kuliah tiroid
TRANSCRIPT
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Epidemiology & Etiology of Goiter
Dr. Lesap Heru Farolan SpB
Bagian Bedah RSUD Sidoarjo
SCHOOL OF HEAD AND NECK SURGERY FOR GENERAL SURGEON
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THYROID GLAND
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Thyroid Gland
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Regulating Anterior Pituitary
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Thyroid (cont)• Regulates basal metabolic rate• Improves cardiac contractility• Increases the gain of catecholamines• Increases bowel motility• Increases speed of muscle contraction• Decreases cholesterol (LDL)• Required for proper fetal neural growth
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Thyroid Physiology
• Uptake of Iodine by thyroid• Coupling of Iodine to Thyroglobulin• Storage of MIT / DIT in follicular space• Re-absorption of MIT / DIT• Formation of T3, T4 from MIT / DIT
• Release of T3, T4 into serum
• Breakdown of T3, T4 with release of Iodine
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Iodine states
• Normal Thyroid
• Inactive Thyroid
• Hyperactive Thyroid
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DEFINITION OF GOITERGoiter = struma = gondok
• A goiter is an enlarged thyroid gland. (lateral lobes greater than the terminal phalanges of the thumbs )
• may be diffuse or nodular
• Function may be normal, overactive (toxic goiter), or underactive (hypothyroid goiter).
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• Mortality/Morbidity Most goiters are benign, causing only cosmetic
disfigurement. Morbidity / mortality may result from -
compression - thyroid cancer - hyper or hypo thyroidism • Race No racial predilection exists• Sex Female-to-male ratio is 4:1. Less frequent in men, but more likely to be malignant.
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Causes of Goiter• Iodine deficiency • Autoimmune thyroiditis• Excess iodine (Wolff-Chaikoff effect)• Goitrogens • Stimulation of TSH receptors• Inborn errors of metabolism• Exposure to radiation • Deposition diseases • Thyroid hormone resistance • Subacute thyroiditis (de Quervain thyroiditis) • Silent thyroiditis • Riedel thyroiditis • Infectious agents • Granulomatous disease • Thyroid malignancy
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Causes of Goiter• Endemic goiter
– Caused by dietary deficiency of Iodide– Increased TSH stimulates gland growth– Also results in cretinism
• Goiter in developed countries– Hashimoto’s thryoiditis– Subacute thyroiditis
• Other causes– Excess Iodide (Amiodarone, Kelp, Lithium)– Adenoma, Malignancy– Genetic / Familial hormone synthesis defects
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Iodine deficiency (ID)• Thyroid hormones, thyroxin and
triiodothyronine (T4 &T3) contain 4 and 3 iodine atoms, respectively.
• Adults need 100-150 g/daily
• Children require less in total, but more per Kg body weight
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Iodine deficiency: consequences
The following are affected by iodine deficiency:
• Thyroid size; enlargement (goiter)
• Mental and neuromotor abilities
• Reproductive results
• Physical growth
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Consequences of ID Neuromotor and cognitive impairment are the
most important effects of ID Where ID is severe and mothers have severe
ID, endemic cretinism is found results include:
cognitive impairment learning, speech deficits psychomotor problems
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Consequences of ID Reproductive effects
Rates of reproduction may be lower Fetal and postnatal survival lower Motor performance in childhood impaired
Iodine correction in a group of Chinese communities doubled the neonatal survival rates
Other effects
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Consequences of ID Economic effects
no clear evidence available ID results in lowered energy, lowered
learning capacity, increase burden of fetal and postnatal mortality probably interfering with social development
Physical growth Hypo-thyrodism retards growth and
development
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TumorTumor
1.Organ apa?
3.Adakah struktur sekitar yang terkena ?
