Tuesday, September 27, 2011

[sehat] Digest Number 16130

Messages In This Digest (25 Messages)

1a.
Stroke di otak kecil From: helen_gultom@yahoo.com
1b.
Re: Stroke di otak kecil From: novalina_sehat@yahoo.com
1c.
Re: Stroke di otak kecil From: Laksmi Purwitosari
1d.
Re: Stroke di otak kecil From: purnamawati.spak@cbn.net.id
1e.
Re: Stroke di otak kecil From: purnamawati.spak@cbn.net.id
1f.
Re: Stroke di otak kecil From: purnamawati.spak@cbn.net.id
1g.
Re: Stroke di otak kecil From: novalina_sehat@yahoo.com
1h.
Re: Stroke di otak kecil From: Laksmi Purwitosari
2a.
Info DSA yg RUM dan bisa Simultan di Hermina Bogor From: bundakirana86
2b.
Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor From: niken qinen
2c.
Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor From: bundakirana86
2d.
Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor From: 'Ita' Elisabeth Dianita
2e.
Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor From: niken qinen
2f.
Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor From: Lydia Amrina
3a.
Re: Kuning pada bayi 2 minggu From: pria ardhana
3b.
Re: Kuning pada bayi 2 minggu From: Pamelia Yulianto
3c.
Re: Kuning pada bayi 2 minggu From: yulianto
4a.
Re: Help...Lg Bingung Ulah si kk yg ga mau si dd nenen (dikasih asi) From: WienTha
5a.
KELAS PERSIAPAN KELAHIRAN & MENYUSUI BANDUNG 29-30 Oktober 2011 From: klasibdg@yahoo.com
6a.
Kelenjar Getah Bening From: nchy
7a.
Apa saja Vaksin yang bisa imunisasi simultan? From: zoe_getme@yahoo.com
7b.
Re: Apa saja Vaksin yang bisa imunisasi simultan? From: hanny.prasetyo@gmail.com
7c.
Re: Apa saja Vaksin yang bisa imunisasi simultan? From: andini.okto@yahoo.com
8.
Bls: [sehat] Apa saja Vaksin yang bisa imunisasi simultan? From: 'Ita' Elisabeth Dianita
9a.
Re: (Tanya) lanjutan - guyur air langsung ke kepala bisa bikin strok From: Laksmi Purwitosari

Messages

1a.

Stroke di otak kecil

Posted by: "helen_gultom@yahoo.com" helen_gultom@yahoo.com   helen_gultom

Tue Sep 27, 2011 12:54 am (PDT)



Dear smart parent n dokter, baru aja dpt kabar kl mertuaku kena stroke di otak kecil, apakah ada yg punya pengalaman ttg hal ini? boleh donk please di sharekan, diagnosa ini diperoleh setelah dilakukan MRI thdp pasien, atau ada yg sudi merekomendasikan dokter tuk konsul lebih lanjutTerima kasih n have a great day all :)

Helen Gultom
Sent from my BlackBerry® smartphone from Sinyal Bagus XL, Nyambung Teruuusss...!
1b.

Re: Stroke di otak kecil

Posted by: "novalina_sehat@yahoo.com" novalina_sehat@yahoo.com   novalina_sehat

Tue Sep 27, 2011 12:59 am (PDT)



Mom Helen,

Ke dokter eka aja, di siloam hospital karawaci.

SOL.

Regards,
Nova.

Sent from my BlackBerry® smartphone from Sinyal Bagus XL, Nyambung Teruuusss...!

-----Original Message-----
From: helen_gultom@yahoo.com
Sender: sehat@yahoogroups.com
Date: Tue, 27 Sep 2011 07:54:21
To: <sehat@yahoogroups.com>
Reply-To: sehat@yahoogroups.com
Subject: [sehat] Stroke di otak kecil

Dear smart parent n dokter, baru aja dpt kabar kl mertuaku kena stroke di otak kecil, apakah ada yg punya pengalaman ttg hal ini? boleh donk please di sharekan, diagnosa ini diperoleh setelah dilakukan MRI thdp pasien, atau ada yg sudi merekomendasikan dokter tuk konsul lebih lanjutTerima kasih n have a great day all :)

Helen Gultom
Sent from my BlackBerry® smartphone from Sinyal Bagus XL, Nyambung Teruuusss...!

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1c.

Re: Stroke di otak kecil

Posted by: "Laksmi Purwitosari" laksmipurwitosari@yahoo.com   laksmipurwitosari

Tue Sep 27, 2011 1:15 am (PDT)



Dear Mom Nova,

Stroke memiliki golden periode, perlu penanganan segera, stroke infark (sumbatan) dengan stroke hemoragik (perdarahan), akan berbeda penanganannya.

Stroke infark jika onsetnya <3 jam, akan bagus hasilnya jika diberikan rTPA (asal syaratpemberian rTPA terpenuhi), segeralah ke dokter spesialis saraf, karena ini kompetensi dokter spesialis saraf.

Jika stroke perdarahan, dan ada indikasi operasi maka ini wewenang dokter speaialis bedah saraf untuk menevakuasi perdarahannya.

Penanganan yang akan diberikan oleh dokter spesialis saraf adalah.
1. Penanganan terhadap sumbatannya dengan pemberian trombolitik dsb, dan menyelamatkan penumbra (daerah yang kurang teraliri darah)
2. Pengendalian faktor risiko, hipertensi, DM, yang berpengaruh terhadap outcome
3. Preventif sekunder, pencegahan stroke berikutnya
4. Neurorestorasi, restorasi untuk pengembalian fungsi motorik, sensorik maupun kognitif
5. Pencegahan dan penanganan komplikasi.

Pesan saya, segera ke dokter spesialis saraf sebelum 3jam dari kejadian, semakin cepat semakin baik hasilnya, mengurangi banyaknya sel otak yang mati, mencegah kecacatan.

Semoga berguna,
Laksmi Purwitosari
Neurolog RSUD Banyumas

[Non-text portions of this message have been removed]

1d.

