FAKULTAS KEDOKTERAN
UNIVERSITAS YARSI
PANDUAN MAHASISWA
BLOK EMERGENSI
SEMESTER VIII
TAHUN AKADEMIK 2019/2020
isi buku dengan cara apapun tanpa izin tertulis dari penulis/penerbit
Segala puji bagi Allah SWT yang telah memberikan segala rahmat dan
hidayahNya sehingga Buku Panduan Blok Emergensi bagi mahasiswa ini dapat
diselesaikan penyusunannya.
Blok ini diberikan pada semester tujuh dan merupakan bagian dari
pemahaman kegawatdaruratan medik, khususnya di Fakultas Kedokteran YARSI
serta penerapan Problem Based Learning (PBL) sebagai salah satu metode belajar
yang efektif untuk meningkatkan kemampuan kognitif, afektif dan psikomotor.
Sumber informasi yang harus dipergunaan mahasiswa meliputi konsultasi pakar,
membaca artikel, jurnal penelitian, akses internet dan buku referensi yang
dianjurkan.
Tim Penyusun
i
DAFTAR ISI
ii
PENANGGUNG J AWAB DAN TIM PENYUSUN
BLOK EMERGENSI
SEMESTER GENAP TA 2020-2021
Penanggung J awab
iii
Pengampu Materi Ilmu Kesehatan Jiwa
Dr. Nasruddin Noor, SpKJ
iv
PENDAHULUAN
Inovasi dalam bentuk PBL ini mempunyai berbagai manfaat baik dalam
bidang kognitif, afektif dan psikomotor. Dalam aspek kognitif, PBL diharapkan
mampu mengaktifkan Prior Knowledge, meningkatkan pengetahuan melalui
diskusi tutorial, mampu memanfaatkan berbagai sumber belajar, baik cetak
maupun digital, serta mampu melakukan integrasi berbagai subjek sehingga lebih
relevan dengan problem-problem professional yang akan dihadapi sebagai dokter.
Dari aspek afektif, PBL akan membawa mahasiswa merasa apa yang mereka
hadapi dan pelajari erat kaitannya dengan calon dokter, meningkatkan motivasi
instrinsik yang kuat dan mengembangkan kemampuan team work melalui diskusi
tutorial. Secara psikomotor, PBL akan meningkatkan kemampuan komunikasi
interpersonal, meningkatkan kemampuan problem solving dan mahasiswa
dibiasakan belajar mandiri sehingga mampu menjadi active learner dan lifelong
learner.
KARAKTERISTIK MAHASISWA
Mahasiswa yang mengikuti Blok KEGAWATDARURATAN pada
semester 7 adalah mahasiswa Fakultas Kedokteran Universitas YARSI yang telah
LULUS Blok pada tahun I dan II dan TELAH PERNAH MENGIKUTI Blok
pada tahun 3.
1. Kompetensi 1: Mampu menggali dan bertukar informasi secara verbal dan non
verbal
1.1. Berkomunikasi dengan pasien
1.1.1. Bersambung rasa dengan pasien
1.1.2. Mengumpulkan informasi
1.1.3. Memahami perspektif pasien
1.1.4. Memberi penjelasan dan informasi
6. Kompetensi 6:
a. Belajar sepanjang hayat
b. Merencanakan, menerapkan dan memantau perkembangan profesi secara
bersinambung
7. Kompetensi 7:
a. Berperilaku profesional dalam praktik kedokteran serta mendukung
kebijakan kesehatan
b. Bermoral, beretika, serta memahami isu-isu etik maupun aspek
medikolegal dalam praktik kedokteran
c. Menerapkan program keselamatan pasien
I. PROSES BELAJ AR
1. Kuliah Pakar
Kuliah dilakukan secara interaktif dan dua arah
Pelaksanaannya 44 x 50 menit, terdiri dari:
o MIKROBIOLOGI: 1 x 50 menit
Virus Dengue penyebab DSS
o PARASITOLOGI: 1 x 50 menit
Peran vektor Dengue pada kasus DSS
o AGAMA: 2 x 50 menit
Kaidah hukum Islam tentang darurat
Maqashid al-syariah (dlaruriyah al-khams)
o OBSGYN : 4 x 50 menit
Perdarahan pada kehamilan muda (1 x 50 menit):
Gawat janin (1 x 50 menit)
Hemorrhagic antepartum:
a. Solutio plansenta (1 x 50 menit)
b. Plasenta previa (1 x 50 menit)
o ANESTESI : 3 x 50 menit
Gagal nafas (2 x 50 menit)
RJP (1 x 50 menit)
o FARMAKOLOGI : 1 x 50 menit
Respon penderita terhadap obat
o NEUROLOGI : 2 x 50 menit
Gangguan kesadaran
Trauma medula spinalis
Langkah 1
I. Membaca skenario
Mahasiswa dihadapkan pada skenario berisi masalah-masalah yang
dapat memicu mahasiswa untuk mendapatkan informasi ilmiah
sehingga diperoleh sasaran belajar
Langkah 3:
Mahasiswa menyajikan materi/informasi yang diperoleh dari langkah II
untuk disintesis dan diuji, serta diakhiri dengan menyusun rangkuman
sebagai jawaban dari skenario yang disajikan
Menggunakan skenario
1. Tekanan darah tinggi dalam kehamilan
2. Trauma pada kepala
3. Kembung pada anak
5. Tugas kelompok
o Membuat laporan skenario (3 kali)
o Membuat laporan textbook / journal reading (1 kali)
III. UJ I KOMPETENSI
1. Diketik pada kertas ukuran A4. Menggunakan Microsoft Word, tipe font
Times New Roman ukuran 12.
