KEGAWATDARURATAN BIDANG

NEFROLOGI DAN
GASTROINTESTINAL
Dr. Ni Wayan Sri Wardani, Sp.PD, K-GH, FINASIM
KSM Ilmu Penyakit Dalam
FKIK Universitas Warmadewa/RSUD Sanjiwani Gianyar*
20 April 2023
Tujuan Pembelajaran:
Mahasiswa mampu:
 Menganalisis jenis-jenis, patofisiologi, gejala (anamnesa) dan tanda klinis
(pemeriksaan fisik) kegawatan bidang Nefrologi dan Infeksi
 Merencanakan penegakkan diagnosis (dengan pemeriksaan penunjang) pada
penyakit yang termasuk kegawatan bidang Nefrologi dan Infeksi.
 Merencanakan pengelolaan emergency penyakit yang termasuk kegawatan
Nefrologi dan Infeksi.
 KEGAWATAN BIDANG NEFROLOGI
DAN GASTROINTESTINAL

1. HIPERTENSI EMERGENCY
2. UREMIC SYNDROME
3. HEMATEMESIS -MELENA
HYPERTENSIVE EMERGENCIES

 DEFINITION
 ETIOLOGY
 CLINICAL PRESENTATIONS OF HYPERTENSIVE EMERGENCY
 SYMPTOMS AND SIGNS
 LABORATORY EXAMINATION
 THERAPY EMERGENCY
 PREVENTION
 PROGNOSIS
Definition of Hipertensive Emergencies

 A hypertensive emergencies is the association of substantially

elevated BP with acute HMOD (Hypertension Mediated Organ
Damage)
 Target organs include the retina, brain, heart, large arteries, and the Kidneys.
 This situation requires rapid diagnostic workup and immediate BP reduction to avoid
progressive organ failure.
 It usually require Intravenous therapy. The choice of antihypertensive treatment is
predominantly determined by the type of organ damage.
ETIOLOGY
POTENTIAL CAUSES OF HYPERTENSIVE EMERGENCY:
 Nonadherence with prescribed antihypertensive drugs,
 Lifestyle changes
 Concomitant use of BP elevating drugs :
 NSAIDS
 Steroids
 Immunesuppressants
 Sympathomimetics
 Cocaine
 Antiangiogenic therapy
PATHOPHYSIOLOGY
The precise pathophysiology of the Hypertensive Emergency remains unclear.
Two different interrelated mechanisms :
1. Failure in autoregulatory mechanism in the vascular bed.
 Autoregulation is defined as the ability of the organs (brain, heart, and kidneys) to
maintain a stable blood flow irrespective of alterations of perfusion pressure.
 If the perfusion pressure drops, the corresponding blood flow decreases temporarily, but
it returns to normal values after the next few minutes.
 In case of autoregulation malfunction, if the perfusion pressure drops, this leads to
decrease in blood flow and an increase in vascular resistance.
 In hypertensive emergency: lack of autoregulation in vascular bed and blood flow an
abrupt increase of BP and systemic vascular resistance  leads to mechanical stress and
endothelial injury.
PATHPHYSIOLOGY
two different interrelated mechanisms
2. The activation of renin–angiotensin system,  vasoconstriction and thus
generating a vicious cycle of continuous injury and subsequently ischemia.
Besides these mechanisms, a prothrombotic state may play a key role in
hypertensive crisis;
P-selectin (an adhesion molecule on the surface activated endothelial cell and
platelet) was significantly higher in patients with hypertensive crisis compared
with normotensive controls  platelet activation is a relatively early finding in
the pathophysiologic sequelae of hypertensive crisis (11) (F
Pathophysiology of hypertensive Crisis
 How is the Clinical Presentation?

 Theclinical presentation of a hypertensive emergency can vary

and is mainly determined by the organ(s) acutely affected.
 There
is no specific BP threshold to define a hypertensive
emergency
 Symptoms and Signs
 Symptoms :
 Headaches
 Visual disturbances
 Chest pain,
 dyspnea,
 neurologic symptoms,
 dizziness,
 and more unspecific presentations
 Physical examination:
 Cardiovascular and neurologic assessment
Specific Clinical Presentations of Hypertensive
Emergencies

Malignant hypertension: Severe BP elevation (commonly

>200/120 mmHg) associated with advanced bilateral retinopathy
(hemorrhages, cotton wool spots, papilledema).

Hypertensive encephalopathy: Severe BP elevation associated

with lethargy, seizures, cortical blindness and coma in the absence
of other explanations.
Clinical Presentations of Hypertensive
Emergencies2
Hypertensive thrombotic microangiopathy: Severe BP elevation associated with
hemolysis and thrombocytopenia in the absence of other causes and improvement with BP-
lowering therapy.

