INTOKSIKASI

INTOKSIKASI
Penyebab intoksisasi ada banyak macam, yang sering terjadi adalah karena kecelakaan atau, disengaja / bunuh diri. Di Amerika intoksikasi ± 75% terjadi pada anak umumnya karena keracunan produk rumah tangga

A. Agen Intoksikasi
Terjadi pada semua umur remaja: obat-obat psikotropik, sedative, transqualizer, antidepresan dan obat-obat narkotik. dewasa umumnya karena kecelakaan kerja (karbon monoksida, pestisida, keracunan makanan, dll)

B. Mekanisme
Mekanisme cidera masing-masing racun memiliki efek patologis yang berbeda-beda dimana masing masing racun memiliki patologi sendiri-sendiri. Efek racun dapat terjadi pada tempat atau sekitar masuknya racun (misalnya reaksi kimia sitotoksin) dan dapat berupa toksisitas sistemik yaitu efek-efek selektif racun atau efek metabolik khusus dari racun itu terhadap target yang spesifik misalkan asetaminofen di liver, methanol diretina, dll.

C. Pengkajian Prioritas Utama
1. Pengkajia riwayat kejadian, tanyakan pada pengantar pasien/pasien sendiri jika kooperatif.
2. Pengjakian fisik : Initial assessment/ Arway- Breathing- Cirkulating ( ABC)
a. Tingkat kesadaran
b. Pernafasan dan efektifitas nafas
c. Irama jantung
d. Ada tidaknya kejang
e. Keadaan dan warna kulit
f. Besar dan reaksi pupil mata
g. lesi, bau mulut, dan lainnya
Terkadang setelah mendapatkan resusitasi (ABC) sering dilanjutkan dengan perawatan suportif di ICU dan dilakukan pengeluaran zat penyebab dari tubuh serta mungkin diperlukan antidotumnya.
Jika didapat pasien tidak sadar dengan penyebab yang Belum jelas, perlu selalu difikirkan adanya kemungkinan intoksikasi. tindakan pertama:menjaga jalan nafas, oksigen ( biasanya tidak kurang dari 6 lt / menit), K/p bantuan nafas, IV line, kemudian cek seluruh tubuh adanya tanda-tanda kemungkinan mendapat obat atau racun, periksa adanya bekas suntikan, zat terminum bau nafas dan lainnya dan perkirakan juga kemungkinan terjadinya hipoglikemi.

D. Evaluasi/outcome umum pd intoksikasi
Stabilisasi & menigkatnya kardiorespirasi, kriteria :
sistolik 100mmHg, nadi 60 – 100X / menit, irama reguler
respirasi 24 X/ menit, tidak ada rales, tidak ada wheezing
meningkatnya kesadaran
1. Carbon Monoxide Poisoning
Carbon monoxide (CO), is a colorless, odorless, toxic gas that is a product of incomplete combustion. Motor vehicles, heaters, appliances that use carbon based fuels, and household fires are the main sources of this poison.
2. Carbon monoxide (CO)
Carbon monoxide (CO) intoxication is the leading cause of death due to poisoning in the United States and also the most common cause of death in combustion related inhalation injury. The incidence of non-lethal CO poisoning is not well established nor is that of unrecognized CO poisonin. Mortality rates as high as 31% have been reported in large series
3. Agent
Most immediate deaths from building fires are due to CO poisoning and therefore, fire fighters are at high risk.
a. Exogenous Sources of CO
b. Car exhaust fumes
c. Furnaces
d. Gas-powered engines
e. Home water heaters
f. Paint removers containing methylene chloride
g. Pool heaters
h. Smoke from all types of fire
i. Sterno fuel
j. Tobacco smoke
k. Wood stoves

