ya mbak?
Aku : (senyum-senyum) yahh namanya juga masih sekolah pak, harus semangat. Gajinya pahala :D
Bapak : Amiin.. Udah punya pacar belom nih mbaknya?
Aku : hehe, belum pak. Mau cariin yah?
Bapak : Sama anak saya gimana? Kuliah di UNJ jurusan Management.
Aku : (shockkkkkk) hehehehehe..... pengen kuliah dulu aja ding pak. (wkakakakakaka)

Hmm, ini sekilas cerita di Dahlia. Tunggu cerita di Melati IV on RS*T part 2 :D

Hypertension

A. Congeniality
Hypertension is an situation where happened the make-up of blood pressure of sistolik more than 160 mmHg and or blood pressure of diastolik more than 90 mmHg most serikit when is different (Brunner and of Suddarth, 2002).
In general hypertension classified pursuant to value of diastolik.
Light hypertension : 90-100 mmHg
Middle hypertension : 100-114 mmHg
Heavy hypertension : 110-118 mmHg
Hypertension of Maligna > 120 mmHg
Hypertension crisis is natural blood pressure increase which quickly so that cause damage of organ quickly repair only can be got with blood pressure.
According to new classification :
Stage I : 90-98 mmHg
Stage II : 100-108 mmHg
Stage III : 110-118 mmHg
Stage IV > 120 mmHg
Blood pressure determined by 2 primary factor
1. Level of dilution volume filling vein determined by pouring heart
2. Prisoner (venous resistensi) of edge (perifer) to blood stream emiting a stream of.

B. Anatomy Physiology
Heart represent especial organ in functioning blood cyrculation as pump. When bud hence blood pumped to aorta with strong forceps pressure later then blood poured into and artery of arteriole with lighter pressure, this pressure very needed to tired blood entire/all tissue and organ and also can return to heart. Blood pressure vena to artery wall can be measured with expressed tensimeter with set of mmHg.
Difference of blood pressure of sistolik is artery blood pressure when bud heart/ konstriksi. Diastolik is blood pressure when dilatation heart return. Blood pressure influenced by pouring heart, prisoner of perifer from and blood volume.
Control system which play a part in to maintain blood pressure:
1. System of Baroreseptor
2. System arrangement of body dilution volume
3. System of Renin angiotensin
4. System of Autoregulasi vascular
( Barbara Engram, 1999)

C. Patofisiologi
Hypertension represent an disparity/symptom of mechanism trouble of regulasi blood pressure. Body have an system to arrange height of blood pressure that is system of renin aldosteron angiostenin (RAAS). Certain Cells of kidney can form hormone of renin discharged if blood pressure downhill glumerolus. Only happened when amount of blood arranging to through kidney decrease. For example because degradation of blood volume or stricture of kidney artery. In plasma, renin joint forces with to become angiostensin I which by enzyme of ACE (Angiostensi Convertury enzyme) can become angiostensin II.
From other side hormone regulasi still there are some physiology factor able to influence blood pressure, for example
1. Volume Stroke
That is amount of blood pumped out of heart every konstriksi, ever greater of this blood pressure volume excelsior. Salt retention improve dilution volume so that volume mount. Hence pressure of wall small channel of blood is increase.

2. Wall artery Elasticity
Artery which its wall have ossified because cholesterol sediment/fat (artherosclerosis) cause higher blood pressure than wall which still is elastic.
3. Release of neurohormon
For example adrenalain of functioning nerodrenalin narrow vein of perifer so that blood pressure mount. At the time of emotion mount or energetic athletic, nerve system of adrenergik reacted and discharge neurohormon. Situation of Stres and smoke also increase product adrenolin neurohormon (Sandra M Hettina, 2002).

D. Factor Cause of Hypertension
1. Primary Hypertension : unknown cause
2. Sekunder Hypertension because of
a. Disease of kidney perenkim or is kidney vascular
b. Endocrine trouble of diabetes
c. Stricture of congenital aorta
d. Tumor Neurogenik, enoufalitas, singe, increase of volume of intravaskuler and psychiatry trouble.
3. Other Risk factor
a. Obesitas
b. Low intake and high salt
c. Smoker
d. Stres
e. Usage of pill anti pregnancy

E. Sign and Symptom
Sign and symptom of hypertensi, that is
1. Headache
2. Epitaksis
3. Confused of migraine
4. Nokturia
5. Finitus
6. Weakness/ worn-out
7. Queasy of puking
8. Out of breath
9. Difficult to sleep
10. Eye have Firefly
11. Feeling buckling weight
12. Increase of BP from is normal
13. Degradation of hand strength
14. Heart frequency mount
15. Takipnea
16. Change of heart rhythm
(Sandra M Hettina, 2002)

F. Pathway

G. Complication
There are some complication able to happened at hypertension that is
a. Damage of vein, manifestasi emerge according to hit organ system
b. Heart sickness of coroner with angiria
c. Left Ventrikel Hipertrofi
d. Change of kidney fatologis
e. Brain blood/ stroke
f. Serebri Infark
(Brunner and of Suddart, 2002)