Other presentations of hypertensive emergencies include :

- severe BP elevation associated with cerebral hemorrhage
- acute stroke
- acute coronary syndrome
- cardiogenic pulmonary edema
- aortic aneurysm/dissection
-severe preeclampsia and eclampsia
 Diagnostic Workup1

 Medical history:
o preexisting hypertension,

o onset and duration of symptoms,

o potential causes (nonadherence with prescribed antihypertensive drugs, lifestyle changes,

concomitant use of BP elevating drugs [NSAIDS, steroids, immunesuppressants,
sympathomimetics, cocaine, antiangiogenic therapy]).
 Symptoms and signs
 Diagnostic Workup2
Essential examinations:
 Laboratory analysis:
o Hemoglobin, platelets
o creatinine
o sodium, potassium,
o lactate dehydrogenase (LDH), haptoglobin
o urinalysis for protein, urine sediment

 Examinations:
o Fundoscopy
o ECG
 Diagnostic Workup3
 Additional investigations may be required and indicated depending on
presentation and clinical findings and may be essential in the context:
o Troponins (chest pain)
o Chest x-ray (congestion/fluid overload)
o Transthoracic echocardiogram (cardiac structure and function)
o CT/MRI brain (cerebral hemorrhage/stroke)
o CT-angiography thorax/abdomen (acute aortic disease)
 Secondary causes can be found in 20%–40% of patients presenting with malignant
hypertension and appropriate diagnostic workup to confirm or exclude secondary forms is
indicated.
 Therapeutic Management
 The overall therapeutic goal is a controlled BP reduction to safer levels to
prevent or limit further hypertensive damage while avoiding hypotension and
related complications.
 There is a lack of randomized controlled trial data to provide clear cut guidance
on BP targets and times within which these should be achieved.
 Most recommendations are based on expert consensus
 The type of acute HMOD is the main determinant of the preferred treatment
choice.
 The timeline and magnitude of BP reduction is strongly dependent on the clinical
context.
Treatment of Hypertensive Emergency
Prognosis

 Risk of Cardiovascular and renal disease Follow-Up Patients

 Reccurent presentations with hypertensive emergencies need investigation of
potential underlying causes and assessment of HMOD
 Achieved target BP and ideally regression of HMOD  recommended :
 Adjustment and simplification of antihypertensive therapy
 Advice for lifestyle modification will assist to improve adherence and long-term BP
control.
 Regular and frequent follow-up (monthly)
Referensi:

1. Unger T, Borghi C, Charchar F , et al. 2020. International Society of

Hypertension Global Hypertension Practice Guidelines.
Uremic Syndrome
Uremic syndrome

 DEFINISi
 ETIOLOGI
 PATOFISIOLOGI
 GEJALA DAN TANDA
 PEMERIKSAAN PENUNJANG
 THERAPI
 PENCEGAHAN
 PROGNOSIS
Definisi

 Uremia adalah: suatu sindrom klinik yang dihubungkan dengan

abnormalitas cairan elektrolit, serta keseimbangan hormon dan
metabolik
 Uremia berkembang parallel dengan perburukan fungsi ginjal
 Uremia pertama kali diperkenalkan oleh Piorry th 1940, sebagai
suatu kondisi klinik yang dihubungkan dengan kegagalan fungsi
Ginjal
Etiologi

 Kegagalan fungsi Ginjal toksin toksin uremik ( Ureum, kreatinin, PTH, beta 2

mikroglobulin, poliamin, AGEs, dan molekul2 dengan berat molekul sedang)

 Gejala muncul umumnya pada PGK stadium V , umumnya pada klirens kreatinin

<10 ml/menit/1,73m2
Patofiosiologi
 Dalam keadaan normal, ginjal berfungsi sebagai:
 Produksi dan sekresi hormon eritropoetin
 Regulasi cairan dan elektrolit
 Eliminasi produk2 sisa
 Bila terjadi penurunan fungsi ginjal, fungsi tersebut tidak berjalan normal  timbul
kelainan2 seperti: ( terutama bila eGFR< 10 ml/menit/1,73m2)
 Anemia
 Asidosis
 Hiperkalemia
 Hiperparatiroidisme
 Hipertensi
Gejala dan Tanda(Pemeriksaan Fisik
Anamnesis Pemeriksaan Fisisk
 Mual  Kulit Pucat
 Bercak bekas garukan
 Muntah
 Uremic frost
 Rasa lemah
 Sklera sedikit ikterik
 Anoreksia  Faring kering
 Kram otot  Stomatitis
 Gatal2  Retensi Cairan : edema paru, edema perifer, HT
 Perikarditis
 Perubahan Status Mental
 Uremic lungs
Gejala memberat dengan penurunan fungsi
 Kelemahan otot, polineuropati
Ginjal
 edema
Pemeriksaan Penunjang