2. Pengetikan menggunakan spasi tunggal.
3. Rangkuman mencantumkan rujukan dan daftar pustaka yang digunakan
4. Halaman judul berisi judul skenario, kelompok dan nama serta NIM
anggota kelompok.
5. Penomoran halaman pada sisi kanan bawah halaman.
6. Jumlah rujukan yang dipakai minimal 5 buah (berbahasa Indonesia
minimal 3 dan berbahasa Inggris 3) dan harus dicantumkan dalam Daftar
Pustaka. Sumber rujukan dapat berupa buku teks, buku saku, artikel dalam
jurnal ilmiah, maupun sumber informasi digital (internet)
7. Diserahkan kepada koordinator pelaksana PBL di Pusat Pendidikan
Kedokteran Fakultas Kedokteran YARSI dalam bentuk print out dan
compact disc (CD)
8. Batas akhir penyerahan rangkuman adalah 3 (tiga) hari sesudah tiap
skenario selesai dibahas.
9. Dari rangkuman yang telah terkumpul, Koordinator PBL akan memilih
satu kelompok untuk setiap skenario. Kelompok yang terpilih harus
memberikan presentasi pada saat acara pleno.
10. Presentasi pleno :
a. Menggunakan power point
b. Durasi presentasi maksimal 30 menit tiap group dilanjutkan dengan
tanya jawab.
c. Kelompok yang tidak melakukan presentasi wajib membuat
pertanyaan minimal 1 buah.
Halaman Judul
I. langkah – 1
II. Langkah – 2 : Individual study
III. Langkah – 3
Daftar Pustaka
Mitsuoka T. 1989. Microbe in the intestine Our Lifelong Partners. Japan, Yakult
Honsa Co., Ltd
Seorang pasien wanita usia 18 tahun datang ke IGD RS dengan keluhan utama
kepala terasa sakit. Pasien ini dengan kehamilan pertama dan usia kehamilan 32
minggu jika dihitung dari hari pertama haid terakhirnya. Pasien melakukan ANC
ke Puskesmas sebanyak 4 kali dan terakhir kontrol 1 minggu yang lalu.
Berdasarkan ANC sebelumnya diketahui pasien memiliki tekanan darah tinggi
dan sudah diberikan obat antihipertensi. Selama kehamilan pasien mengalami
kenaikan berat badan 20 kg dan tidak ada edema pada tungkai. Dari riwayat
penyakit keluarga tidak ada keluarga yang menderita penyakit
jantung,ginjal,diabetes dan hipertensi. Pada pemeriksaan fisik didapatkan pasien
tampak sakit sedang, tekanan darah 180/120, nadi 92x/menit, nafas
22x/menit,suhu 36,3oC. Dari status obstetri didapatkan tinggi fundus uteri 26cm
dan denyut jantung janin 154x/menit. Tanda tanda persalinan tidak ada.
Selanjutnya dilakukan pemeriksaan penunjang usg dengan hasil janin hidup
tunggal intra uterin presentasi kepala dan hasil pemeriksaan laboratorium urin
protein positif 3. Dari hasil pemeriksaan darah didapatkan Hb 10.5 gr %, leukosit
12.000/mm3, trombosit 95.000/mm3.
Tanda Vital
Airway: terdengar bunyi snoring
Breathing: frekuensi nafas 10 x/menit
Circulation: tekanan darah 160/90 mmHg, frekuensi nadi 40x/menit
Wajah
Terlihat adanya brill hematoma.