H. Diagnostic Inspection
a. Hb/HCL to assess relation between cells of blood viskositas as risk factor of hiperkoagulasi, enemia, etc
b. BUN/ creatinin to know kidney function
c. Glucose, hiperglikemia effect of height of katekolamin will add hypertension
d. System of Potasium. If found the existence of this hipokalamia represent sign of existence of primary aldostenon as side effects of diuretika
e. Calcium serum, if high usually signifikan at hypertension
f. Serum of Trigliserida and cholesterol if high represent factor of predisposisi hypertension
g. Tiroid. Hipertirordisme cause vascular vasokontriksi
h. WP to identify cause of hypertension, do representing disease of kidney parenkim or is kalikulo renal.
(Brunner and of Suddart, 2002)

I. Therapy
a. Program degradation of BB to fat
b. Low salt and lower fat diet
c. Altering ugly habit pursuant to health
d. Regular Athletic
e. Check blood pressure regularly
f. Therapy of Farmakologis
1. Diuretik : HCT, lasix
2. Beta of Blocker : propanaol
3. Alpha of Blocker : phentolamin, vrozqazine (minipres)
4. Simpatolik
5. Vasodilator
6. Calcium of Antagonis
(Barbara Engram, 1999)

J. Assessment
1. Assessment
This study cover patient identity, old age, work, disease history now is, former, and family
In study of Doengoes (1999) covering practice and activity, eliminasi, habit of defecate and urinate, eat and dilution cover habit of consumed food and beverage of fatty food type, high cholesterol have, alcohol, high salt, etcetera. Sensori Neuron : headache symptom, weaken, rest, and sleep, existence of sleepless, habit of sleep, cognate perception, perception of pandemic client while for all important physical examination is vital marking that is blood tension, existence of increase
2. Diagnosa and Intervention Treatment
According to Doengoes (1993) at hypertension client can be found by the following treatment intervention and diagnosa
a. Trouble perfuasi of tissue referring to decrease of O2supply to perifer tissue
1) Target of : supply of O2 to tissue fufilled
2) Criterion result of :
a) Visible Husk squeezing do not cyanosis
b) Temperature body in normal boundary 36°C s.d 37°C
c) Nadi in normal boundary (60-80 x/mnt)

3) Intervention
a) Monitor blood pressure, to evaluate early using accurate technics and correct manset.
Rationalization : comparison of pressure give more complete picture about involvement of vascular problem
b) Note existence, quality of perifer central pulsation
Rationalization : pulsation of karotis, juguralis, and radialis of femoralis possible perceived/throb terpolasi at downhill to tungkai possible express and effect of vasokontriksi and of kongesti vena
c) Perceive husk colour, dampness, temperature, and a period of/to capillary admission filling.
Rationalization : existence of turning pale, to be chilled, damp husk and a period of/to tardy capillary refil, possible its bearing with vasokontriksi or express dekompensasi/bulk heart degradation
d) Note the existence of oedem / certain
Rationalization : earn identification fail heart, damage of kidney or is vascular.
e) Create balmy environment
Rationalization : assisting to degrade stimulus of simpatis, improving relaksasi
f) Limit activity
Rationalization : degrading stress and stress which blood pressure effect and journey of disease
g) Conduct action balmy like heightening head in place sleep
Rationalization : lessening uncomfortable and can degrade stimulus of simpatis.
h) Watch respon to drug to control blood pressure
Rationalization : respon to drug therapy, depended effect individual of sinergis medicinize because effect of sampinh, hence important to use drug in number a few/little and low dose.
Kolaborasi : giving drug according to indication.
b. Acute pain (headache) relate to the make-up of serebral vascular pressure
1) Target of : pain in bone decrease / lose
2) Criterion result of :
a) Blood pressure go down / maximal normal 140 / 90mmHg
b) Client do not feel dizzy / neck lost to stiff again
c) Visible peace client
3) Intervention
a) Maintain lie down during a period of/to is acute
Rationalization : minimization of stimulasi / increase of relaxation.
b) Give non farmakologik action to eliminate headache, for example : compress cool water at forehead, squeeze back.
Rationalization : action of massage aim to to degrade vascular pressure of serebral and slow down sympathetic respon, effective in eliminating pain in bone.
c) Eliminate / activity minimization of vasokontriksi able to improve headache, for example : cough length and moving many
Rationalization : activity which mounting vasokontriksi cause headache make-up of vascular pressure.
d) Assist client in ambulasi according to requirement.
Rationalization : confused and blurry eyesight often relate to client headache also earn hypertension episode mengalamio of postural.
e) Give dilution , soft food which is easy to be swallowed.
Rationalization : improving public freshment and lessen requirement of energi/ tired.
f) Give analgetik according to therapy indication.
Rationalization : degrading pain in bone and stimulate nerve system of simpatis.
c. Activity Intoleran relate to fatigue
1) Target of : activity client can be unassisted
2) Criterion result of :
a) Client able to have activity
b) Client can do simple activity
1) Intervention :
a) Study family respon to activity
Rationalization : studying physiological respon to activity stress and if any representing indicator of activity work related to activity storey;level.
b) Intruct client about thrift of energi technical
Rationalization : thrift of energi lessen technics degradation of energi, also balance help supply and requirement of O2.
c) Give motivation to conduct activity / treatment of x'self in phases, giving aid according to requirement.
Rationalize : progress of activity in phases prevent the make-up of heart activity sudden. Giving aid only limited to requirement will push independence in conducting activity.
d. Trouble take a rest and sleep relate to sekunder confusedly with make-up of Intra Cranial Pressure (ICP)
1) Target of : patient can take a rest and sleep quietly
2) Criterion result of :
a) Patient can sleep ± 8 hours a day.
b) Eye do not see to squeeze
3) Intervention
a) Study habit of sleep / rest
Rationalization : study and identify correct intervention.
b) Study habit usage of sedative drug
Rationalize : habit of sedative drug usage very is influencing sleep pattern.
c) Create calm atmosphere
Rationalization : giving situation of kondusif for sleep.
d) Suggest technicsly of relaxation
Rationalization : assisting to induce sleep.
e) Balmy Berry sleep position
Rationalization : change of position alter the way of pressure and improve rest.
e. Less knowledge relate to cognate limitation
1) Target : patient understand pandemicly
2) Criterion result of : patient can lay open about hypertension, symptom, sign, cause, complication, and prevention
3) Intervention
a) Study the readiness of and resistance in learning the including people closest
Rationalize : Assess mount ability of client, which can influence client enthusiasm/ people closest to study disease, progress of and therapy of prognisis and also resistance that happened in course of medication.
b) Specify and determine normal blood pressure, explaining about hypertension and effect at heart, venous, brain and kidney.
Rationalization : giving real correct knowledge base about blood pressure and also explain risk factors which show in supporting hypertension and disease of kardiovaskuler.
c) Assist client in risk factors identify of kardiovaskuler able to be altered, for example obesitas, diet high of saturated fat and cholesterol, smoke, alcoholic, and pattern live full of stress
d) Explain about therapy, drugs and also side effects that happened.
Rationalize : explaining risk factor and altered possibility and also benefit able to be taken.
e) Suggest client for consultancy with giver of commemoration before using drug which recipe and or which do not recipe
Rationalize : important care in prevention of drug interaction which is dangerous possibility.