Laboratorium
 Kliren Kreatinin (laju filtrasi Glomerulus)
 Urinalisis

Pemeriksaan Pencitraan
 USG
 CT scan
 MRI

Biopsi Ginjal
Penentuan Stadium
Penatalaksanaan
Nonfarmakologik
 Diet :
 protein 0,6 – 0,8 gram/ kgBB/hari (Predialitik)

1.0 – 1.2 gram/kgBB/hr (hemodialitik)

1.3- 1.5 gram /kgBB/hr (Peritoneal Dialitik)

 Kalori 30 -35 kkal/ kg BB/hari

 Restriksi Garam < 5 gr NaCl/hari (< 2.4 gr Natrium)

 Air disesuaikan dg jumlah urinenya
 Restriksi Kalium (batasi/hindari buah2an) bila hiperkalemia
Farmakologik

 Kalsium karbonat/asetat  diberikan bila hipokalsemia (sesuai kadar Kalsium)

 Kalsitriol : hipokalsemia, hiperfosfatemia

 Kayeksilat : sodium polysrene sulfonate (bila hiperkalemia)

 Eritropoetin : pada anemia

 Preparat besi : pada defisiensi besi

 Tablet bikarbonat : pada asidosis metabolik

Komplikasi

 Perdarahan spontan

 Henti Jantung

 Kejang dan Koma

 Osteoporosis dan fraktur patologis

Prognosis

 Uremia yang penyebabnya dapat diobati prognosisnya lebih baik

 Prognosis tergantung kecepatan diagnosis dan kecepatan memberikan obat2an

 Henti jantung
KEGAWATANGASTROINTESTINA
L
Perdarahan Saluran Cerna
 Perdarahan Saluran Cerna
# PERDARAHAN DARI MULUT SAMPAI ANUS
Terbagi menjadi:
Perdarahan saluran cerna Atas dapat berupa.
 Perdarahan Varices Esofagus
 Ulkus Peptikum
 Mallory Weiss Syndrome
 Gasstritis erosive
 Perdarahan usus halus
 Perdarahan Lain

Perdarahan Saluran Cerna bawah

 Perdarahan divertikel
 Angiodisplasia
 Kolitis Iskemik
 Penyakit Kolon inflamatif
 Neoplasma
PERDARAHAN SALURAN CERNA
 PERDARAHAN DARI MULUT SAMPAI ANUS
 TERBAGI:
 PERDARAHAN SMBA
 PERDARAHAN SMBB
 BATAS LIGAMENTUM TREITS
 Perdarahan dapat berupa :
 Hematemesis : Muntah darah berwarna merah kehitaman.
 Melena : Buang air besar dengan kotoran seperti ter, lengket, bercampur dengan
darah kehitaman.
 Hematokhesi : Keluar darah merah segar dalam jumlah banyak melalui rektum.
 Perdarahan terselubung : Warna tinja normal, tetapi pada pemeriksaan kimiawi
mengandung darah.
 SMBA BS SEMUA, SMBB BUKAN HEMATEMESIS
PERDARAHAN SALURAN MAKANAN
ATAS, (SMBA)
 PERDARAHAN SMBA

PENYEBAB
 Variseal: Perdarahan dari Varises Esofagus
atau Varises Lambung

 Non-variseal: Perdarahan Ulkus Peptikum

(Ulkus Gaster Atau Ulkus Duodenal),
Sindroma Mallory-weiss, Gastritis Erosiva,
Perdarahan Esofagitis
DIAGNOSIS PERDARAHAN SMBA