E. Pathophysiology
In patients who die early following CO poisoning the brain is edematous, and there are diffuse petechia and hemorrhages. If the victim survives initially but dies within a few weeks, findings typical of ischemic anoxia are prominent. Interestingly, the severity of the lesions appears to correlate best with the degree of hypotension rather than with hypoxia.
1. Hypoxia and cellular asphyxia
CO combines preferentially with hemoglobin to produce COHb, displacing oxygen and reducing systemic arterial oxygen (O2) content. CO binds reversibly to hemoglobin with an affinity 200- 230 times that of oxygen. Consequently, relatively minute concentrations of the gas in the environment can result in toxic concentrations in human blood. Possible mechanisms of toxicity include: decrease in the oxygen carrying capacity of blood. Alteration of the dissociation characteristics of oxyhemoglobin, further decreasing oxygen delivery to the tissues. Decrease in cellular respiration by binding with cytochrome a3. Binding to myoglobin, potentially causing myocardial and skeletal muscle dysfunction.
2. Ischemia.
In addition to causing tissue hypoxia, CO can cause injury by impairing tissue perfusion, indicate that myocardial depression, peripheral vasodilation, and ventricular arrhythmia causing hypotension may be important in the genesis of neurologic injury.
3. Reperfusion injury
Many of the pathophysiologic changes are similar to those seen with postischemic reperfusion injuries, and similar pathology occurs in the brain in the absence of CO when hypoxic hypoxia precedes an interval of ischemia.
F. Symptomatology
Many victims of CO poisoning die or suffer permanent, severe neurological injury despite treatment. In addition, as many as 50% of those who recover consciousness and survive may experience varying degree of more subtle but still disabling neuropsychiatric sequela.
The features of acute CO poisoning are more dramatic than those resulting from chronic exposure. The clinical presentation of acute CO poisoning is variable, but in general, the severity of observed symptoms correlates roughly with the observed level of COHb:
COHb Levels and Symptomatology
a. 10% Asymptomatic or may have headaches
b. 20% Dizzyness, nausea, and syncope
c. 30% Visual disturbances
d. 40% Confusion and syncope
e. 50% Seizures and coma
f. 60% Cardiopulmonary dysfunction & death

G. Management
The mainstay of therapy for CO poisoning is supplemental O2, ventilatory support and monitoring for cardiac arrhythmias. There is general agreement that 100% oxygen should be administered prior to laboratory confirmation when CO poisoning is suspected. The goal of oxygen therapy is to improve the O2 content of the blood by maximizing the fraction dissolved in plasma (PaO2).36 Once treatment begins, O2 therapy and observation must continue long enough to prevent delayed sequelae as carboxymyoglobin unloads.
The most controversial and widely debated topic regarding CO poisoning is the use of hyperbaric oxygen (HBO). The most controversial and widely debated topic regarding CO poisoning is the use of hyperbaric oxygen (HBO) severe poisoning should be treated with 100% oxygen, with endotracheal intubation in patients who cannot protect their airway. In these patients, consideration should be given to transfusion of packed red blood cells.
H. Prognosis
30% of patients with severe poisoning have a fatal outcome.49 One study has estimated that 11% of survivors have long-term neuropsychiatric deficits, including 3% whose neurologic manifestations are delayed. One third of CO poisoning victims may have subtle but lasting memory deficits or personality changes.40. Indicators of a poor prognosis include altered consciousness at presentation, advanced age, patients with underlying cardiovascular disease, metabolic acidosis, and structural abnormalities on CT or MRI scanning.
Organophosphate and Carbamate Poisioning
Although OPC and carbamates are structurally distinct, they have similar clinical manifestations and generally the same management. Although most patients with OPC and carbamate poisoning have a good prognosis, severe poisoning is potentially lethal. Early diagnosis and initiation of treatment are important. The ED physician has access to a number of therapeutic options that can decrease morbidity and mortality.

I. Pathophysiology
OPCs and carbamates bind to 1 of the active sites of acetylcholinesterase (AChE) and inhibit the functionality of this enzyme by means of steric inhibition. The main purpose of AChE is to hydrolyze acetylcholine (ACh) to choline and acetic acid. Therefore, the inhibition of AChE causes an excess of ACh in synapses and neuromuscular junctions, resulting in muscarinic and nicotinic symptoms and signs.
Excess ACh in the synapse can lead to 3 sets of symptoms and signs. First, accumulation of ACh at postganglionic muscarinic synapses lead to parasympathetic activity of smooth muscle in lungs, the GI tract, heart, eyes, bladder, and secretory glands, and increased activity in postganglionic sympathetic receptors for sweat glands. This results in the symptoms and signs that can be remembered with the mnemonic SLUDGE/BBB. Second, excessive ACh at nicotinic motor end plates causes persistent depolarization of skeletal muscle (analogous to that of succinylcholine), resulting in fasciculations, progressive weakness, and hypotonicity. Third, as OPs cross the blood-brain barrier, they may cause seizures, respiratory depression, and CNS depression for reasons not completely understood.