SOURCE

Engram, Barbara,1999, Rencana Asuhan Keperawatan, Medikal Bedah, Volume I, Alih Bahasa, Suaryati, Samba.
Hettina., Sandra M. Pedoman Keperawatan Medikal Bedah. Edisi 3. Vol. 3. Jakarta. EGC. 2002.
NIC. Nursing Intervention Classification. 2005.
NOC. Nursing Outcomes Classification. 2005.
Panduan Diagnosa Keperawatan Nanda 2005-2006. Alih Bahasa Budi Santosa. Prima Medika. 2005.
Potter, R.A. Derry A.G. Fundamental of Nursing; St. Louis. Mosby.2000
Smeltzer, S.C. Bare, B.G., Keperawatan Medikal Bedah. Brunner dan Suddarth. Alih Bahasa. Monica Ester. Jakarta : EGC. 2002.

Pleura Effusion

PLEURA EFFUSION

A. Congeniality
Effusion of Pleura is heaping of cavity dilution of pleura (I Schwartz seymour, 2000).
Effusion of Pleura is gathering of abnormal dilution in pleural cavum (Wise [of] Mansjoer, ed. 1999).
Effusion of Pleura is gathering of dilution in room of pleura which lay between surface of and visceral of parietal. (Suzanne C Smeltzer and of Brenda G. Bare, 2002

B. Etiology
According to Selbacher, dkk (2000) etiology of pleura effusion that is as follows: pleura dilution accumulate if pleura dilution forming exceed pleura imbibition dilution. Normally, dilution enter pleura cavity from capillary in panetalis pleura and transported to tissue of limfatik located in parietalis pleura. Dilution also can enter pleura cavity room of interstisium pulmo through viseralis pleura or from peritoneum cavum through puncture exist in diaphragm. channel of limfe have capacities under normal circumstances. For the reason, pleura effusion can be formed if there is forming of dilution of pleura abundant (parietalis pleura, pulmonary interstisium room, or peritoneum cavum) or if there is degradation transportation of dilution by passing limfatik, normal pleura dilution is 15-20 cc.
According to Wisdom of Mansjoer, ed (1999) etiology of pleura effusion shall be as follows:
1. Neoplasma like bronkogenik neoplasma and of metastatik
2. Cardiovascular like failing heart of kongesti, pulmonar embolus, and perikarditis
3. Disease at abdomen like pankreatitis, asites, and abscess
4. Infection caused by bacterium, virus, mushroom, parasite and mikobakterial
5. Others systematical eritematosus like lupus, arthritis rheumatoid, syndrome of nefrotik and of uremia.

C. Classification of pleura effusion pursuant to formed dilution (Suzanue C Smeltezer and of Brenda G. Bare, 2002)
1. Transudat
Representing plasma filtrat emiting a stream of to penetrate intact capillary wall, happened if factors influencing and forming of reabsorbsi pleura dilution annoyed that is because pressure imbalance of hidrostaltik or ankotik. Transudasi designate the condition of like asites, perikarditis. Disease kongestik heart failur or fail kidney so that happened heaping of dilution.
2. Eksudat
Ekstravasasi dilution into tissue or cavitas. As effect of inflammation by bacterium or humor product which hitting the pleura for example TUBERCULOSIS, chest trauma, virus infection. Pleura effusion possible represent komplikasi kongestif heart fail. TUBERCULOSIS, pneumonia, infection of paru, nefrotik sindroma, bronkogenik karsinoma, hepatis serosis, embolism of paru, infection of parasitik

D. Patofisiologi
Change of dilution movement into and exit of pleura cavity caused by the existence of hydrostatic pressure imbalance and colloid osmotic pressure in capillary surface and pleura.
Difference between eksudat and transudat relied on its trasudat protein content (hidrotoraks) produced when dilution free of protein emit a stream in pleura cavity become annoyed. Visible dilution pure or turn pale yellow. Specific gravity 1,015 or less with normal protein content less than 3 gr/dl, calculate corpuscle type. Make-Up of capillary pressure at failing heart and onkotik pressure reduction plasma in kidney or hepar disease have been known to cause dilution of transudat.