2. Proses patologis yang terjadi ?
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1. Organ apa ? Kulit : Epidermis : - hiperkeratosis; scc - basalioma (bcc) Dermis : - fibroma; fibrosarkoma - lipoma - neurinoma; schwanoma; neurofibroma - hemangioma - lymphangioma - adenoma - nevus
Jaringan lunak subkutisKelenjar getah bening regional
Organ spesifik (kelenjar tiroid, liur; muskulus, dsb.)Tulang ( Mandibula; maksila)
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2. Proses patologi yang terjadi
I. Hiperplasi/hipertrofi
II. Inflamasi/infeksi
III. Neoplasma
IV. Kelainan kongenital
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3. Adakah gangguan pada organ/struktur sekitar
Gangguan fungsi
Invasi (fixed; peau de orange)
Nyeri
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STRUMA : Pembesaran kelenjar tiroid1. Hipertrofi dan hiperplasi
Kompensasi akibat Tiroid dipacu lebih berat untuk bekerja menghasilkan hormon : defisiensi Jodium, masa pertumbuhan, gravid,
2. Inflamasi / Infeksi- Tiroiditis akut-Tiroiditis Sub akut ( de quervain )- Tiroiditis Kronis ( hashimoto )
3 NeoplasmaJinak ( adenoma )Ganas ( adenokarsinoma )
4. Kongenital– 1 Tiroid ektopik : Tiroid terletak ditempat lain, gangguan migrasi tiroid– 2 Kista / fistula duktus tiroglosus : Gagalnya obliterasi duktus tiroglosus
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Struma
Morfologi
Fungsi
Histopatologi (Ca)
difusa
nodosa
uninodosa
hipotiroid
eutiroid
hipertiroid
Papiler Folikuler Meduler Anaplastik
multinodosa
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THE ROLE OF SURGICAL TREATMENT IN GOITRE
SCHOOL OF HEAD AND NECK SURGERY
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INDIKASI OPERASI STRUMA
1. STRUMA UNINODOSA CURIGA GANAS2. STRUMA DENGAN GANGGUAN3. BASEDOW GAGAL DGN TX MEDIKA MENTOSA4. KOSMETIS
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1. STRUMA UNINODOSA NONTOKSIKA CURIGA GANAS
STRUMA UNINODOSA NON TOKSIKA
SUB TOTAL LOBEKTOMI
VC JINAK VC GANAS
VC GANAS PROGNOSTIK BAIK
VC GANAS PROGNOSTIK JELEK
TOTAL LOBECTOMI
SUBTOTAL LOBEKTOMI
TOTAL TIROIDEKTOMI
PATOLOGI ANATOMI
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2. STRUMA DENGAN GANGGUAN
Menekan jalan nafas, baik benign maupun ca thyroid
-Thiroiditis chronis (Riedel’s Struma; Hashimoto ds)
isthmectomi -Anaplastik Ca Thyroid trakeostomi Menekan saluran makan -Operasi Subtotal tiroidektomi -Operasi Total tiroidektomi Retrosternal Goiter (gangguan nafas dan
gangguan sal. Pencernaan) -Opreasi Total Tiroidektomi Gangguan “psikis” curiga keganasan;
kosmetis
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3. BASEDOW GAGAL DGN TX MEDIKAMENTOSA. BASEDOW YG SUDAH MENIMBULKAN GANGGUAN.
-STRUMA BESAR -EXOPHTHALMOS -CARDIOLOGIS
Segera siapkan (“crash program”) untuk operasi,
setelah euthyroid lakukan lugolisasi (10-14 hari)
kemudian operasi subtotal tiroidektomi
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4. KOSMETIS
• Struma yang besar dan dirasa mengganggu penampilan penderita Struma kecil (<4 cm),
endoskopic thyroidectomy minimally access thyroidectomy
• Struma besar, tiroidektomi konvensional
• Lakukan pemeriksaan PA, evaluasi dan follow up sehingga tidak terjadi kekambuhan dengan terapi hormonal.