J. Signs & Symptoms
Patients often present with evidence of a cholinergic toxic syndrome, or toxidrome. SLUDGE/BBB mnemonic :
S = Salivation
L = Lacrimation
U = Urination
D = Defecation
G = GI symptoms
E = Emesis
B = Bronchorrhea
B = Bronchospasm
B = Bradycardia

DUMBELS mnemonic
D = Diarrhea and diaphoresis
U = Urination
M = Miosis
B = Bronchorrhea, bronchospasm, and bradycardia
E = Emesis
L = Lacrimation
S = Salivation

K. Lab & Test
Serum cholinesterase and RBC AChE activity, which are used to estimate neuronal AChE activity. Other Tests: ECG, prolonged QTc interval is the most common ECG abnormality. Elevation of the ST segment, sinus tachycardia, sinus bradycardia, and complete heart block (rare) may also occur. (Sinus tachycardia occurs just as commonly as sinus bradycardia.)




L. Prehospital Care
Identification of the type of chemical is important. As a general rule, dimethyl OPCs undergo rapid aging, which makes early initiation of oximes critical. In comparison, diethyl compounds may cause delayed toxicity, and oxime therapy may need to be prolonged.

M. Emergency Department Care
1. ABC
Care of the ABCs should be initiated first because intubation may be necessary in cases of severe poisoning. Because succinylcholine is metabolized by means of plasma cholinesterase, OPC or carbamate poisoning may cause prolonged paralysis. Increased doses of nondepolarizing agents, such as pancuronium or vecuronium, may be required to achieve paralysis because of the excess ACh at the receptor.
Providers with appropriate personal protective equipment (PPE) can address the ABCs before decontamination atropine can precipitate ventricular fibrillation in hypoxic patients. Paradoxically, the early use of adequate atropine will dry respiratory secretions, improve muscle weakness and thereby improve oxygenation. The following should be monitored on a regular basis to assess the patient's respiratory status:
a. Respiratory rate
b. Tidal volume/ vital capacity
c. Neck muscle weakness
d. Ocular muscle involvement eg. diplopia
e. Arterial blood gas analysis
f. Cardiac monitoring, a wide range of cardiac manifestations can occur and careful haemodynamic and electrocardiac monitoring hypoxaemia, metabolic and electrolyte abnormalities can all contribute to cardiac arrhythmias. Some arrhythmias may require cardiac pacing.
2. Decontamination:
Important part of the initial care, decontamination depends on the route of poisoning. The patient's body should then be thoroughly washed with soap and water to prevent further absorption from the skin. Washing the poisioned person and removing contaminated clothes nosocomial poisoning in staff members treating patients who have been exposed to OPCs and carbamates; the odors often smelled when one cares for a patient poisoned from pesticide are commonly due to the hydrocarbon solvent, which may cause symptoms independent of the OPC agent. The patient's clothes must be removed and isolated, and his or her body washed with soap and water.GI decontamination: Oral administration of activated charcoal is a reasonable intervention after GI poisoning. Gastric emptying should then be considered if the patient presents within 1 hour of ingestion. Gastric lavage is the only means of emptying the stomach in unconscious patients in which case the airway needs to be protected.
3. Atropine
Atropine is a pure muscarinic antagonist that competes with ACh at the muscarinic receptor.
most commonly given in intravenous (IV) form at the recommended dose of 2-5 mg for adults and 0.05 mg/kg for kids with a minimum dose of 0.1 mg to prevent reflex bradycardia. Atropine may be redosed every 5-10 minutes. Severe OP poisonings often require hundreds of milligrams of atropine. In 1 case report, a patient required frequent doses of atropine and was eventually converted to an atropine infusion to a total of 30 g over 5 days.
Most sources recommend starting atropine on patients with anything more than ocular effects and then observing the drying of secretions as an endpoint in titrating to the appropriate dose. From the Tokyo sarin experience, patients poisoned by nerve agents had modest atropine requirements, with none requiring more than 10 mg. The recommended starting dose of atropine is a 2mg IV bolus. Subsequent doses of 2-5mg every 5-15 minutes should be administered until atropinization is achieved. The signs of adequate atropinization include an increased heart rate (>100 beats/min.), moderately dilated pupils, a reduction in bowel sounds, a dry mouth and a decrease in bronchial secretions.
4. Benzodiazepines
Seizures are an uncommon complication of OP poisoning. When they occur, they represent severe toxicity.
5. Other treatments
magnesium and fresh-frozen plasma as adjunctive therapy. both must be evaluated. Nebulized ipratropium bromide as an adjunct agent.