E. Sign and Symptom
1. Trakea deviasi avoid hit side
2. The impelling of mediastinum at adversative side with dilution
3. Deaf at percussion
4. Degradation of sound respiration of hit side at auskultasi
5. Out of breath or short breath
6. Chest pain of pleuritik (blunt feeling in chest)
7. Noisy of heart at heart weakness
8. Weaken progressive, downhill body weight
9. Cough sometime bleed at smoker (Bronchus Karsinoma)
10. Fever of Subfebril (tuberkulosis)
11. Anxietas (liver cirrhosis)

F. Supporter Diagnosa
1. Inspection of laboratory (effusion dilution analysis which in thorakosentesis)
2. Inspection of radiology
Thorax photo seen the corner loss of kostofrenikus and will seen tortous surface if amount of effusion dilution more than 300 ml, friction of mediastinum sometime found .
3. Chest CT Scan will seen difference of dilution densitas with vinicity tissue
4. Ultra Sono grafi at pleura can determine pleura cavity dilution
5. Bronkoskopi at cases of neoplasma, aleunum korpus and abscess of pulmo
6. Thorakoskopi (pleura optic tiber) at case with pleura tuberculosis neoplasma
7. Biopsy of Pleura.


G. Threatment
1. Dilution drainage if effusion of pleura generate symptom of subjek, pain, dipsnea, etc. Dilution effusion counted 1-1,5 litre released immediately to prevent to to improve oedema. Amount of more effusion dilution hence expenditure of dilution following conducted 1 hour later.
2. Antibiotic if there are emprema
3. Pleurodesis that is adhere viseralis pleura and pleura parietalis to prevent happening of again effusion of pleura after aspiration (effusion of pleura maligna)
4. Opreatif, when pus jell dilution difficult so that exit or its multilokulara
5. Lie down

H. Komplikasi
1. Pneumonia
2. Fibrosis Paru
3. Pneumotorak
4. Emfisema
5. Arelektasis

I. Functional Health Pattern Study
1. Activity and Practice Pattern
a. Anamnesis existence of dyspnea, weaken, or fatigue
b. At effusion area there no fremitus, gloomy percussion, breath voice decrease
c. Unsimmetrical chest ekspansi
d. Out of breath or short breath
e. Tachipnea
f. Heart noisy at heart weakness
g. Heaping return dilution after action of thorakosintesis, study sign of distress respiration
h. Kardiovaskuler respon after thorakosintesis, hipotensi, tachicarchi, aritmia, insensible, pale and sweaty husk
i. Bronkhopulmonary infection: temperature, sputum for the culture of and of sensitivitas
2. Sleep and rest pattern
a. Habit of sleep
b. Condition of sleep
c. Time got off to sleep
d. Quality of sleep
e. Moment sleep trouble
f. Habit of deliverer of sleep.
3. Cognate Perception pattern
a. Existence of sigh of chest pain
b. Perception of pain in bone, PQRST pain
c. Intensity scale mount pain.

J. Nursing Care Plan
1. Ineffective Breath Pattern related to degradation of pulmo ekspansi (Heaping of dilution).
Target of
a. Client can reach normal respirasi status by way of clean breath.
Indikator 1 2 3 4 5
- Easy to breath
- Syspnea after exercise
- Normal chest expantion
- Not anxiety
- Good condition
- Reguler breath pattern
- RR normal
Boldness:
1 : Very inappropriate
2 : Seldom according to
3 : Sometime according to
4 : Often according to
5 : Always according to

b. Client can reach normal vital marking status
Indikator 1 2 3 4 5
- Temperature
- Perifer pulse
- Central perifer
- RR
- Diastolik
- Sistolik
Boldness:
1 : Most digressing from normal
2 : Digressing many from normal
3 : Digressing from normal
4 : Light digress from normal
5 : Do not digress from normal
Intervention:
- RR Observation, breath pattern, breath deepness effort and respiration
- Observation result of chest rongten
- Give air numidifikasi/oxygen if precisely
- Positioning balmy patient on course to maximize ability of breathing
- Teach patient for breathing slow and regular
- Teach family and patient about usage of O2 at home
- Colaborate with family for observation and know symptom and sign in change respiration and report at health team

2. Ineffective Airway Breathing
That is disability in cleaning or secretion of bronchi obstruksi to take care of cleanness airway breathing
Characteristic definition:
- Dispnea
- Degradation of breathing voice
- Orthopnea
- Breathing voice additional: rales, creakles, ronkhi, wheezing
- Ineffective cough/cannot cough
- Production of Sputum
- Sianosis
- Difficulty talking
- Change of respiration frequency and ritme
- Jumpy
Coresponding Factor :
- Environment
- Smoke
- Smoke Cigarette
- Inhalaksi Smoke
- Passive Smoker
Obstruksi airway
- Spasme airway
- Mucus many
- Ineffective sekresi
- Existence of artificial respiration way
- Foreign object in airway
- Sekresi in bronkus
- Eksudat in alveoli
Physiology
- Disfungsi Neuromuscular
- Hyperplasia Wall of bronchial
- Disease of kronik obstruksi paru
- Infection
- Asthma
- Allergic
Target : Client can reach status of respirasi normal with ventilation after conducted treatment during …..hours
Criterion result of
Indikator 1 2 3 4 5
- Regular breathing
- Breath rythm normal
- No noisy breath voice
- Easy to breath .
- Orthopnea is never
1 : very it to
2 : always it to
3 : often it to
4 : sometime it to
5 : expectation inappropriate
Intervention:
Management Respiration:
1. Observing deepness rhythm level and effort in breathing
2. Observing exhalation sound
3. Teaching technique of relaksasi special
4. Auskultasi breath voice
5. Give O2