Re: Stroke di otak kecil

Posted by: "purnamawati.spak@cbn.net.id" purnamawati.spak@cbn.net.id

Tue Sep 27, 2011 1:24 am (PDT)



So sorry to hear
Ada perdarahan? Hipertemsi tadinya?
Kalau perdarahan harus operasi (umumnya) - cmiiw

Wati
Patient Safety, first

1e.

Re: Stroke di otak kecil

Posted by: "purnamawati.spak@cbn.net.id" purnamawati.spak@cbn.net.id

Tue Sep 27, 2011 1:30 am (PDT)



So sorry to hear
Ada perdarahan? Hipertemsi tadinya?
Kalau perdarahan harus operasi (umumnya) - cmiiw

Wati
Patient Safety, first

1f.

Re: Stroke di otak kecil

Posted by: "purnamawati.spak@cbn.net.id" purnamawati.spak@cbn.net.id

Tue Sep 27, 2011 1:46 am (PDT)



So sorry to hear
Ada perdarahan? Hipertemsi tadinya?
Kalau perdarahan harus operasi (umumnya) - cmiiw

Wati
Patient Safety, first

1g.

Re: Stroke di otak kecil

Posted by: "novalina_sehat@yahoo.com" novalina_sehat@yahoo.com   novalina_sehat

Tue Sep 27, 2011 2:12 am (PDT)



Hi dr laksmi,

Setuju bangeet, mama ku kena stroke hemoragik, dlm wkt 1 jam sdh ditangani oleh dr eka, kena jam 10 pagi, sore jam 3 dioperasi oleh beliau dan tim nya. Alhamdulillah, pasca operasi langsung sadar, dan tidak ada kelumpuhan sama sekali, memori jg tdk ada yg berkurang, walau otak nya sempat bengkak.

Semoga membantu ya mom helen..

Regards,
Nova.
Sent from my BlackBerry® smartphone from Sinyal Bagus XL, Nyambung Teruuusss...!
1h.

Re: Stroke di otak kecil

Posted by: "Laksmi Purwitosari" laksmipurwitosari@yahoo.com   laksmipurwitosari

Tue Sep 27, 2011 2:41 am (PDT)



Dear All,
Tidak semua stroke perdarahan dilakukan tindakan operatif, dibawah ini dicantumkan indikasi dan bagaimana tindakan operatif pada stroke perdarahan.
Saya ambil dari emedicine.

http://emedicine.medscape.com/article/1163977-treatment#a1128

Consider nonsurgical management for patients with minimal neurological deficits or with intracerebral hemorrhage volumes less than 10 mL.
Consider surgery for patients with cerebellar hemorrhage greater than 3 cm, for patients with intracerebral hemorrhage associated with a structural vascular lesion, and for young patients with lobar hemorrhage. The common hypertensive hemorrhages in the basal ganglia have not been shown clearly to benefit from surgery, although case series with favorable outcomes after stereotactic needle evacuation or endoscopic drainage have been reported. In the past, standard craniotomy with evacuation of the hematoma did not appear to improve outcomes.
Other surgical considerations include the following:
Clinical course and timing
Patient's age and comorbid conditions
Etiology
Location of the hematoma
Mass effect and drainage patterns
Surgical approaches include the following:
Craniotomy and clot evacuation under direct visual guidance
Stereotactic aspiration with thrombolytic agents
Endoscopic evacuation
Dan untuk stroke infark, penanganannya seperti ini,

http://emedicine.medscape.com/article/1916852-treatment#aw2aab6b6b5

Multiple factors contribute to delays in seeking care for symptoms of stroke. Many strokes occur while patients are sleeping (also known as "wake-up" stroke) and are not discovered until the patient wakes. Stroke can leave some patients too incapacitated to call for help. Occasionally, a stroke goes unrecognized by the patient or their caregivers. (See Diagnostic Considerations).[30, 48]

The median time from symptom onset to ED presentation ranges from 4-24 hours in the United States.[18] Prehospital care providers are essential to timely stroke care. Course curricula for prehospital care providers are beginning to include more information on stroke than ever before. Through certification and ACLS instruction, as well as continuing medical education classes, prehospital care providers can remain current on stroke and promote stroke awareness in their own communities.

Physician and nursing staff involved in the care of patients who have had a stroke, in the ED and in the hospital, should participate in scheduled stroke education. This will help them to maintain the skills required to treat stroke patients effectively and to remain current on medical advances for all stroke types.

Establishing the time at which stroke symptoms first occurred is of paramount importance when considering patients for possible thrombolytic therapy. An essential question is, "When was the patient last seen to be normal?" It is advisable for emergency clinicians to rapidly enlist the assistance of family members or relatives to establish time of symptom onset and to identify other pertinent components of the patient's presentation history.

The central goal of therapy in acute ischemic stroke is to preserve the area of oligemia in the ischemic penumbra. The area of oligemia can be preserved by limiting the severity of ischemic injury (ie, neuronal protection) or by reducing the duration of ischemia (ie, restoring blood flow to the compromised area).

Recanalization strategies, including IV recombinant tissue-type plasminogen activator (rt-PA) and intra-arterial approaches, attempt to establish revascularization so that cells in the penumbra can be rescued before irreversible injury occurs. Restoring blood flow can mitigate the effects of ischemia only if performed quickly. Neuroprotective strategies are intended to preserve the penumbral tissues and to extend the time window for revascularization techniques; however, at the present time, no neuroprotective agents are available and approved for use in ischemic stroke.

The ischemic cascade offers many points at which such interventions could be attempted. Multiple strategies and interventions for blocking this cascade are currently under investigation. The timing of the restoration of cerebral blood flow appears to be a critical factor. Time may also prove to be a key factor in neuronal protection. It is expected that neuroprotective agents, which block the earliest stages of the ischemic cascade (eg, glutamate receptor antagonists, calcium channel blockers), will be effective only in the proximal phases of presentation.