Trauma di daerah sepertiga tengah wajah, pada pemeriksaan terlihat adanya
cerebrospinal rhinorrhea, mobilitas dari maxilla, krepitasi dan maloklusi dari gigi.
Hidung
Inspeksi: adanya edema atau deformitas pada hidung tidak ada
Palpasi: terdapat krepitasi pada hidung
Pemeriksan fisik menggunakan rinoskopi anterior: terdapat clothing perdarahan
aktif tidak ada, tampak laserasi di septum dan konka inferior
Telinga
Liang telinga: lapang, terdapat laserasi, clothing (+), tidak terdapat perdarahan
aktif dan membran timpani utuh
Status Neurologi
GCS E1 M1 V1, pupil: bulat, anisokor, diameter 5 mm/3 mm, RCL -/+, RCTL -
/+, kesan hemiparesis dekstra, reflex patologis Babinsky +/-
Cunningham FG., Gant N, et al. 2001, “William Obstetrics” 21st ed. McGraw-
Hill, Medical Publishing Division: 567-618.
Kosim MS. Yunanto A. Dewi R. Sarosa GI, dkk. 2008. Buku Ajar Neonatologi
edisi 1, UKK Perinatologi IDAI. IDAI, Jakarta.
Kuniyoshi S, Suarez JI. 2004. Traumatic head injury. In: Suarez JI, Tarsy D.
Critical care neurology and neurosurgery. New Jersey: Humana Press; 395-
415.
Miller C. 2009. Traumatic brain injury. In: Frontera JA. Decision making in
neurocritical care. New York: Thieme Medical Publishers, Inc.; 20-35.
Pedersen GW. 1992. Buku Ajar Praktis Bedah Mulut. Jakarta. EGC. (221-263)
(293-324)
Ropper AH, Brown RH. 2005. Adams and Victors principles of neurology. 8th
edition. New York: McGraw-Hill; 452-79.
Sjamsuhidajat. Wim de Jong. 2004. Buku Ajar Ilmu Bedah. Edisi 2. Jakarta.
EGC: 769 – 772.
Abstract
Background: The widespread use of pesticides in public health protection and agricultural pest control has caused
severe environmental pollution and health hazards, especially in developing countries, including cases of severe
acute and chronic human poisoning. Diabetic ketoacidosis is an uncommon manifestation of acute pesticide poisoning.
Suicidal pesticide poisoning by injection is also an unusual way to take poison. We report a severe pesticide mixture
poisoning case with diabetic ketoacidosis in an adult with improved outcome after supportive treatment and large
doses of atropine.
Case presentation: A 30-year-old unmarried Moroccan Arab male with a previous history of active polysubstance abuse
and behavior disorders had ingested and self injected intravenously into his forearm an unknown amount of a mixture
of chlorpyrifos and cypermethrin. He developed muscarinic and nicotinic symptoms with hypothermia, inflammation in
the site of the pesticide injection without necrosis. Red blood cell cholinesterase and plasma cholinesterase were very
low (<10%). By day 3, the patient developed stroke with hypotension (80/50 mmHg) and tachycardia (143 pulses /min).
Laboratory tests showed severe hyperglycemia (4.49 g/dL), hypokaliemia (2.4 mEq/L), glycosuria, ketonuria and low
bicarbonate levels (12 mEq/L) with improvement after intensive medical treatment and treatment by atropine.
Conclusion: Suicidal poisonings with self-injection of insecticide were rarely reported but could be associated with
severe local and systemic complications. The oxidative stress caused by pyrethroids and organophosphates poisoning
could explain the occurrence of hyperglycemia and ketoacidosis.
Keywords: Hyperglycemia, Pesticide, Poisoning, Ketosis
© 2014 Badrane et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain
Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article,
unless otherwise stated.
Badrane et al. BMC Research Notes 2014, 7:485 Page 2 of 4
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religious delusions. The patient had never consulted a acidosis. Cardiac enzymes and echocardiography were
psychiatrist. normal. Blood and urine were sterile. Procalcitonine was
In the emergency room, vital signs revealed a pulse 1.90 ng/mL and C-reactive protein (CRP) was 2.70 mg/L.