3. Acute Pain related to biological injuri agent
Target: client can reach balmy level.
Indikator 1 2 3 4 5
- Comfortable physic
- Reporting to satisfy to ability control x'self / symptom and sign
- Reporting psychical freshment.
- Comfort with the environment
- Comfort with the relationship
- Satisfy to its independence
- Satisfy to ability control pain
Boldness:
1 : Have never demonstrated
2 : Seldom demonstrate
3 : Sometime demonstrate
4 : Often demonstrate
5 : Always demonstrate
Intervention:
1. Analgesic Administration
- Determining location, characteristic, quality of and degree of pain before giving drug
- Monitor vital sign before and after giving analgesic at first time
- Give timely analgesic especially super pain moment
- Effectiveness evaluation of analgesic, symptom and sign (side effects)
2. Pain Management
- Conduct pain study comprehensively cover characteristic location, onset, durasi, frequency, quality of, factor and scale.
- Teach good relaksasi and distraksi technique before, moment or after pain
- Report at doctor if given pain handling less effective
- Give optimal analgetik drug to lessen pain
- Kolaborasi with one who mean with patient, other health team to determine pain management to non invasif action.

4. Less knowledge about disease process related to
- Lack of information
- Mistake of information interpretation
- Cognate delay
Target: Client can know about its disease process
Indikator 1 2 3 4 5
- Knowing the name of disease
- Can explain about the disease
- Can explain about the risk factor
- Can explain about the sign and symptom
- Can explain about the complication
Boldness:
1 : Cannot
2 : Seldom can
3 : Sometime can
4 : Often can
5 : Always can
Intervention
1. Teach: disease process
- Descripting disease sign and symptom
- Explaining disease process and identify cause
- Intruct to client to report sign and symptom
- Discussing about therapy.


SOURCE

Doengoes, Marllyn E. Rencana Asuhan Keperawatan, 2000.
Isselbacher, et.al. Harison Prinsip-prinsip Ilmu Penyakit dalam, Edisi 13. Jakarta: EGC. 2000.
Mansjoer, Arif ed.et.all, Kapita Selekta Kedokteran, Jilid 1. Edisi 3. EMdia Aesculapius, FKUI: 2001.
Nanda Nursing Diagnoses Definitions and Clasification, Philadelphia. 2002.
Nettina, Barbara M. Pedoman Praktik Keperawatan Alih Bahasa. Setiawan Sari, Monica Ester, Jakarta: EGC. 2002.
Schwartz, Saymour I, Intisari Prinsip-prinsip Ilmu Bedah. Jakarta: EGC. 2000.
Smeltzer, Suzanne C. Buku Ajar Keperawatan Medikal Bedah. Jakarta: EGC. 2000.

Anemia

A. Definition
Anemia is an condition of where rate of Hb and/or count lower eritrosit of normal price. Told as anemia when Hb < 14 g/dl and Ht < 41% at man and Hb < 12 g/ dl and Ht < 37 % at woman. (Arif Mansjoer,Dkk. 2001)
Anemia is decreasing of amount of eritrosit and also the amount of haemoglobin in 1mm3 blood or decreasing compacted cell volume (volume cells red packed) in 100 blood ml. (Ngastiyah, 1997)

B. Etiology
Anemia caused by various disease type, but all the damage by significant will lessen to the number of oxygen which available to tissue. According to Brunner and of Suddart (2001), some cause of anemia in general for example:
a. Physiologically anemia happened when there are lacking amount of haemoglobin to transport oxygen to tissue
b. Effect of premature red corpuscle or crushing of abundant red corpuscle
c. Red corpuscle production falling short
d. Other factor cover losing of blood, lack of nutrisi, clan factor, chronic disease and lacking of ferrum.

C. Classification
By patophisiology anemia consist of:
1. Degradation of production : deficiencies anemia, anemia of aplastic
2. Make-Up of crushing : anemia because blood, anemia of hemolitik.
Generally anemia grouped become:
1. Mikrositik hipokrom anemia
a. Deficiencies iron anemia
To make red corpuscle needed ferrum (Fe). Requirement of Fe about 20 mg/day, and only about 2 mg absorbent. Full scale of Fe in body about 2-4 mg, about 50 mg/kg of BB at man and 35 mg/kg of BB at woman. This anemia generally caused by chronic bleeding. In Indonesia many because of hookworm infestation (ankilostomiasis), it will not cause anemia when do not accompany by malnutrisi. This anemia type is also caused by:
1) Diet which fall short
2) Downhill imbibition
3) Requirement which mounting at pregnant woman and suckle
4) Bleeding at channel digest, menstruating, blood transfussion
5) Hemoglobinuria
6) Depository of iron decrease, like pulmo hemosiderosis.
b. Chronic anemia disease
This anemia recognized also by the name of anemia sideropenic of with siderosis reticuloendothelial. This disease attributed to many various disease of infection like kidney infection, pulmo (abscess, empisema, etc).