Thrombolytics restore cerebral blood flow among some patients with acute ischemic stroke and may lead to improvement or resolution of neurologic deficits. Unfortunately, thrombolytics can also cause symptomatic intracranial hemorrhage, defined as radiographic evidence of hemorrhage combined with escalation of the NIHSS score by 4 or more points. Therefore, if the patient is a candidate for thrombolytic therapy, a thorough review of the inclusion and exclusion criteria must be performed. The exclusion criteria largely focus on identifying risk of hemorrhagic complication associated with thrombolytic use.

While streptokinase and rt-PA have been shown to benefit patients with acute MI, only alteplase (rt-PA) has been shown to benefit selected patients with acute ischemic stroke.

In May 2009, the American Heart Association/American Stroke Association (AHA/ASA) guidelines for the administration of rt-PA following acute stroke were revised to expand the window of treatment from 3 hours to 4.5 hours to provide more patients with an opportunity to receive benefit from this effective therapy.[4, 5, 54] Eligibility criteria for treatment in the 3-4.5 hours after acute stroke are similar to those for treatment at earlier time periods, with any 1 of the following additional exclusion criteria:

Patients older than 80 years
All patients taking oral anticoagulants are excluded regardless of the international normalized ratio (INR)
Patients with baseline NIHSS greater than 25
Patients with a history of stroke and diabetes
Caution should be exercised in the administration of rt-PA to patients with major deficits. Patients with evidence of low attenuation (edema or ischemia) involving more than a third of the distribution of the MCA on their initial NCCT scan are less likely to have favorable outcome after thrombolytic therapy and are thought to be at higher risk for hemorrhagic transformation of their ischemic stroke.[32] In addition to the risk of symptomatic intracranial hemorrhage (6.4% in the NINDS trial), other complications include potentially hemodynamically significant hemorrhage and angioedema or allergic reactions.[18]

Streptokinase has not been shown to benefit patients with acute ischemic stroke, but it has been shown to increase their risk of intracranial hemorrhage and death.

Researchers have studied the use of transcranial ultrasound as a means of assisting rt-PA in thrombolysis. By delivering mechanical pressure waves to the thrombus, ultrasound can theoretically expose more of its surface to the circulating thrombolytic agent. Further research is necessary to determine the exact role of transcranial Doppler ultrasound in assisting thrombolytics in acute ischemic stroke.

No human trials comparing the IV versus intra-arterial administration of thrombolytics exist. Theoretic advantages to intra-arterial delivery may include the possibility that higher local concentrations of thrombolytic would allow lower total doses of the agent (and theoretically less risk of systemic bleed) and a longer therapeutic window; however, the longer time to administration via the intra-arterial approach versus the IV approach may mitigate some of this advantage.

Antiplatelet Agents
The International Stroke Trial and the Chinese Acute Stroke Trial (CAST) demonstrated modest benefit from the use of aspirin in the setting of acute ischemic stroke. The International Stroke Trial randomized 20,000 patients within 24 hours of stroke onset to treatment with aspirin 325 mg, subcutaneous heparin in 2 different dose regimens, aspirin with heparin, and a placebo. The study found that aspirin therapy reduced the risk of early stroke recurrence.[55, 56]

CAST evaluated 21,106 patients and had a 4-week mortality reduction of 3.3% contrasted to 3.9%. A separate study also found that the combination of aspirin and lowâ€"molecular-weight heparin did not significantly improve outcomes.[57]

The early initiation of aspirin plus extended-release dipyridamole is likely to be as safe and effective in preventing disability as is later initiation after 7 days following stroke onset, according to a German study. The study’s authors attempted to assess the precise time to initiate dipyridamole following ischemic stroke or TIA.[58] Patients from 46 stroke units who presented with an NIHSS score of 20 or less were randomly assigned to receive aspirin 25 mg plus extended-release dipyridamole 200 mg bid (early dipyridamole regimen) (n=283) or aspirin monotherapy (100 mg once daily) for 7 days (n=260). Therapy in either group was initiated within 24 hours of stroke onset.

After 2 weeks, all patients received aspirin plus dipyridamole for up to 90 days. At day 90, 154 (56%) patients in the early dipyridamole group and 133 (52%) in the aspirin plus later dipyridamole group had no or mild disability (P=0.45).

Other antiplatelet agents are also under evaluation for use in the acute presentation of ischemic stroke. In a preliminary pilot study, abciximab was given within 6 hours to establish a safety profile. A trend toward improved outcome at 3 months for the treatment versus the placebo group was noted.[59] Further clinical trials are necessary.

Semoga bermanfaat,
Laksmi Purwitosari

[Non-text portions of this message have been removed]

2a.

Info DSA yg RUM dan bisa Simultan di Hermina Bogor

Posted by: "bundakirana86" bundakirana86@yahoo.com   bundakirana86

Tue Sep 27, 2011 1:03 am (PDT)



Dear Sps..

Saya berencana mau cacth up imunisasi MMR, Typhoid dan Hep A. Ada Sps yg punya info DSA yg RUM dan bisa simultan di Hermina Bogor? Terimakasih.

Lia

2b.

Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor

Posted by: "niken qinen" nikenqinen@gmail.com   qinen_q9

Tue Sep 27, 2011 1:11 am (PDT)



Dear mba Lia...
Maaf ga bisa kasih jawaban.
Cuma mau kasih usul, gimana kalo imunisasinya di Markas Sehat mba?
Jarang lho nakes mau simultan 3 suntikan, lha wong 2 suntikan aja
susah bujuk rayunya... :)

Salam,
-Niken-

On 9/27/11, bundakirana86 <bundakirana86@yahoo.com> wrote:
> Dear Sps..
>
> Saya berencana mau cacth up imunisasi MMR, Typhoid dan Hep A. Ada Sps yg
> punya info DSA yg RUM dan bisa simultan di Hermina Bogor? Terimakasih.
>
> Lia
>
>

2c.

Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor

Posted by: "bundakirana86" bundakirana86@yahoo.com   bundakirana86

Tue Sep 27, 2011 1:19 am (PDT)



Iya mba Niken... kemaren pas ikut pesat 2 Bekasi, dr.Endah menyarankan juga ke Markas Sehat saja... sekalian jalan2 dari Bogor.. hehe.. Ok deh, aku mau telp2 dulu ke Markas.. Thanks

Salam,
Lia

2d.

Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor

Posted by: "'Ita' Elisabeth Dianita" ita_sehat@yahoo.com   ita_sehat

Tue Sep 27, 2011 1:23 am (PDT)



Kalo ke markas, sms aja mbak. Kalo telp jarang diangkat, tp kalo sms pasti dibalas kok.

Sori gak potek


salam sehat,
ita (ibuke Saka & Ambar)
Sent from my BlackBerry®
powered by Sinyal Kuat INDOSAT

-----Original Message-----
From: "bundakirana86" <bundakirana86@yahoo.com>
Sender: sehat@yahoogroups.com
Date: Tue, 27 Sep 2011 08:19:04
To: <sehat@yahoogroups.com>
Reply-To: sehat@yahoogroups.com
Subject: [sehat] Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor

Iya mba Niken... kemaren pas ikut pesat 2 Bekasi, dr.Endah menyarankan juga ke Markas Sehat saja... sekalian jalan2 dari Bogor.. hehe.. Ok deh, aku mau telp2 dulu ke Markas.. Thanks

Salam,
Lia





[Non-text portions of this message have been removed]

2e.

Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor

Posted by: "niken qinen" nikenqinen@gmail.com   qinen_q9

Tue Sep 27, 2011 1:31 am (PDT)



Huahahaaa...mba Lia ikut pesat2 bekasi yaaa?
Saya juga ikutan lho mba?heheheeee...

Salam,
-Niken-

On 9/27/11, bundakirana86 <bundakirana86@yahoo.com> wrote:
> Iya mba Niken... kemaren pas ikut pesat 2 Bekasi, dr.Endah menyarankan juga
> ke Markas Sehat saja... sekalian jalan2 dari Bogor.. hehe.. Ok deh, aku mau
> telp2 dulu ke Markas.. Thanks
>
> Salam,
> Lia
>
>
>
>

2f.

Re: Info DSA yg RUM dan bisa Simultan di Hermina Bogor

Posted by: "Lydia Amrina" l_amrina@yahoo.com   l_amrina

Tue Sep 27, 2011 2:22 am (PDT)



mba lia, mbak niken ...

sepertinya emang belum ada deh mbak dsa di Hermina yg mau simultan, dsa anak saya juga gak mau.
Rencananya saya juga mau bawa anak saya ke Markas aja ( Alhamdulillah, suami mau mau aja nganterin )

o,ya, rencananya kita juga mau buat pesat-3 Bogor tahun depan, tp karena mba qq dan mba sita ( hai mbak ),
lagi persiapan mau lahiran, makanya belum jadi kopdar nih. ( maaf oot..he..he.. )

salam

Lydia
*Bunda Abyan & Lubna

[Non-text portions of this message have been removed]

3a.

Re: Kuning pada bayi 2 minggu

Posted by: "pria ardhana" priaardhana@yahoo.co.uk   priaardhana

Tue Sep 27, 2011 1:32 am (PDT)



Nambahin sharing, baby saya Waja (8 days, lahir Senin 19 September kemarin, SC) udah 2 hari ini di perina karena jaundice. Waktu masuk perina kadar bilirubinnya sampai 21,9. Sepulang dari RS usia 4 hari belum menunjukkan tanda kuning dan anaknya sangat aktif nenen, nangis dan gerakannya. Sampai-sampai ibunya kewalahan ASInya. Tapi usia 5 hari mulai kelihatan kuning dan lebih suka tidur, malas-malasan nenen. Suhu badan 39,5 dercel dibawa ke dokter cuma dikasih parcet ama disuruh jemur. Besoknya (sabtu malam) makin lemas dan kayaknya kena diare juga soalnya BABnya cair dan kuning, udah 5-6 kali dalam 5 jam. Anaknya tidur mulu sampek digelitikin gak respon, gak mau nenen. Langsung tengah malam saya bawa ke IGD dan mulai masuk perina.
Alhamdulillaah kemarin pagi bili-nya udah 18,5 dan pagi tadi 16,5. Dan ternyata kena diarenya itu karena ibunya minum jamu.., maklum dikasih ortu dari Solo...--"

Tadi saya baca di imel sebelumnya tentang breastfeeding jaundice, itu seperti apa ya..?? Apakah karena kurang nenennya, atau menyusuinya yang caranya kurang tepat..??
Kemudian, apakah ada hubungannya juga ama golongan darah? Golongan darah Waja itu O (+) sama seperti saya, sedangkan ibunya A (+).

Salam,
Ardhana

________________________________
From: nankrist <nankrist@yahoo.com>
To: sehat@yahoogroups.com
Sent: Tuesday, 27 September 2011, 14:01
Subject: [sehat] Re: Kuning pada bayi 2 minggu

 
Chitra,

Nara juga jaundice.
lahir 25 April 2011/Senin/3,02kg
27 April 2011/Rabu dicek bili nya 9, (sekian, lupa persisnya),
masih ok, jadi 28 April 2011/Kamis blh pulang.

Begitu pulang,
makin kuning, tidur trus, pipis jarang, gak mau nenen (begitu ketemu pd lgsg pules tnp ngenyot), jadi ngasi asiP pake sendok.
bbm dsa nya disuruh perbanyak asiP,
pantau trus frek pipis nya (saya bikin log book).

Senin 2 Mei 2011,
dicek bili lagi 14,6, masih oke.
berat baru 2,99 kg, blm balik ke berat lahir,
kuning baru sebatas setengah perut.

Syukur nya sjk Senin 2 Mei 2011 ini ud mau nenen.
sejak mau nenen, frek pipis nya lebih dari 6x.
Tapi kuning masih lanjut trus, sampe pupil mata yg putih juga kuning kyk kunyit.

Umur sebulan imunisasi,
masih kuning tp krn beratnya ud jadi 4,01 kg jadi dsa yakin ini breastmilk jaundice.
Disuruh nunggu sampe 2 bulan, kl blm hilang juga jaundice nya test isk.