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GRAVES DISEASESTRUMA BASEDOW
STRUMA DIFUSA TOKSIK
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PHYSIOLOGY OF THYROID HORMONE
hypothalamus releases TRH↓
stimulates release of TSH from anterior pituitary↓
binds to receptors in the thyroid gland↓
controls production and release of T3 and T4↓
inhibit further release of TSH
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12
3
4
5
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PATHOGENESIS OF GRAVES’ DISEASE
Immunology of thyroid glandTSH receptor-stimulating antibodiesAnother thyroid antibody in Graves’ diseaseImmune mechanism on the pathogenesis of
Graves’ diseasePathogenesis of ophthalmopathy and
dermopathy in Graves’disease
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• Activate both the adenyl cyclase-cAMP and the protein kinase C-phosphoinositide signal transduction systems →
a. release of thyroid hormone and thyroglobulin b. stimulation of iodine uptake and organification c. protein synthesis d. thyroid follicular-cell growth
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TSH receptor-stimulating antibodies
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Immunology of thyroid gland
• The thyroid gland is a primary site of thyroid autoantibody production
• The B cells that accumulate within the thyroid gland of patients with Graves’ hyperthyroidism have greater basal immunoglobulin secretion than peripheral blood B cells (indicative of an activated state)
• These thyroid B cells also may secrete thyroid autoantibodies spontaneously (in vitro)
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TSH receptor-stimulating antibodies
• In pts with Graves’ hyperthyroidism, the thyroid gland is no longer under the control of pituitary TSH but is continuously stimulated by antibodies with TSH-like activity
• Antibodies that bind to the TSH receptor may or may not initiate an intracellular signal transduction process :
a. TSH receptor-stimulating antibodies b. TSH receptor-blocking antibodies
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DIAGNOSIS • Tanda tanda KLINIS hipertiroidi :
- takikardi (nadi ≥100) - nervous (threshold sistem syaraf ↓) - diare (peristaltik usus ↑) - cepat payah, cepat lapar, makan banyak tapi - badan tetap kurus (pulsus celler) - kulit palmar basah dan hangat - tremor - eksoptalmus - BMR > 10• LABORATORIUM - T3 dan T4 tinggi - TSH rendah
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Basal metabolisme rate
• Secara empiris klinis bisa kita hitung dengan menggunakan rumus Reed :
BMR = 0,72{ 0,72(s-d)} s=sistole, d=diastole diukur kondisi basal pada
saat penderita tidur nyenyak BMR normal berkisar antara -10 sampai +10
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ASK-DNC
Clinical Patterns and Differentials Clinical Patterns and Differentials(Summarized : Tjokroprawiro 2005, 2006)(Summarized : Tjokroprawiro 2005, 2006)
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Thyroid Storm (TS) = Thyroid Crisis (TC)Thyroid Storm (TS) = Thyroid Crisis (TC)
DIFFERENTIALS : CNS Infections, Malignant Hyperpyrexia, Sepsis, Adrenergic Drugs, Etc.
1 GENERAL SYMPTOMS :- Fever (>38.50C, Frequently >400C) Tachycardia >120/min- Profuse Sweating, Respiratory Distress, Fatigue
2 PHYSICAL SIGNS OF THYROTOXICOSIS : Orbital Signs, Goiter
3 CNS : Agitation, Psychosis, Seizures, Coma
4 CARDIOVASCULAR : Tachycardia disproportionates to FeverIncreased Blood Pressure with Wide Pulse Pressure, CHF, AF
5 GI SYMPTOMS : Diarrhea, Vomiting, Abdominal Pain, Jaundice
CLINICAL PATTERNS : a Life Threatening – Clinical Extreme of Thyrotoxicosis
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ASK-DNC