2. Anemia of Makrositik
a. Anemia of Pernisiosa
Anemia that happened by lack of vitamin of B12 effect of intrinsic factor because trouble of absorbtion representing disease of autoimun herediter and also factor of ekstrinsik for lack of vitamin B12 suply
b. Deficiencies of folat acid anemia
This anemia generally relate to malnutrisi, but degradation imbibition of folat acid seldom be found because imbibition happened in all channel digest. Folat acid there are in flesh, milk, and green leaf
3. Anemia because bleeding
a. Acute bleeding
Possible when expenditure of blood quite a lot, while degradation of Hb rate happened a few days later
b. Chronic bleeding
Expenditure of blood usually a little so that unknown by patient. For example caused by peptikum ulcus, menometroragi, channel blood digest, and epistaksis.
4. Hemolitik anemia
Hemolitik anemia happened degradation of red corpuscle age (normal 120 day), good whereas or continuously. This anemia caused by disparity of membrane, disparity of glikolisis, disparity of enzyme, immured system disorder, infection, hipersplenisme, and singe. Patient usually ikterus and of splenomegali.
5. Aplastik anemia
Happened because bone marrow can not form corpuscles. Its cause can be congenital, idiopatik, kemoterapi, radiotherapy, toxin, etc.

D. Clinical Manifestation
At anemia, because all organ system can involve hence can generate wide of clinical manifestation. This manifestation base on
a. Speed of anemia occurence
b. Duration
c. Requirement of pertinent client metabolism
d. Existence of defect or other disparity
e. Certain complication or situation causing anemia.
Because red blood count decrease, hence is slimmer delivered oxygen to tissue. Losing of blood which quickly counted 30% can cause vascular kolaps at same individual. But degradation of hemoglobin and hematokrit without visible symptom or clear disability step by step usually earn tolerance until 50%. Compensation body mechanism work through
a. Bulk improvement of respiration and heart, in consequence add delivery of oxygen to tissues by red corpuscle
b. Improving release of haemoglobin and oxygen
c. Developing plasma volume attractively dilution from tissue
d. Redistribusi blood stream to vital organs.
Individual which have experienced of sufficient anemia during with haemoglobin rate between 9-11 g/dl, only experiencing of a few symptom or no symptom at all besides light takikardi during practice. Takikardi depict work load and pour heart which mounting. Dispnea practice usually happened when hemoglobin rate below/under 7,5 g/dl representing manifestation decrease delivery of oxygen. Weakness only happened when haemoglobin rate below/under 6 g/dl. Dispnea take a rest when below/under 3 g/dl and fail heart only at very low rate 2-2,5 g/dl, this matter caused by heart muscle which lacking of inadaptable oxygen x'self with heart work load which mounting.
One of the most sign often related to anemia is turning pale. This resulted decreasing blood volume, and hemoglobin of vasokontriksi to enlarge delivery of oxygen to vital organs. Nail colour, palm, tire of mukosa trap and konjungtiva can be used to assess paleness.

E. Supporter Data
At laboratory test result met
a. Amount of lower Hb from is normal (12-14 g/dl)
b. Rate of Ht downhill (normal 37-41)
c. Make-Up of total bilirubin (hemolitik anemia)
d. Seen and retikulositosis of sferositosis at edge blood5. There are pansitopenia, empty bone marrow changed by fat (aplastik anemia)

F. Threatment
Threatment of anemia addressed to look for cause and change missing blood. Anemia threatment pursuant to its type, that is
a. Aplastik anemia
The threatment cover bone marrow transplantation and therapy of immunosupresif with globulin antithimocyte (needed ATG) through central band during 7-10 day. Ugly prognosis if bone marrow transplantation fail to. If needed can be given by transfusion of RBC low and platelet leucocyte (Phipps, Cassmeyer, Sanas & Lehman, 1995)
b. Deficiencies iron anemia
Overcome by curing its cause and change ferrum by farmakologis during one year. Men require 10 mg/day, woman menstruating 15 mg/and day of postmenaupouse require 10 mg/day
c. Megaloblastik anemia
For the anemia of caused by megaloblastik is vitamin deficiencies of B12 (anemia of pernisiosa) and sour deficiencies of folat dosed with giving vitamin of B12 and oral folat acid 1 mg/day
d. Cell scythe anemia
Its medication include giving hydration and antibiotic swiftly and big dose. Gife sour addition of folat every day needed to fill lacking of acid folat caused by the existence of kronik hemolisis. Transfusion only needed during happened crisis of aplastik or hemolitik. Education and continuous tuition including tuition of genetik, conducted important for the prevention of and medication of scythe cell anemia.

G. Complication
There are three common complication happened at anemia that is failing heart, and spastic of parestesia (feeling which digressing like feeling burnt and ant).