Umur 2 bulan imunisasi,
sudah gak kuning, berat juga ud jadi 4,99 kg.

Kl saya baca2 di
http://www.klinikdrtiwi.com/article/normal-berat-badan-bayi-baru-lahir-akan-turun
http://www.ayahbunda.co.id/Artikel/Gizi+dan+Kesehatan/berat.badan.bayi.turun/001/001/1603/1/4
http://bidanku.com/index.php?/Tanda-Penyebab-Bayi-Tidak-Mendapat-Cukup-ASI

batas maksimal berat harus balik ke berat lahir itu 2 minggu/14 hari.
Saran saya, kl Chitra kuatir better ditimbang dulu (pake timbangan yg sama ya jgn beda2 timbangannya),
kl ud balik ke berat lahir, frek pipis oke,
saya rasa cmiiw gak perlu test2 darah segala.
kl pun masih kuatir better kontrol dulu ke dsa minta tolong liat kuningnya masih batas aman atau tdk (makin ke bawah kuningnya makin harus aware), jd jgn tll mudah test2 darah ke Alya, kasian.

Kuatir mah wajar,
saya juga kuatir, bbrp kali bbm Hilda, Lucy (mamanya Alena),
plus juga pernah bc sharing di milis ini ttg jaundice,
dan mereka matok breastmilk jaundice s.d 2 bulan mestinya hilang kuningnya.
dan emang Nara pas 2 bulan deh hilang kuningnya;p

Tapi jgn sampe kekuatiran kita bikin si anak jd korban under treatment, dan jgn sampe jg over treatment.

TSH harus dgn periksa darah deh.
g6pd gak tau.
browsing aj, Chit.

Pamelia,
kl kyk nya asi nya kurang,
setelah dinenenin disambung dgn suapin asiP pake sendok (jgn botol dot ya).
Kl asiP nya masih dikit dan Pamelia gak masalah dgn donor asiP,
cari aj donor asiP.
Pengalaman saya, dgn ada donor asiP, saya jd lbh tenang dan asi saya jadi lancar.

gut luck ya.
cy

--- In sehat@yahoogroups.com, chitra.tifanny@... wrote:
...> Salam,
> Chitra
> Mulai khawatir :(
> Sent from my AXIS Worry Free BlackBerry® smartphone

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3b.

Re: Kuning pada bayi 2 minggu

Posted by: "Pamelia Yulianto" hidupsehat.pam@gmail.com   pamelia_yulianto

Tue Sep 27, 2011 2:00 am (PDT)



Pak Ardhana
Breastfeeding jaundice itu 'kuning' akibat bayi krg asupan asi nya

Kl breastmilk jaundice itu 'kuning' krn ada zat dlm asi yg memblok pemecahan bilirubin cmiiw

Ringkasnya begitu

Di atas usia 72 jam mmg harus PT kl bili di atas 20. Smg anaknya lekas baik keadaannya

- p a m e l i a -
"Stop Judging, Start Supporting"

Powered by my children's existance

3c.

Re: Kuning pada bayi 2 minggu

Posted by: "yulianto" yuliantosk@gmail.com   anto_sk

Tue Sep 27, 2011 3:03 am (PDT)



dear smart parents,

bila kuning >2 mg, disarankan periksa dokter (riwayat kelahira,
pertumbuhan dan pemeriksaan fisik) dan diperiksa pemeriksaan penunjang
yang mungkin diperlukan (mis : bilirubin direk dan indirek, urine )
untuk sampai diagnosis jaundice fisiologis, atau breastmilk jaundice
melalui rangkaian algoritma dahulu.

http://www.rch.org.au/clinicalguide/cpg.cfm?doc_id=5282

salam,
-anto-

4a.

Re: Help...Lg Bingung Ulah si kk yg ga mau si dd nenen (dikasih asi)

Posted by: "WienTha" Muhammad.athaya@gmail.com

Tue Sep 27, 2011 2:16 am (PDT)



Wah ini sama bgt ma sy mba, msh blm berhasil ngasih pengertian ma kk(27bl) buat gantin ma adiknya(12wk), sampe skrg kknya msh ngambek kalo adenya minta nyusu,kalo ditandem jg yg ada adiknya ditendang2/dijawil2,pdhl dulu wkt sy hamil kk smpt on off nyusunya.
Paling kalo adenya udah nangis laper/pengen nyusu minta tlg suami buat bawa pergi dl, atau kalo lg ga ada siapa2 sblm adiknya laper(kan biasanya jadwal nyusunya on time,udah ketebak jam2 lapernya) kknya dl yg minta nyusu soalnya kknya udah apal gesture adenya pengen nyusu,kalo ga kknya sy sogok pake eskrim,lumayan lupa nyusu kalo pake eskrim yg ada kantong jebol :D

Br,
Wiwinn
*msh blm melewati jeritan+nangis ngeraung2 AthArka rebutan nen*
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5a.

KELAS PERSIAPAN KELAHIRAN & MENYUSUI BANDUNG 29-30 Oktober 2011

Posted by: "klasibdg@yahoo.com" klasibdg@yahoo.com   klasibdg

Tue Sep 27, 2011 2:17 am (PDT)



Dear Smart Parents,

Sadarkah kita bahwa ASI, TataLaksana Kehamilan & Kelahiran dan juga Penangananan Bayi Baru Lahir ternyata sangat berkaitan? Alangkah baiknya jika kesadaran itu kita munculkan sekarang, sebelum tugas sebagai orangtua kita jalani.

Yuk, maksimalkan setiap usaha dalam memberikan yang terbaik dan juga benar sesuai tata laksana kepada buah hati kita.

Klub Peduli ASI YOP hadir untuk memfasilitasi orangtua menjalani salah satu perannya dengan menyediakan informasi seputar persiapan kelahiran dan menyusui serta media support group orangtua peduli ASI.