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(Burch - Wartofsky 1993, Summarized : Tjokroprawiro 2005, 2006)(Burch - Wartofsky 1993, Summarized : Tjokroprawiro 2005, 2006)
Diagnostic Criteria for Thyroid StormDiagnostic Criteria for Thyroid Storm
Below 25 is Unlikely TS25-44 is Impending TS
45-Greater is Highly Suggestive TS
3 Central Nervous System Effects : 0-30Absent : 0Mild : Agitation 10Moderate : Delirium 20
Psychosis Extreme Lethargy
Severe : Seizure 30 Coma
4 Gastrointestinal-Hepatic Dysfunction : 0-20Absent : 0Moderate : Diarrhea 10
Nausea/Vomiting Abdominal Pain
Severe : Unexplained Jaundice 20
5 Precipitant History : 0-10Negative : 0Positive : 10
Thermoregulatory Dysfunction : 5-30Temperature : 37.2 - 37.7 5
37.8 - 38.3 1038.4 - 38.8 1538.9 - 39.4 2039.5 - 39.9 25> 40 30
1
Cardiovascular Dysfunction : 0-25Tachycardia : 99 - 109 5
110 - 119 10120 - 129 15130 - 139 20> 140
25Congestive Heart FailureAbsent : 0Mild : Pedal Edema 5Moderate : Bibasilar Rales 10Severe : Pulmonary Edema 15Atrial FibrillationAbsent : 0Present : 10
2
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ASK-DNC
I General Supportive Care : A Must
II Spec. Measures : FORMULA TS–41668.24.6 and CS-7.3.7
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Chlorpromazine is needed to treat Agitation and Hyperpyrexia
(Its Effect in Inhibiting Central Thermoregulation)
4
Supplemental Oxygen, if needed : Ventilatory Support5
Treatment of Thyroid StormTreatment of Thyroid StormTreatment of Thyroid StormTreatment of Thyroid Storm(Clinical Experiences : Tjokroprawiro 2002-2006)(Clinical Experiences : Tjokroprawiro 2002-2006)(Clinical Experiences : Tjokroprawiro 2002-2006)(Clinical Experiences : Tjokroprawiro 2002-2006)
NG Tube (if needed) : many drugs should be given orally1
IV Fluids :
Dextrose and Electrolytes are preferred for the Hypermetabolic Demand
2
Hyperpyrexia : Cooling Blanket. ASA should be Avoided
Acetaminophen 15 mg/kg, q 4 h; or Chlorpromazine 25-100 mg I.M
3
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ASK-DNC
FORMULA TS–41668.24.6FORMULA TS–41668.24.6
Description
4-1-6-6-8—24-6 : Each Figure shows Time of Treatment Period
Practical Guidelines for the Treatment of Thyroid StormPractical Guidelines for the Treatment of Thyroid Storm
(Clinical Experiences : Tjokroprawiro 2002-2006)(Clinical Experiences : Tjokroprawiro 2002-2006)
Based on BW-Score > 45 (1993) and/or TTS-Score > 50 (2005)Based on BW-Score > 45 (1993) and/or TTS-Score > 50 (2005)
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Continued
6 Hourly for Lugol-Administration66 Hourly for Propranolol-Administration68 Hourly for Hydrocortisone/Dexamethasone/Prednisolone Treatment8
1 Hour Interval between PTU (first) and Lugol (later) Administrations1
24 Clinical Improvement should occur within Hours24
6 Adequate Therapy should Resolve the Crisis within Days6
44 Hourly for PTU-administration
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ASK-DNC
Practical Guidelines in the Treatment of Thyroid StormPractical Guidelines in the Treatment of Thyroid Storm
(Clinical Experiences : Tjokroprawiro 2002-2006)(Clinical Experiences : Tjokroprawiro 2002-2006)
This Formula should be given in a SEQUENTIAL MANNERThis Formula should be given in a SEQUENTIAL MANNER
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4 Loading Dose (if needed) 400 mg PTU or 40 mg Thyrozol OrallyMaintenance : 100-200 mg PTU or 10-20 mg Thyrozol 4 Hoursly
1 Minimally, 1 Hour after PTU or Thyrozol, and then Lugol can be given6 Lugol's Sol. can be given 6 gtt / 6 h (6 drops 6 Hourly)
Or, Sodium Iodide 0.25 g IV 6 Hourly6
Or, 1-3 mg/dose slow IV Propranolol, not to exceed 1 mg/min,and Repeat in 2 min, if needed
Oral Propranolol (Empty Stomach) can be given 10-40 mg 6 Hourly
Continued