NURSING CARE PLAN FORMAT

A. ASSESSMENT
1. Activity/Rest
a. Iethargy, weakness, common malaise
b. Losing of productivity, dispiriting to work
c. Tolerance to low practice
d. Requirement more for the rest and sleep
2. Sirculation
a. History losing of chronic bleeding
b. History of endokarditis chronic infektif
c. Palpitasi
3. Integrity Ego
Confidence of culture or religion influence election of medication, for example: deduction of blood tranfusi
4. Elimination
a. History of Pielonenepritis, fail kidney
b. Flatulen, syndrome of malabsobsi
c. Hematemesi, melana
d. Diarrhoea or constipation
5. Food/dilution
a. Passion eat downhillly
b. Queasy/puking
c. Downhill body weight
6. Pain/freshment
Location pain especially abdomen area and head
7. Respiration
Short breath at rest or doing actifity
8. Seksualitas
a. Change of menstuasi for example menoragia, amenore
b. Downhill of sexual function
c. Impotent

B. DIAGNOSA TREATMENT
1. Trouble tissue perfusion relate to degradation of oxygen supply/nutrition to cell, marked with:
a. Palpitasi,
b. Pale husk, dry mukosa membrane, brittle hair and nail,
c. Cool ekstremitas
d. Change of blood pressure, tardy capillary admission filling
e. Disability of have concentration, disorientasi
Target: showing adekuat tissue perfusion
2. Intoleran activity relate to oxygen supply imbalance, marked with:
a. Weakness and fatigue
b. Complaining degradation of actifity/practice
c. More needing rest/sleep
d. Palpitasi,Takikardi, make-up of blood pressure
Target: happened the make-up of tolerance of aktifitas
3. Change of nutrition less than requirement relate to failure to digest, food absorbtion, Marked with:
a. Degradation of normal body weight
b. Degradation of husk turgor, change of mouth mukosa.
c. Passion eat downhillly, queasy
d. Losing of muscle tonus
Target: requirement of nutrisi fufilled which followed by make-up of body weight.
4. Constipation or diarrhea relate to degradation of food amount, change of ingestion , side effects usage of drug, Marked with :
a. Existence of fesesfrequency, characteristic, and amount change
b. Queasy, puking, degradation of passion eat
c. Abdomen pain
d. Peristaltic disorder
Target: pattern of eliminasi normal as according to its function
5. High risk of infection relate to defence of skunder which inadekuat, Marked by can not be applied by the existence of symptom and marking-symptom making actual diagnosa.
Target of: happened degradation of infection risk.


C. INTERVENCE
Diagnosa 1
1. Vital sign study, husk colour, mukosa membrane, nail elementary
2. Give semi fowler position
3. Study pain scale and existence of palpitasi
4. Maintaining ambient temperature and patient body
5. Avoid usage of hot water or warmer.
Kolaboration
1. Monitor laboratory test result for example Hb/amount and ht of SDM
2. Give complete SDM blood/pocket
3. Give additional O2 as according to indication

Diagnosa 2
1. Study ability of patient actifity
2. Vital sign study when doing actifity
3. Assist requirement of patient actifity if needed
4. Suggest to patient to discontinue actifity if happened palpitasi
5. Use energy thrift technics for example bath sat

Diagnosa 3.
1. Study history of nutrisi the including food took a fancy to
2. Observation and note patient food input
3. Deliberate body weight every day
4. Giving food a few/little and frequency which often
5. Observation for queasy, puking, other related symptom and flatus
6. Assist and give good mouth hygiene
Kolaborasi
1. Consul at nutritionist
2. Give drug as according to indication for example: mineral and vitamin of suplemen
3. Give nutrisi suplemen.

Diagnosa 4
1. Observ colour of feses, consistency, amount and frequency
2. Sound intestine study
3. Dilution giving 2500-3000 ml/day in heart tolerance
4. Avoid to eat gasiform
5. Study condition of husk of perianal
Kolaborasi
1. Consul nutritionist for giving well-balanced diit
2. Give laksatif
3. Give anti diarrhea drug

Diagnosa 5
1. Improving to clean hand better
2. holding up of aseptic technics tighten in each action
3. Assist treatment of husk of perianal and of oral carefully
4. Limit visitor
Kolaborasi
1. Take spesemen for culture
2. Give topikak antiseptic, systematical antibiotic.


SOURCE

Brunner & Suddarth. 1997. Buku Ajar Keperawatan Medikal Bedah. Jakarta : EGC.
Doenges, Marilynn, dkk. 1993. Rencana Asuhan Keperawatan, Pedoman Untuk Perencanaan dan Pendokumentasian Perawatan Pasien. Jakarta : EGC.
Long, Barbara C.1996. Perawatan Medikal Bedah ( Suatu Pendekatan Proses Keperawatan ). Bandung : Yayasan Ikatan Alumni Pendidikan Keperawatan Pajajaran Bandung.
Manjoer, Arief. 2001. Kapita Selekta Kedokteran. FK UI : Media Aeskulatius
Ngastiyah. 2001. Ilmu Keperawatan Anak. Jakarta : EGC.

Meski Pialaku Terbang

Haha....
Yang terbang biarlah terbang. Mungkin dia bosan nangkring di almari kelas qt. Mungkin dia bosen liat tampang-tampang qt, kelakuan qt yang ‘autis’..... wotever laaa.... toh kalo qt menang juga ntu piala cuma buat hiasan...hoho....

Heyy, piala boleh terbang. Tapi semangat jangan ikut terbang ;-)

Hmm, ayolah ngaku.... seneng kan bisa memporakporandakan kelas? Seneng kan bikin pohon harapan yang dikasi nama HAMINALOUZ (ah, bahasa mana sih ntu)? Heboh juga kan bikin gundul sapu kelas buat bikin atap mading? (kalo ini mah,ide yang beneran gila.... dasar hakim autiss.. haha).