KELAS PERSIAPAN KELAHIRAN & MENYUSUI BANDUNG

Pelaksanaan :Hari : Sabtu , 29 Okt  dan Minggu, 30 Okt 2011
Waktu : Pukul 09:00 â€" 14:00 WIB
Tempat : ‎​Koffielosophy.
Jl.Anggrek 36 Bandung.
Tel : (022) ‎​7234227

Materi di dalam Kelas Persiapan Kelahiran & Menyusui ini adalah semua hal yang penting diketahui setiap orangtua/calon orangtua, atau siapapun yang berhubungan erat dengan pengasuhan anak. 

Kelas ini dibagi menjadi 2 Sesi.
Sesi I: ASI dan Seputar Kehamilan (29 Okt 2011)
- Inisiasi Menyusu Dini (IMD)
- Keuntungan ASI
- Posisi Menyusui (latch-on)
- Prinsip dasar
- Persiapan menjelang kelahiran
- Hamil ≠ sakit, suplemen, makanan, mitos-mitos
- Indikasi caesar
- Perawatanbayi baru lahir
- Kegawatdaruratan pada kehamilan 

Sesi II: Masalah-masalah Menyusui dan Pasca Kehamilan (30 Okt 2011)
- Memerah ASI
- ASI Perah dan Penyimpanannya
- Mastitis, Inverted Nipple , Cracked Nipple
- Nursing Strike
- Self Weaning
- Hal-hal penting dalam check-up bayi sampai dengan 6 bulan.
- Kecukupan ASI dari segi nutrisi, terutama ASI perah
- Mengenali dan mencegah gagal tumbuh pada neonatus
- Jaundice
- Cara memantau pertumbuhan dengan kurva pertumbuhan
- Cara memantau perkembangan dan milestones
- Prinsip Rational Use of Medicines (RUM) 

Materi akan disampaikan oleh dokter dan TIM ASI YOP disertai dengan praktek, pemutaran video dan diskusi grup.

Melalui kelas ASI ini diharapkan peserta akan memperoleh pengetahuan yang komprehensif mengenai persiapan kelahiran dan menyusui sekaligus mendapatkan kelompok support yang bisa saling mendukung dan berbagi.

Biaya Rp 130.000,- per orang, atau Rp. 230.000 untuk pasangan. Biaya ini sudah termasuk handout materi, CDmateri, snack dan makan siang. Bagi yang berminat menjadi peserta, silakan mengisi dan mengirimkan formulir pendaftaran di bawah ini kirim ke
klasibdg@yahoo.com dengan Subject: “Kelas Persiapan Kelahiran & Menyusui”.

Untuk informasi lebih lanjut dapat hubungi : Monika . Tlp : 081320678893

http://klasibandung.com/kelas-persiapan-kelahiran-dan-menyusui-29-30-oktober-2011

Tempat Terbatas!
Salam SEHAT, Tim KLASI YOP (Bandung) Proudly Supports Breastfeeding

FORMULIR PENDAFTARAN KELAS PERSIAPAN KELAHIRAN &MENYUSUI 29-30 Oktober 2011

Nama Lengkap 1 :_____ (diisi oleh peserta perorangan)

Nama Lengkap 2 :_____ (diisi apabila mengajak pasangan)

Alamat :_____

Telepon/HP :_____

Email aktif :_____ (untuk mengingatkan peserta)

Jumlah anak:_____

Usia anak:_____ bulan/tahun

Due Date (tanggal perkiraan kelahiran): ____ (jika sedang hamil)

Ibu bekerja di luar rumah:_____ (ya/tidak)

Apakah sudah pernah mengetahui ilmu tentang laktasi / menyusui?_____ (ya/tidak)

Jika ya, dari mana sumbernya?_____ (buku/milis/tenaga kesehatan/lainnya …)

Apakah sudah pernah menyusui?_____ (ya/tidak)

Jika ya, apakah berhasil melakukan ASI eksklusif?_____

Permasalahan yang sedang atau pernah dihadapi dalam proses menyusui:_____

Apa yang diharapkan dari kelas Persiapan Kelahiran dan Menyusui yang akan

diikuti?_____

Salam SEHAT,

Tim KLASI YOP (Bandung) Proudly Supports Breastfeeding

http://klasibandung.com/

klasibdg@yahoo.com

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6a.

Kelenjar Getah Bening

Posted by: "nchy" nchy@yahoo.com   nchy

Tue Sep 27, 2011 2:35 am (PDT)



Dear All,

Baru saja saya ronsen dada, dengan hasil :
CTR < 50 %
PULMO : Infiltrat di apex kanan
Sinus dan diafragma normal

Kira2 artinya apa ya?
Saya jelaskan kronologisnya knp saya ronsen,
Sdh seminggu lebih, bdan saya, lemas, meriang tdk jelas, badan ngilu2, dan hari kamis kmrin, tgl 22 sept, timbul benjolan kelenjar getah bening, didkt tulang dada atas yg spt mangkok (namanya saya lupa, td sdh spt browsing) , akhirnya dokter dikantor merujuk utk ronsen, dan cek lab jg, dikhawatirkan sy terkena TB.

Terima kasih

Leslie

7a.

Apa saja Vaksin yang bisa imunisasi simultan?

Posted by: "zoe_getme@yahoo.com" zoe_getme@yahoo.com   zoe_getme

Tue Sep 27, 2011 2:39 am (PDT)



Dear all smart moms,
Mohon infonya dong "gandengan" vaksin apa saja yg bisa imunisasi simultan utk anak 1 thn ke atas dan dilakukan saat usia brp tahun?maaf sy ga bisa ubek2 arsip milis krn entah knp browsernya eror.trims ya moms

Bunda etzel
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7b.

Re: Apa saja Vaksin yang bisa imunisasi simultan?

Posted by: "hanny.prasetyo@gmail.com" hanny.prasetyo@gmail.com   nyai_loh

Tue Sep 27, 2011 2:44 am (PDT)



Bunda Etzel,




Pada dasarnya semua vaksin bisa simultan kok mbak. Jd kalo misalnya sekarang anaknya bunda umur 12 bulan, dan imunisasi sebelumnya sudah lengkap en komplit semua, berarti di umur 12 bulan jadwal imunisasi nya adlh varicela simultan dengan hepatitis A. Trus umur 15 bulan MMR simultan dengan varicela. Nanti 18 bulan DPT dan HiB combo.