FORMULA TS–41668.24.6FORMULA TS–41668.24.6
8 Hydrocortisone 100 mg or Prednisolone 25 mg or Dexamethasone 2 mg IV8 Hourly by Formula CS–7.3.7 07.00 - 13.00 - 17.00
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Peningkatan produksi dari hidrofilik glycosamino-glycans (GAGs) pada jaringan orbita
Infiltrasi sel-sel imunokompeten yang didominasi oleh limfosit T (tersering adalah CD4+), makrofag dan limfosit B
Peningkatan produksi dari hidrofilik glycosamino-glycans (GAGs) pada jaringan orbita
Infiltrasi sel-sel imunokompeten yang didominasi oleh limfosit T (tersering adalah CD4+), makrofag dan limfosit B
EXOPTHALMUS PatogenesisEXOPTHALMUS Patogenesis
Otot-otot ekstra okuler mengalami edema
Reseptor limfosit T pada CD4+ akan mengenali antigen dan mensekresi cytokines Reseptor limfosit T pada CD4+ akan mengenali antigen dan mensekresi cytokines
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Cytokines merangsang : Terbentuknya Major Histocompatibility Complex
Class II dan Heat Shock Protein 72 (HSP-72) berperan dalam pengenalan antigen
Fibroblast membentuk dan mensekresi GAGsmenarik cairan menuju ruang retro orbita pembengkakan periorbita, proptosis dan
pembengkakan otot–otot ekstra okuler
Cytokines merangsang : Terbentuknya Major Histocompatibility Complex
Class II dan Heat Shock Protein 72 (HSP-72) berperan dalam pengenalan antigen
Fibroblast membentuk dan mensekresi GAGsmenarik cairan menuju ruang retro orbita pembengkakan periorbita, proptosis dan
pembengkakan otot–otot ekstra okuler
…Patogenesis…Patogenesis
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Fibroblast melindungi sel T yang menginfiltrasi orbita dari apoptosis reaksi imun berjalan terus.
Sel-sel preadiposit adiposit peningkatan volume jaringan lemak orbita
Fibroblast melindungi sel T yang menginfiltrasi orbita dari apoptosis reaksi imun berjalan terus.
Sel-sel preadiposit adiposit peningkatan volume jaringan lemak orbita
…Patogenesis…Patogenesis
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• Modalitas terapi penyakit Graves• Indikasi & kontra indikasi pembedahan• Persiapan pra-bedah• Prinsip pembedahan• Komplikasi pembedahan• Perawatan pasca bedah• Follow-up
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Modalitas terapi penyakit Graves
• 1. Obat anti tiroid (OAT)PTU : 3x100 mgMethymazol ( Rthyrozol ) ; 1 x 20 mg
• 2. Ablasi Iodium radioaktif ( I131 )• 3. Operasi
• Cepat • Komplikasi rekuren < (dibanding terapi OAT)• Komplikasi hipotiroidi < (dibanding terapi I131)• Resiko komplikasi - lesi n.rekuren
- hipoparatiroidi
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Indikasi & kontra indikasi pembedahan
• Indikasi– Usia < 40 tahun– Disertai nodul tiroid– Anak-anak– Wanita hamil– Problem kardiologis akibat penyakit Graves
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• Kontra indikasi– Penyakit Graves rekuren– Alergi OAT– Resiko tinggi untuk bedah/ anestesi
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Persiapan pra-bedah
• 1. USG tiroid• 2. OAT - Sampai fase eutiroidi
( terapi ± 1-3 bulan)
• 3. Lugolisasi 7-14 hari : ( Iodium solusio ) Tujuan membuat kel. Tiroid lebih padat sehingga mengurangi perdarahan 10 – 15 tetes Lugol fortior dalam 1 gelas air ( 3 kali sehari )
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Prinsip pembedahan• 1. Exsposure harus cukup• 2. Manipulasi harus gentle• 3. Lapangan operasi bersih dari perdarahan • 3. Ligasi pembuluh darah tiroid• 4. Preservasi n.laringikus superior• 5. Preservasi kel.paratiroid & n.rekuren• 6. Sisakan jaringan tiroid 5 gr di tiap sisi• 7. Kontrol perdarahan• 8. Pasang drain• 9. Overtight dressing
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Komplikasi pembedahan