rate of 100 beats per minute, blood pressure of 170/ Amylasemia, lipasemia and glycosylated hemoglobin and
100 mmHg, a respiratory rate of 25 breaths per minute abdominal ultrasound were normal. Treatment, including
and plenty of oral secretions. The patient was afebrile IV fluids, insulin infusion, parenteral potassium, sodium bi-
and had rhonchi all over his chest. Oxygen saturation carbonate, adrenaline at the rate of 6 mg per hour and
was 80%, and Glasgow Coma Scale was 6/15. There were hydrocortisone-hemisuccinate was started. Treatment with
no fasciculations. The patient had also a miosis. He atropine and supportive care was continued.
required ventilator support and he was admitted to the At day 5, he developed hyperthermia with chills. His
Medical Intensive Care Unit (MICU). chest X-ray was normal. The level of procalcitonin and
He developed, in few hours, hypothermia (34°C), bra- CRP increased. Streptococcus pneumoniae was isolated
dychardia (35 beats per minute) with generalized fascicula- from protected distal bronchial samples. Two bacteries,
tions, tremor, excessive salivation, bronchial secretions and Klebsiella pneumoniae and Staphylococcus hominis were
bronchospasm. Physical examination revealed hyperemia isolated from the blood. Empirical antibiotic therapy
extending from the proximal third of the forearm to the with ceftriaxone and gentamicin was started and modi-
axillary region with severe edema in the antecubital fossa fied to imipenem once bacteriological results became
without indurations or necrosis. The capillary refill time available. The glucose levels were normal and needed no
was normal and the pulses were present. Urine was disco- further insulin therapy, and the acidosis was resolved at
lored to a reddish brown. Investigations at admission to day 5.
MICU, showed hyperglycemia (2.42 g/L), rhabdomyolysis Treatment with adrenaline was stopped on day 6. The
(level of creatine kinase in the blood was 1188 UI/L) patient required ventilator support for 7 days and atro-
and low bicarbonate levels (16 mEq/L). Renal and pine for 10 days. The patient received 700 mg as the
liver functions and serum levels of sodium, potassium, total dose of atropine. Edema and inflammation in
calcium, and magnesium were normal. Blood picture the left upper limb regressed without requiring sur-
showed leukocytosis. Screening for benzodiazepine, antiep- gery. Red blood cell cholinesterase and plasma cho-
ileptic drugs, amphetamines, ethanol, cocaine, exstasy, linesterase were still very low (<10%). A psychiatric
tetrahydrocannabinol, morphine and its derivatives was consultation conducted during hospitalization revealed a
negative. Red blood cell cholinesterase and plasma cholin- suicide attempt in the context of psychosis in the patient.
esterase were very low (<10%). The chest X-ray and elec- He was discharged after 13 days to a medical department
trocardiogram were normal. to continue the antibiotic therapy, clinical monitoring
OP and pyrethroid (PYR) mixture poisoning was as- and to start the prescribed antipsychotic drugs. The
sumed on the basis of the medical interview, the com- serum cholinesterase has been recovered four weeks after
pound identification made based on the container poisoning.
brought by the patient’s relatives, cholinergic syndrome
associated with pyrethroid effects, tremor and excessive Discussion
salivation supported by low plasma and red cell cholin- There is an increased commercial interest in developing
esterase levels. insecticide mixtures. The use of two active compounds
He was treated with, intravenous (IV) fluids, atropine, in a mixture may provide rapid action and more residual
phenobarbital, IV sodium bicarbonate and passive exter- effect than any of them if applied singly in sequence [1].
nal rewarming. Atropine (2 mg) was given every 10 mi- One of the most popular insecticide combinations is OP
nutes for four hours, followed by infusion at the rate of and PYR. The trend toward increased marketing of
2.5 mg per hour, and the dose was adjusted as per his OP- PYR mixtures is likely to result in the creation of new
clinical response. The use of phenobarbital was empirical patterns of mixed toxicity. The product used by our patient
because an electroencephalogram to look for subclinical to attempt suicide was a mixture of CPF and CM.
seizures was not available. The patient was not treated Coexposure to CPF and CM inhibits the carboxylester-
with oxime because this antidote was not available. ase mediated hydrolysis of CM, leading to an increased
At day 3, the patient developed stroke with hypotension tissue concentration of this compound and a decreased
(80/50 mmHg) and tachycardia (143 beats per minute). urinary excretion of 3-phenoxybenzoic acid, the major
Laboratory tests showed severe hyperglycemia (4.49 g/dL), metabolite of PYR [1]. Similarly, CPF oxon (the toxic
hypokaliemia (2.4 mEq/L), glycosuria, ketonuria, and low metabolite of CPF) strongly and irreversibly inhibits CM
bicarbonate levels (12 mEq/L). Arterial blood gas analysis hydrolysis [1]. These data could explain the severity of
revealed pH 6.99, PaCO2 73 mmHg, PaO2 195 mmHg the clinical presentation of our patient. Indeed, the pa-
(FiO2 70%), and HCO3ˉ 17.6 mEq/L, suggesting mixed tient presented clinical signs related to the inhibition of
Badrane et al. BMC Research Notes 2014, 7:485 Page 3 of 4
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acetylcholine esterase (ChE) by CPF but also prolonged Acute pancreatitis can occur with OP intoxication and
tremor and hypersalivation because of the prolongation may result in hyperglycemia [9]. We eliminated acute
of the CM action by the inhibition of CM hydrolysis. pancreatitis because of the normal amylase and lipase
Many experimental, clinical and in vitro studies have level and the normality of the abdominal ultrasound.