Cheers,




Hanny Prasetyo
Sent from my cuteBerry®
7c.

Re: Apa saja Vaksin yang bisa imunisasi simultan?

Posted by: "andini.okto@yahoo.com" andini.okto@yahoo.com   andini.okto

Tue Sep 27, 2011 2:51 am (PDT)



Mba hanny,
Kemarin saya baru vaksin DPaT di combo dgn Hib, lebih bagus lagi sebenernya kalo simultan yah? Trus bulan dpn dijadwalin IPD, tp bisa ga kalo saya memilih Hep B3, HiB, sama DPT secara simultan?

Thank u...
Sent from my BlackBerry® smartphone from Sinyal Bagus XL, Nyambung Teruuusss...!
8.

Bls: [sehat] Apa saja Vaksin yang bisa imunisasi simultan?

Posted by: "'Ita' Elisabeth Dianita" ita_sehat@yahoo.com   ita_sehat

Tue Sep 27, 2011 2:46 am (PDT)



Mom,
Semua vaksin bisa disimultan kok. Tinggal pinter2nya aja ber tenggo sama dokternya..


salam sehat,
ita (ibuke Saka & Ambar)
Sent from my BlackBerry®
powered by Sinyal Kuat INDOSAT
9a.

Re: (Tanya) lanjutan - guyur air langsung ke kepala bisa bikin strok

Posted by: "Laksmi Purwitosari" laksmipurwitosari@yahoo.com   laksmipurwitosari

Tue Sep 27, 2011 2:48 am (PDT)



Dear Mba lilis adn SP semua,

Och ternyata yang dimaksud heat stroke toch, kalo di Indonesia kayaknya sepanas panasnya udara gak pernah nyampe 40 derajat.

Heat stroke beda dengan stroke (gangguan peredaran darah otak) yang sering kita bicarakan.

Heat stroke artinya serangan panas.

Silahkan mampir disini http://emedicine.medscape.com/article/166320-clinical

Heat illness may be viewed as a continuum of illnesses relating to the body's inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (ie, prickly heat), heat cramps, and tetany, as well as heat syncope and heat exhaustion. Heatstroke is the most severe form of the heat-related illnesses and is defined as a body temperature higher than 41.1°C (106°F) associated with neurologic dysfunction.

Two forms of heatstroke exist. Exertional heatstroke (EHS) generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment. Classic nonexertional heatstroke (NEHS) more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons. Classic NEHS occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years. Both types of heatstroke are associated with a high morbidity and mortality, especially when therapy is delayed.

With the influence of global warming, it is predicted that the incidence of heatstroke cases and fatalities will also become more prevalent. Because behavioral responses are important in the management of temperature elevations, heatstroke may be entirely preventable.

Pathophysiology
Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body's mechanisms of heat loss, the body temperature rises, and a major heat illness ensues. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death. The exact temperature at which cardiovascular collapse occurs varies among individuals because coexisting disease, drugs, and other factors may contribute to or delay organ dysfunction. Full recovery has been observed in patients with temperatures as high as 46°C, and death has occurred in patients with much lower temperatures. Temperatures exceeding 106°F or 41.1°C generally are catastrophic and require immediate aggressive therapy.

Heat may be acquired by a number of different mechanisms. At rest, basal metabolic processes produce approximately 100 kcal of heat per hour or 1 kcal/kg/h. These reactions can raise the body temperature by 1.1°C/h if the heat dissipating mechanisms are nonfunctional. Strenuous physical activity can increase heat production more than 10-fold to levels exceeding 1000 kcal/h. Similarly, fever, shivering, tremors, convulsions, thyrotoxicosis,sepsis, sympathomimetic drugs, and many other conditions can increase heat production, thereby increasing body temperature.

The body also can acquire heat from the environment through some of the same mechanisms involved in heat dissipation, including conduction, convection, and radiation. These mechanisms occur at the level of the skin and require a properly functioning skin surface, sweat glands, and autonomic nervous system, but they also may be manipulated by behavioral responses. Conduction refers to the transfer of heat between 2 surfaces with differing temperatures that are in direct contact. Convection refers to the transfer of heat between the body's surface and a gas or fluid with a differing temperature. Radiation refers to the transfer of heat in the form of electromagnetic waves between the body and its surroundings. The efficacy of radiation as a means of heat transfer depends on the angle of the sun, the season, and the presence of clouds, among other factors. For example, during summer, lying down in the sun can result in a heat gain of up to 150 kcal/h.

Under normal physiologic conditions, heat gain is counteracted by a commensurate heat loss. This is orchestrated by the hypothalamus, which functions as a thermostat, guiding the body through mechanisms of heat production or heat dissipation, thereby maintaining the body temperature at a constant physiologic range. In a simplified model, thermosensors located in the skin, muscles, and spinal cord send information regarding the core body temperature to the anterior hypothalamus, where the information is processed and appropriate physiologic and behavioral responses are generated. Physiologic responses to heat include an increase in the blood flow to the skin (as much as 8 L/min), which is the major heat-dissipating organ; dilatation of the peripheral venous system; and stimulation of the eccrine sweat glands to produce more sweat.

As the major heat-dissipating organ, the skin can transfer heat to the environment through conduction, convection, radiation, and evaporation. Radiation is the most important mechanism of heat transfer at rest in temperate climates, accounting for 65% of heat dissipation, and it can be modulated by clothing. At high ambient temperatures, conduction becomes the least important of the 4 mechanisms, while evaporation, which refers to the conversion of a liquid to a gaseous phase, becomes the most effective mechanism of heat loss.