• 1. Perdarahan & hematoma• 2. Lesi n. rekuren• 3. Hipoparatiroidism• 4. Hipotiroidism• 5. Hipertiroidism rekuren• 6. Krisis tiroid
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• n. rekuren terpotong 0-0,6%, lesi temporer 2-4% sembuh dalam beberapa minggu atau bulan
Wheeler, Surgery 1988; 3:1480 1485‑
• Hipotiroidi 10%(5 th), 18%(10 th), 20%(30 th)
Hipertiroidi rekuren 6% (5 th), 10%(10 th), 15%(30 th)
Sugrue Br J Surg 1983;70:408-411
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• Hipotiroidi 43% (4 g), 20% (4-6 g)Hipertiroidi rekuren 0% (4 g), 6% (4-6 g), 23% (>6 g)
Takai, Nippon Nibunpi Gakkai Zasshi 1995; 71: 27 38‑
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Perawatan pasca-bedah
• Pasca-bedah dirawat di ICU 1 malam• OAT diteruskan 2 hari• Lugol distop• Propanolol tapering off• Drain dilepas bila produksi <10 ml/hr• Angkat jahitan hr 7
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Follow-up• Waktu
• Tahun I : tiap 3 bulan• Tahun II : tiap 4 bulan• Tahun III : tiap 6 bulan• Tahun IV dst : tiap tahun
• Periksa• Leher : nodul• Komplikasi : hipoparatiroidi, hipotiroidi, hipertiroidi
rekuren
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KARSINOMA TIROID
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NODUL TIROID :
Bisa pada semua usiaMeningkat dengan bertambahnya usiaPuncak : 21 – 40 thPada populasi : 5 – 8 %Wanita 2-4 kali laki-laki
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KEGANASAN PADA NODUL TIROID :
Riccabona (1987) : 2,5-24,3 %Sarda (1994) : 11,2 %Reksoprawiro (1999) : 9,97 %
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1. STRUMA UNINODOSA CURIGA GANAS
• Anamnesa - Umur < 20 tahun atau > 50
tahun - Riwayat terpapar radiasi leher
pada waktu kanak2 - Pembesaran kelenjar tiroid yang
progresif - Disertai disfagi - Disertai rasa nyeri - Suara parau / serak - Ada riwayat pada keluarga yang
menderita kanker - Struma yg. diduga hiperplasi,
diterapi hormon tetap membesar
- Struma dengan sesak nafas
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2. STRUMA UNINODOSA CURIGA GANAS
• Pemeriksaan fisik - Nodul kenyal – keras - Infiltrasi kekulit sehingga tidak bisa
di”jumput“ , - Infiltrasi kedasar sehingga fixed terhadap dasar
- Pembesaran kelenjar getah bening leher - Pulsasi a. karotis begeser ke posterolateral (
Berry Sign ) - Metastase jauh (+) : kranium, sternum,
pelvis : benjolan berdenyut
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(Riccabona score in Thyroid cancer its epidemiology, clinical feature and treatment, Springer Verlag, Berlin Heidelberg,1987)
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ADENO CARSINOMA PAPILER :
Merupakan 80 dari keganasan tiroidDapat terjadi pada semua umurPuncak : 40-49 thDelapan persen (8 %) multisentrisSering pada nodul tunggal
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ADENOCARSINOMA FOLIKULER
5-20 % dari keganasan tiroid
Sering timbul pada usia lebih tua
Puncak pada usia 50-59 th
Lebih sering pada nodul ganda
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TUMOR SEL HURTHLE
Merupakan 5 % dari keganasan tiroid
Sering bilateral
Invasi kapsul dan pembuluh darah, keluar tiroid
Sering metastase KGB
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KARSINOMA MEDULER
5 % dari keganasan tiroid
Sering sebagai bagian dari MEN
Sering bilateral
Usia muda
Bentuk non-MEN jarang, sering pada dewasa
dan prognosa jelek
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LIMFOMA
Merupakan 5 % dari kasus limfoma
Riwayat tiroiditis
Sering disertai hipotiroid
Sebagian besar Non-Hodgkin limfoma
derajat keganasan tinggi
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KARSINOMA ANAPLASTIK
5-15 % dari keganasan tiroid
Sering pada dekade 6-8, terutama wanita
Prognosa jelek (1 tahun sejak diagnosa)