N. Management of Organophosphorus compunds poisoning
1. Skin decontamination **
2. Airway protection if indicated **
3. Gastric lavage
4. Activated charcoal 0.5-1gm/kg every 4hr
5. Anticholinesterase: Atropine/glycopyrrolate **
6. Cholinesterase reactivator: Pralidoxine
7. Ventilatory support
8. Inotropic support
9. Benzodazepines ( if seizure) **
10. Feeding-enteral/parental
** = useful

O. Further Inpatient Care
Patients who require continuous monitoring or treatment should be admitted to the ICU. Patients with clinically significant poisoning should be evaluated frequently to monitor their airway and respiratory secretions. In addition, frequent neurologic examination should be performed to evaluate for neuromuscular blockade. Therapy is largely titrated to the physical findings. Atropinization is based on the drying of respiratory secretions, and oxime therapy is based on an improvement in neuromuscular signs. A toxicologist may be of help in determining specific aging and reactivation times of the particular OPC or carbamate agent.

P. Further Outpatient Care:
Patients without any symptoms and with questionable or minimal exposure to OPs or carbamates may be considered for discharge after 6-12 hours of observation. Patients with residual neurologic symptoms should be given a follow-up appointment with a neurologist. Follow-up with a psychiatrist should be arranged as indicated.

Q. Complications
1. Intermediate syndrome, Intermediate syndrome was first described in 1987 as a sudden respiratory paresis, with weakness in cranial nerves and proximal-limb and neck flexor muscles. These clinical features appear 24-96 hours after exposure and are distinct from the previously described delayed neurotoxicity (see below). Although intermediate syndrome is incompletely understood, more recent reports suggest this is due to presynaptic and postsynaptic dysfunction of neuromuscular transmission and that it may result from insufficient oxime treatment.
2. OPC-induced delayed neurotoxicity (OPCIDN), OPCIDN is a sensorimotor polyneuropathy that typically occurs 9-14 days after OP exposure. The patient initially presents with distal motor weakness and sensory paresthesias in the lower extremities, which may progress proximally and eventually affect the upper extremities. Most sources suggest the mechanism involves inhibition of neuropathy target esterase (NTE), an enzyme that metabolizes esters in nerve cells. Some patients may recover over 12-15 months, but permanent losses with spasticity and persistent upper motor neuron findings have been reported.
3. Pancreatitis, Pancreatitis has been reported as a rare complication. One case series reported that 12.76% of OP poisonings were associated with acute pancreatitis, though this has not been the experience in other series.

R. Prognosis
In severe poisoning, death usually occurs within the first 24 hours if it is untreated. With nerve-agent poisoning, death may occur within minutes if untreated. Even with adequate respiratory support, intensive care, and specific treatment with atropine and oximes, the mortality rate is still high in severe poisonings. A delay in treatment can also lead to late and permanent neurologic sequelae. Most patients with minimal symptoms fully recover.

S. Special Concerns
Pregnant women should receive the same treatment as that given to other adults. Both atropine and pralidoxime are class C drugs in pregnancy. In the Tokyo subway attacks, 5 pregnant women were mildly poisoned, and all had normal babies without complications.

WASSALAM
Sumber : perkuliahan Ibu Sri Setyorini, 2008

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POWER, POLITIK DAN PENGARUH DALAM KEPERAWATAN

POWER, POLITIK DAN PENGARUH

Introduksi:

• Profesi keperawatan dilahirkan di AS pada waktu wanita mempunyai keterbatasan hukum/peraturan.
• Pada abad ke-19 adalah masa yang digambarkan sebagai kekuatan bukan politik, wanita dan kekuatan secara praktis merupakan kontradiksi.
• Pada abad ke-20 status dan peran wanita berubah sehingga memiliki status dan peran dari perawat, seperti ekonomi dan kekuatan sosial dari wanita telah meningkat maka perawat memiliki power.

Histori:

Power adalah satu kali pertimbangan yang hampir tabu dalam keperawatan. Dalam profesi akhir beberapa tahun, latihan kekuatan dipertimbangkan tidak cocok, tidak disukai oleh wanita dan tidak profesional. Banyak keputusan keperawatan tentang pendidikan keperawatan dan praktik yang sering dibuat oleh orang-orang di luar keperawatan (Ashley, 1976 cit Wise, Y, 1996)