Ada cerita di jalan deket singosaren plaza. Judulnya “Meski Styrofoamku Terbang”. Garagara ana nih bwa motor 30km/jam. Jadi terbang kann?? Tengsin gw.....

Ada cerita tentang hebohnya semarak ICON di medan pertandingan. Apapun hasilnya, yang penting menggilaaaaaa......... ayee............

Bosen yah denger kalimat, “biar gk jadi juara yang penting seneng”?
Gw ganti dah......
“biar gk jadi juara yang penting heppi” haha.......

Sumpah.... emang ini porseni yang hebat, temann...
Porseni taun ini, kue leker jadi inovasi baru di 2B. Seribuu seribuuu.... (enak tenan eg kue yang masaknya pke tevlon kebalik ituh). Heh Indah..... ayo ke kue leker lagii, menunaikan tantanganmu pesen kue leker setengah bokong tevlon full choco.

Porseni taun ini kita belajar bagaemana mengendalikan keadaan. Huh, emang smtime gk bisa ngampet. Tapi salut laaa......

Porseni taun ini, kebersamaan 2B jadi menyenangkaaaaannnn........... :D

Dedicated to ICON

Bismillah......
Untuk yang berkenan silakan dibaca tulisan ini.

Mungkin aku akan sedikit memaksa, menutup telinga ketika ada yang berkata, “ah, kurang kerjaan kie sing nulis.” Tapi ini bukan tulisan iseng, kawan... aku pengen menyampaikan yang mungkin belum tersampaikan. Entah karena sulit atau memang kemampuanku terbatas untuk menyampaikan di hadapan kalian. Ini tentang kita semua. Semoga bisa diambil manfaatnya.

Kawan......
Aku sering kepikiran, kok adaaaaa aja masalah yang mampir di antara kita. Entah ini aku yang berlebihan atau memang kalian juga merasakan hal yang sama. Tapi besar atau kecil, yang namanya masalah tetep masalah. Yang kecil didiemin malah jadi besar. Kalo udah besar mau jadi apa? (jangan dijawab jadi perawat -.-).

Hmm, 1st step.... yok bikin pathway.....
Gambaran aja deh, masalah itu dimunculkan bukan muncul dengan sendirinya. Ya, memang sebagian dimunculkan tanpa disadari. Dari hal sepele, jadi masalah pribadi (dianggap gak penting), kebawa sampe forum (bisa diatasi, tapi apa di belakang baik-baik saja?).

Teman, dalam keadaan composmentis... sadar sepenuhnya... bukan aku tak pernah melakukan kesalahan. Faktanya kita sama-sama masih belum benar-benar pandai dalam menyikapi sebuah kehidupan. Aku pernah berburuk sangka, aku pernah memendam emosi, aku pernah tak peduli dan bukan berarti aku tak pernah membenci.

Kita ini hidup diantara perbedaan, kawan. Sakit hati itu manusiawi.... dan kesalahan itu wajar karena memang manusia tempatnya salah. Disini, kita sama-sama belajar bagaimana cara menghargai, bagaimana cara bersosialisasi, belajar mengerti bahwa persaudaraan itu hal yang luar biasa, dan menjadikan tiga puluh tujuh insan yang berbeda menjadi suatu kekuatan yang hebat.

Jika kita benar-benar sudah dewasa, aku yakin kita bisa berfikir jauh ke depan. Memilah mana yang prioritas dan mana yang bisa ditunda. Jika kita berkomitmen untuk suatu kebersamaan, aku yakin kita telah belajar arti dari sebuah pengorbanan. Jika memang tak bisa dipaksakan, Insya Allah kita semua bisa bersikap bijaksana dalam mengambil keputusan.

Sudah saatnya kita berbenah, kawan. Mulai dari diri kita sendiri (karena mungkin Cuma kita yang tau keadaan diri kita sendiri). Sebuah karakter biarlah menjadi karakter. tapi bukan berarti tidak ada yang perlu dirubah dari diri kita. Apakah kita akan puas dengan keadaan yang statis?

Kawan...
Yok kita sama-sama berjuang.
Kayaknya lebih enak kalo kita saling membantu. Hmm, liat deh betapa hebatnya kepala suku kita memperjuangkan nasib anak buahnya. Kalo seandainya kita di posisinya, apa kita msih sabar menghadapi anak buah yang (kadang) susah dikendalikan. Termasuk ane nih yang kadang juga bandel....
Kalo di posisi dia, apa kita cukup bijaksana mengambil keputusan untuk kepentingan bersama.... bahkan tak jarang suatu kebijaksanaan yang bermaksud baik, justru kita yang membuat jadi rumit. Bukan tak berarti ketua kita kesulitan mengambil sebuah keputusan, tapi karena dia menganggap kita ada, kawan.... :)
Dan sebagai anak buah, ane salutt sama pak kepala suku.... (walopun kadang sempet komplen ini itu. Hehe...)

Semoga note ini bukan cuma sekedar note. Semoga ada pelajaran yang bisa diambil dari note ini, sebagai umpan balik kedewasaan kita. Semoga kita tidak akan pernah terhenti dalan sebuah putaran roda ‘proses’ ini. Kita mulai bersama, melangkah bersama, dan sukses bersama. amin.....