Insular karsinoma : varian prognosa lebih baik
bisa up-take I131
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Rangsangan TSH jangka panjangRadiasi ionisasiFaktor genetikTiroiditis limfositikNodul tiroid (tunggal)
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Kekurangan yodium
Hipotiroid
TSH naik
pembesaran tiroid
Nodul tiroid
Ca tiroid
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Wanita 2-4 kali laki-lakididuga ada pengaruh hormonal
Nodul tunggal : 15-20 % ca tiroid
Nodul tunggal + riwayat radiasi : 33-37 % ca tiroid
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PEMERIKSAAN FISIK NODUL TIROID
Posisi pemeriksa dibelakang pasien
Deskripsikan
1.Lokasi : lobus kanan atau kiri2.Ukuran : dalam cm. diameter terpanjang3.Jumlah nodul : Uninodosa atau multinodosa4.Konsistensi : ksitik, lunak, kenyal, keras5.Nyeri6.Mobilitas : ada / tidak perlekatan terhadap trakea atau m. sternocleido 7.Pembesaran kelenjar getah bening di sekitar tiroid8.Benjolan metastase di tempat lain
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pemeriksaan penderita dari arah belakang, ibujari ditengkuk dan keempat jari lainnya didepan
tumor.
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Palpasi tumor, evaluasi konsistensi, batas tumor, penderita disuruh menelan cek batas bawah tumor
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Cek batas pool bawah tumor
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Evaluasi mobilitas tumor terhadap trakea: tangan kanan mengidentifikasi trakea, tangan kiri menggoyangkan tumor
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Konsistensi tumor: dua jari tangan kiri menjadi pengamat dan telunjuk kanan menekan, bila tekanan dirasakan oleh kedua jari pengamat kistous.
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Adakah invasi kekulit? Bila tidak ada maka kulit masih bebas dan bisa dijumput (tampak pada gambar insert), bila terjadi invasi tidak bisa dijumput dan tampak seperti kulit jeruk (peau de orange)
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Kulit diatas tumor yang terinvasi tidak bisa di “jumput”
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Cari, periksa pembesaran kgb leher
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Cari, periksa pembesaran kgb leher
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Berry sign, pulsasi arteri karotis teraba dibelakang muskulus sternokleidomastoideus
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Dibedakan atas Resiko tinggiResiko rendah
Klasifikasi AMES Baik BurukAge : Wanita < 50 th > 50 th
Pria < 40 th > 40 th Metastatic Disease : Negatif Positif
Extrathyroidal Extension : Negatif PositifSize : < 5 cm > 5 cm
AMES BAIK : TOTAL LOBEKTOMIAMES BURUK : TOTAL TIROIDEKTOMI
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Terapi Karsinoma Tiroid• Operasi Tiroidektomi ± Neck dissection (FND )• Radiasi Internal ( Iodine Radioaktif )• Radiasi external
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Pemeriksaan klinis untuk evaluasi paska operasi
• Produksi Redon drain, daerah operasi hematom, penderita sesak nafas
• Suara parau• Penderita terasa kesemutan (parestesia) pada
ekstremitas, Chovstek”s sign (+), Troussou’ s sign (+)
karena terjadi hipokalsemia akibat kel. Paratiroid terpotong / terbuang saat operasi
• Carpopedal spasme • Tanda2 hipotiroidi
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Chovstek’s sign; bila di”ketuk” pada daerah pangkal nervus fasialis
akan twitching pada otot2 mimiknya
Pasang tensimeter pada lengan, pertahankan tekanan > sitole ( 200mmHg) selama 2 menit, bila penderita hipokalsemia maka akan terjadi spasme pada tangannya Troussou’s sign (+); Obstetrician’s hand sign (+)
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