Sejumlah trend sosial, teknologi, ilmiah, dan ekonomi telah membentuk keperawatan, para perawat dan kemampuan kami melakukan latihan kekuatan pada beberapa abad terakhir.
Seiring pergantian abad, para perawat harus memiliki rasa percaya diri dan ketrampilan dalam latihan kekuatan untuk menjamin pengembangan profesi yang berkelanjutan. Bagaimanapun, bahkan dalam profesi keperawatan kontemporer, ada perawat yang melihat diri mereka tidak berdaya dan tertindas yang menggambarkan aspek perilaku kelompok yang tertindas. Seperti banyak orang yang tertindas secara politis dan ekonomis, sejumlah perawat tetap bertahan bekerja dalam kelompok intra konflik (contoh, permusuhan) dan mereka menjaga jarak antara perawat yang satu dengan lainnya (contoh, kegagalan perawat untuk bergabung dengan organisasi profesional. (Robert, 1983).
Oleh karenanya perawat memiliki kebutuhan yang terus menerus untuk memperluas pengetahuan mereka tentang konsep power/kekuatan dan untuk mengembangkan ketrampilan mereka dalam latihan kekuatan. Menghindari campur tangan dalam politik keperawatan, baik di tempat kerja maupun pada profesi lainnya yang lebih luas, membatasi kekuatan individual perawat dan profesi sebagai kolektivitas yang utuh.

Politik

Sejumlah perawat masih menganggap tabu politik, memperlakukan politik seolah-olah adalah kata yang “kotor”. Politik dapat didefinisikan dalam banyak cara. Contoh : ilmu pemerintah, proses alokasi sumber daya, atau suatu proses interaksi formal manusia. Politik secara sederhana adalah suatu proses interaksi manusia dalam organisasi. Politik menyebar ke seluruh bagian organisasi, mencakup tempat kerja, legislatif, profesi dan bahkan dalam lingkungan keluarga. Aktivisme politis adalah format keterlibatan profesional kuat. Kalisch and Kalisch (1982) menguraikan empat tingkatan aktivisme atau partisipasi politik :

Apathetis : sikap masa bodoh  partisipasi yang kecil atau bahkan sama sekali tidak berpartisipasi.
Spektator : penonton/penyemangat.
Transitionals : transisi
Gladiator

Power

Power berasal dari bahasa Latin dari kata “ POTERRE” yang berarti “be able”. Power adalah kemampuan untuk mempengaruhi yang lainnya dalam pencapaian tujuan.Perawat sering memandang power seolah-olah adalah sesuatu tabu, merusak, dan bertentangan terhadap nilai keperawatan alamiah. Bagaimanapun, definisi di atas menunjukkan naturalitas esensial power pada keperawatan.
Hersey, Blanchard and Natemeyer (1979) menawarkan suatu formulasi berbasis kekuatan sosial. Mengidentifikasi tujuh basis power, yang sangat mudah dipahami sebagai sumber atau tipe kekuatan sosial. Para perawat sering menggunakan semua tipe ini, baik dalam manajemen maupun praktek klinis.

TUJUH TIPE SOFT SOCIAL POWER IMAGE

• Coercive power
• Reward power
• Expert power
• Legitimate power
• Referent power
• Information power
• Connection power

EMPOWERMENT/STRATEGI PENGEMBANGAN POWERFUL IMAGEStrategi 1. Pengembangan Powerful Image Self image : citra diri

• Grooming and dress : penampilan
• Speech : gaya bicara
• Body language : bahasa tubuh
• Belief in power as a positive force : Mempercayai bahwa power sebagai kekuatan positif.
• Belief in value of nursing to society : Mempercayai nilai-nilai keperawatan dalam masyarakat.
• Carrier commitment
• Continuing professional education : pendidikan profesi berkelanjutan.

2. Strategi Pesonal Power Tambahan Bersikap jujur

• Selalu ramah, sehingga membuat orang merasa senang.
• Bertanggung jawab atas kesalahan kita dan belajar dari kesalahan tersebut.
• Berani mengambil resiko
• Menerima kekelahan dan kemenangan dengan iklas.
• Berusaha bersikap tenang dalam menghadapi konflik dan kekacauan, hal tersebut merupakan kejadian normal kemanusiaan.
• Kondisi
• Memberikan kepercayaan kepada orang lain bilamana diperlukan.
• Mengembangkan kemampuan untuk membangun sikap kritis yang tepat.
• Belajar dari sikap kritis yang salah “rool off your back”
• Gunakan kartu bisnis ketika memperkenalkan diri anda pada orang baru dan kumpulkan kartu bisnia yang anda peroleh ketika melakukan networking.