ANAMNESIS PEMERIKSAAN FISIK PEMERIKSAAN PENUNJANG

• PASTIKAN MUNTAH DARAH BUKAN BATUK • VITAL SIGN: STATUS HEMODINAMIK,

DARAH TENSI, NADI • DARAH LENGKAP
• MUNTAH HITAM SEPERTI KOPI • LAKUKAN RESUSITASI SEGERA BILA SYOK • LFT
• JUMLAHNYA • TEMUKAN TANDA-TANDA PENYAKIT YANG
• LAMANYA MENDASARI • RFT
• DISERTAI BERAK HITAM? • SIROSIS HEPATIS
• GEJALA LAIN YANG MENYERTAI: DEMAM, • ULKUS PEPTIKUM • VIRUS MARKER
GEJALA MUNTAH BERLEBIHAN? GEJALA
ULKUS? SINDROME DISPEPSIA? GEJALA
• TANDA GASTRITIS EROSIVA PASIEN • ENDOSKOPI
• KONSUMSI ANALGETIK KRONIS,
SIROSIS? • MENDERITA PENYAKIT REMATIK • USG
• LAKUKAN PEMERIKSAAN COLOK • EKG
DUBUR/RT
STRATIFIKASI RISIKO
PERDARAHAN
 TATA LAKSANA PERDARAHAN
MAYOR
1. Resusitasi aktif :
 a.Perdarahan < 750cc : Nadi < 100, tekanan darah normal, tekanan
nadi meningkat, respirasi 14-20, produksi kencing > 30cc/jam,
sedikit gelisah. Resusitasi dengan: cairan kristaloid (iv line)
 b. Perdarahan 750-1500cc : Nadi > 100, tekanan darah normal,
tekanan nadi menurun, respirasi 20-30, produksi kencing
20-30cc/jam, status mental: gelisah. Resusitasi dengan:
 - Cairan kristaloid (tetesan cepat),
 - Persiapan tranfusi
 c.Perdarahan 1500-2000cc : Nadi > 120, Tekanan darah menurun,
tekanan nadi menurun, respirasi 30-40, produksi urin 10-20
cc/jam, status mental : gelisah dan kebingungan Resusitasi
dengan :
 - Cairan kristaloid/koloid (tetesan cepat) dan tranfusi darah -
Pemantauan vena sentral.
 d. Perdarahan > 2000cc : Tanda klinis : Nadi > 140, syok, tekanan
nadi lemah, respirasi >40, produksi urin < 10 cc/jam, status mental
: lemas Resusitasi dengan : - Cairan kristaloid 1 liter dalam 1 jam.
- Bila tetap syok berikan koloid tetesan cepat dan tranfusi darah.
CVP, OKSIGEN
2. Kumbah lambung: Setelah berhasil melakukan resusitasi, kalau
keadaan umum lebih baik segera pasang pipa nasogastrik untuk
kumbah lambung dengan air es 150 cc setiap 2, 4, 6 jam tergantung
aktivitas perdarahannya untuk tujuan persiapan melakukan
endoskopi agar dapat menentukan sumber perdarahan dengan tepat.
3. Inhibitor pompa proton dosis tinggi: Pada perdarahan ulkus
peptikum segera berikan inhibitor pompa proton (PPI) dosis
tinggi : omeprazol 80 mg dilanjutkan dengan drip 8 mg setiap jam
sampai 72 jam.
4. Obat lain yang masih ada tempatnya adalah : Antacid, sukralfat.
5. Terapi endoskopi : Jika perdarahan masih aktif dalam 24 jam dan
endoskopi menunjukkan adanya stigmata perdarahan aktif (forrest
I, IIa, IIb), maka indikasi untuk melakukan terapi endoskopi dan
dikombinasi dengan PPI dosis tinggi. Jika pada endoskopi
ditemukan forrest IIc, III maka diberikan terapi ulkus peptikum
pada umumnya.
6. Vasokonstriktor: Sandostatin iv
7. Pembedahan : Jika terapi endoskopi gagal, perforasi,
striktur/stenosis berat.
 TATA LAKSANA PERDARAHAN
MINOR
1. Infus-IVFD NaCl 0,9%
2. Kumbah lambung dengan air es.
3. Inhibitor pompa proton.
4. Obat lain yang masih ada tempatnya: antacid, sukralfat.
5. Endoskopi dilakukan secara elektif.
6. Penatalaksanaan Perdarahan Varises
7. Bila variseal/Sirosis: Vit K 3 x 1 ampul, Lavement @12 jam, sterilisasi usus
dengan Neomisin, laktulosa. Tentukan prognosis dengan skor Child-Pugh
CHILD-TURCOTTE-PUGH
SCORE
PERDARAHAN SALURAN
MAKANAN BAWAH (SMBB)
 PERDARAHAN SMBB

PENYEBAB:
 Divertikulosis
 Hemorrhoid interna
 Kolitis iskemik
 Ulkus rectum/ proctitis
 Penyakit peradangan usus (IBD) : kolitis ulseratif, penyakit crohn. - Polip kolon
 Kanker kolon
 Angioma kolon
 Demam tifoid
 Disentri basiler/amoeba
DIAGNOSIS PERDARAHAN SMBB

• ANAMNESIS • Pemeriksaan fisik • Pemeriksaan

• Umumnya tanpa • Evaluasi penyakit penunjang
hematemesis ekstraintestinal • DL, LFT
• Berak darah • Adakah tumor • Radiologi: BOF,
segar, kecuali • RT: hemoroid foto kontras, USG
volume banyak • Kolonoskopi
TATA LAKSANA

 TINDAKAN UMUM
 RESUSITASI CAIRAN
 TENTUKAN VOLUME PERDARAHAN- TRANSFUSI DARAH
 APAKAH DISERTAI PERDARAHAN SMBA? LAKUKAN KUMBAH
LAMBUNG
 TINDAKAN KHUSUS: LASER, INJEKSI EPINEFRIN,KOAGULASI,
HEATER PROBE, HEMOCLIP, LIGASI, RESEKSI
Referensi

 BUKU EIMED Papdi I

 Terima Kasih
https://www.youtube.com/@sriwardanisppd