The efficacy of evaporation as a mechanism of heat loss depends on the condition of the skin and sweat glands, the function of the lung, ambient temperature, humidity, air movement, and whether or not the person is acclimated to the high temperatures. For example, evaporation does not occur when the ambient humidity exceeds 75% and is less effective in individuals who are not acclimated. Nonacclimated individuals can only produce 1 L of sweat per hour, which only dispels 580 kcal of heat per hour, whereas acclimated individuals can produce 2-3 L of sweat per hour and can dissipate as much as 1740 kcal of heat per hour through evaporation. Acclimatization to hot environments usually occurs over 7-10 days and enables individuals to reduce the threshold at which sweating begins, increase sweat production, and increase the capacity of the sweat glands to reabsorb sweat sodium, thereby increasing the efficiency of heat dissipation.

When heat gain exceeds heat loss, the body temperature rises. Classic heatstroke occurs in individuals who lack the capacity to modulate the environment (eg, infants, elderly individuals, individuals who are chronically ill). Furthermore, elderly persons and patients with diminished cardiovascular reserves are unable to generate and cope with the physiologic responses to heat stress and, therefore, are at risk of heatstroke. Patients with skin diseases and those taking medications that interfere with sweating also are at increased risk for heatstroke because they are unable to dissipate heat adequately. Additionally, the redistribution of blood flow to the periphery, coupled with the loss of fluids and electrolytes in sweat, place a tremendous burden on the heart, which ultimately may fail to maintain an adequate cardiac output, leading to additional morbidity and mortality.

Factors that interfere with heat dissipation include an inadequate intravascular volume, cardiovascular dysfunction, and abnormal skin. Additionally, high ambient temperatures, high ambient humidity, and many drugs can interfere with heat dissipation, resulting in a major heat illness. Similarly, hypothalamic dysfunction may alter temperature regulation and may result in an unchecked rise in temperature and heat illness.

On a cellular level, many theories have been hypothesized and clinically scrutinized. Generally speaking, heat directly influences the body on a cellular level by interfering with cellular processes along with denaturing proteins and cellular membranes. In turn, an array of inflammatory cytokines and heat shock proteins (HSPs) (HSP-70 in particular, which allows the cell to endure the stress of its environment), are produced. If the stress continues, the cell will succumb to the stress (apoptosis) and die. Certain preexisting factors, such as age, genetic makeup, and the nonacclimatized individual, may allow progression from heat stress to heatstroke, multiorgan-dysfunction syndrome (MODS), and ultimately death. Progression to heatstroke may occur through thermoregulatory failure, an amplified acute-phase response, and alterations in the expression of HSPs.

An index used by some, including the American College of Sports Medicine, is the Wet Bulb Globe Temperature (WBGT). It is an environmental heat stress index used to evaluate the risk of heat of heat-related illness on an individual. It is calculated using 3 parameters: temperature, humidity, and radiant heat. There is low risk if the WBGT is < 65 º F, moderate risk if it is between 65-73 º F, high risk if between 73-82 º F, and very high risk >82 º F.

Infants, children, and elderly persons have a higher incidence of heatstroke than young, healthy adults.

Infants and children are at risk for heat illness due to inefficient sweating, a higher metabolic rate, and their inability to care for themselves and control their environment.

Elderly persons also are at increased risk for heat-related illnesses because of their limited cardiovascular reserves, preexisting illness, and use of many medications that may affect their volume status or sweating ability. In addition, elderly people who are unable to care for themselves are at increased risk for heatstroke, presumably because of their inability to control their environment.

EHS is the second most common cause of death among high school athletes, surpassed only by spinal cord injury. Lack of acclimatization is a major risk factor for EHS in young adults.

Exertional heatstroke
EHS is characterized by hyperthermia, diaphoresis, and an altered sensorium, which may manifest suddenly during extreme physical exertion in a hot environment.

A number of symptoms (eg, abdominal and muscular cramping, nausea, vomiting, diarrhea, headache, dizziness, dyspnea, weakness) commonly precede the heatstroke and may remain unrecognized. Syncope and loss of consciousness also are observed commonly before the development of EHS.

EHS commonly is observed in young, healthy individuals (eg, athletes, firefighters, military personnel) who, while engaging in strenuous physical activity, overwhelm their thermoregulatory system and become hyperthermic. Because their ability to sweat remains intact, patients with EHS are able to cool down after cessation of physical activity and may present for medical attention with temperatures well below 41°C. Despite education and preventative measures, EHS is still the third most common cause of death among high school students.

Risk factors that increase the likelihood of heat-related illnesses include a preceding viral infection, dehydration, fatigue, obesity, lack of sleep, poor physical fitness, and lack of acclimatization. Although lack of acclimatization is a risk factor for heatstroke, EHS also can occur in acclimatized individuals who are subjected to moderately intense exercise.

EHS also may occur because of increased motor activity due to drug use, such as cocaine and amphetamines, and as a complication of status epilepticus.

Nonexertional heatstroke
Classic NEHS is characterized by hyperthermia, anhidrosis, and an altered sensorium, which develop suddenly after a period of prolonged elevations in ambient temperatures (ie, heat waves). Core body temperatures greater than 41°C are diagnostic, although heatstroke may occur with lower core body temperatures.

Numerous CNS symptoms, ranging from minor irritability to delusions, irrational behavior, hallucinations, and coma have been described.

Anhidrosis due to cessation of sweating is a late occurrence in heatstroke and may not be present when patients are examined.

Other CNS symptoms include hallucinations, seizures, cranial nerve abnormalities, cerebellar dysfunction, and opisthotonos.

Patients with NEHS initially may exhibit a hyperdynamic circulatory state, but, in severe cases, hypodynamic states may be noted.

Classic heatstroke most commonly occurs during episodes of prolonged elevations in ambient temperatures. It affects people who are unable to control their environment and water intake (eg, infants, elderly persons, individuals who are chronically ill), people with reduced cardiovascular reserve (eg, elderly persons, patients with chronic cardiovascular illnesses), and people with impaired sweating (eg, patients with skin disease, patients ingesting anticholinergic and psychiatric drugs). In addition, infants have an immature thermoregulatory system, and elderly persons have impaired perception of changes in body and ambient temperatures and a decreased capacity to sweat.

Laksmi Purwitosari

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