3. Networking
Merupakan strategi power dan ketrampilan politis yang penting. Network/jaringan adalah suatu sistem kontak yang dikembangkan, dijaga dan dipertahanakan sebagai sumber informasi, penyedia saran dan dukungan moral (Schutzenhofer, 1992)

• Jaringan
• Organisasi Profesional

4. Mentoring
Pada beberapa tahun terakhir ini telah menjadi suatu daya penggerak dalam perawatan. Para mentor/penasihat berkompeten, para profesional berpengaralaman mengembangkan hubungan dengan orang baru untuk kepentingan penyediaan nasehat, dukungan, informasi dan umpan balik dalam rangka mendorong pengembangan diri individual (Houston and Marquis, 1988).

5. Goal Setting / Penentuan Sasaran

• Penentuan sasaran adalah strategi power yang lain
• Pengembangan ketrampilan
• Visi yang besar

LATIHAN POWER DAN PENGARUH DI TEMPAT KERJA
DAN ORGANISASI LAIN
Untuk dapat menggunakan pengaruh secara efektif dalam organisasi apapun, pemahaman mengenai bagaimana suatu sistem bekerja dan pengembangan organisasional strategis merupakan hal yang kritis. Pengembangan ide organisasional meliputi pengidentifikasian pembuat keputusan riil dan orang-orang yang memiliki tingkat pengaruh yang lebih tinggi dari para pembuat keputusan tersebut.

KOLLEGIALITAS DAN KOLABORASI

• Unity : kesatuan
• Collegiality
• Volunteerisme
• SIKAP PENGUASAAN
• Status Sosial
• PENGEMBANGAN KOALISI
• Negosiasi
• Negosiasi
• Persetujuan timbal balik
• Penawaran kolektif
  

Politik adalah seni mempengaruhi pengalokasian sumber daya (The art of influencing the allocation of scare resources) (Mason& Talbott, 1985)
Sumber daya tersebut meliputi : uang, waktu, personil, dan material. Politik berarti pengaruh terhadap kegiatan dan keputusan orang lain (Stevens, 1980)
Politik adalah suatu usaha keras interpersonal, yang meliputi ketrampilan komunikasi dan persuasi. Dengan kemampuan komunikasi akan menjadikan para perawat bertindak efektif dalam aktivitas politik.
Politik adalah suatu usaha kolektif.
Politik juga merupakan analisa dan perencanaan.
Nilai analisa politis yang baik mencakup suatu penilaian yang teliti/seksama.
Politik juga merupakan gambaran/citra. Apakah orang-orang berpikir anda dapat membuat suatu perubahan?
Apakah orang-orang berpikir perubahan tersebut berbahaya bagi mereka?
Apakah orang-orang percaya kepada anda?

Kerangka Tindakan Politik
Walaupun kebanyakan orang menghubungkan politik dengan pemerintah, hal ini berkaitan dengan masing-masing aspek kehidupan yang melibatkan kompetisi pengalokasian sumber daya atau pengaruh dalam pengambilan keputusan pengaruh, sedemikian sehingga menjadi relevan.
Politik di tempat kerja
Politik dalam Pemerintahan
Politik keuangan
Politik dalam organisasi
POLITIK dapat difenisikan sebagai prinsip yang mengarahkan tindakan pemerintah.
Politik dalam masyarakat
POWER DAN KEPEMIMPINAN
Prinsip power riil memusatkan power sebagai basis penghargaan, penghormatan, loyalitas dan komitmen. Pemusatan power tidaklah dipaksakan tetapi merupakan suatu ajakan (Covey, 1990).

Kepemimpinan power kemudian menjadi kapasitas untuk menciptakan order dari konflik, pertentangan, dan kekacauan.
Kepemimpinan power berasal dari kemampuan untuk menopang pengaruh proaktif, yang dipertahakan karena kepercayaan dari para pengikutnya dan sebagai respek kepada pemimpin untuk mengerjakan sesuatu yang dengan benar dan dengan alasan yang tepat. Sebagai pemimpin dalam bidang perawatan kesehatan, perawat harus memahami dan memilih perilaku yang mengaktifkan prinsip kepemimpinan terpusat.

Perilaku tersebut, meliputi :
Mengenali orang-orang
Bersikap terbuka
Mengetahui nilai-nilai dan visi anda
Mempertajam kompetensi interpersonal anda
Menggunakan power untuk memberi kemungkinan pada orang lain.
Memperluas pengaruh dan hubungan. Power terkadang berkembang di luar kebutuhan seseorang.

pertanyaan buat kita semua:
DISKUSI: Bagaimana perkembangan power dalam profesi keperawatan di Indonesia???

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