shown that CPF is associated with slower serum cholin- However, diabetic ketoacidosis is an uncommon mani-
esterase recovery and some animal studies confirmed festation of pesticide poisoning. The OP poisoning was
that the inhibitory effect of CPF on ChE activity is not the cause of the coma, hyperglycemia, glycosuria and
influenced by co-exposure to PYR [5]. The serum cho- keto-acidosis in a 3-year-old boy who was in contact
linesterase of our patient was very low (<10%) and re- with parathion [10]. OP intoxication can mimic diabetic
covered four weeks after poisoning. ketoacidosis and its diagnosis may be delayed [4].
A prospective study has showed that, in humans, OP Akyildiz et al. have also reported a case of a 5-year-old
poisoning causes an initial fall in body temperature, girl with OP intoxication who presented as diabetic
followed by a period of normal to high body temperature. keto-acidosis [11]. Swaminathan et al. have discussed
However, there are factors such as infections and treatment the case of a 15-year-old girl with diabetic ketoacidosis
that could alter thermoregulation in the patients with OP after an intentional overdose with OP pesticide [12].
poisoning [6]. Some adults with OP intoxication have presented with
In our patient, it’s difficult to confirm that the cause of non-ketotic hyperglycemic coma [6]. However, no pesti-
hyperthermia was the OP poisoning because of the pres- cide poisoning cases with diabetic ketoacidosis have
ence of a major factor of confusion like nosocomial in- been reported in adult patients.
fection confirmed by the isolation of bacteria from The other originality of our observation was the
protected distal bronchial samples and blood. unusual intravenous way used by the patient to at-
Hyperglycemia, after OP exposure, has been confirmed tempt suicide. Suicidal poisonings with self-injection
in animal studies [3]. Mechanisms of hyperglycemia of insecticide have been rarely reported but could be
demonstrated in these studies were the oxidative stress, associated with severe local and systemic complica-
inhibition of paroxanase, stimulation of adrenal glands tions [3,13]. Most patients had mental problems, such
and release of catecholamines, and the effect on metab- as depression, substance abuse, or both [3]. Our patient
olism of liver tryptophan [3]. had a history of drug abuse and a diagnosis of psychosis
Transient hyperglycemia and glycosuria are also found was established in our department after a psychiatric
in severe OP poisoning [7]. consultation, which explains the patient’s choice of poi-
The oxidative stress caused by PYR poisoning could soning way.
explain the occurrence of hyperglycemia in PYR poison- Because of the severity of the intoxication, our pa-
ing cases. An animal study showed that CM decreased tient required a large dose of atropine. A recent clin-
the cellular antioxidant activity, altered marker enzyme ical study has shown that following atropinization, the
activity and effected histopathological changes in the maintenance dosage of atropine can be usually kept
brain, heart, liver, kidney and testis of male rats [8]. low at 0.005 mg h − 1 kg − 1 and doses of more than
To our knowledge, no study has shown the effect of 0.06 mg h − 1 kg − 1 are only required when AChE is
pesticide mixtures on glucose metabolism. OP and PYR completely inhibited [14].
are responsible for an oxidative stress that could possibly
explain the hyperglycemia induced by the mixture of OP Conclusion
and PYR. In fact, Wielgomas and Krechniak have shown To our knowledge, this is the first case of diabetic ketoa-
that both CM and CPF administered as single com- cidosis caused by pesticide poisoning reported in adults.
pounds, or in combination, cause an impact on different The oxidative stress caused by OP and PYR could play a
free radical mediated parameters in wistar rats [1]. role in the development of metabolic disturbances of
In our case, we have excluded diabetes. There was no glucose. The exact mechanisms of this action need fur-
patient history of diabetes, the glycosylated hemoglobin ther investigation.
was normal and no other episode of hyperglycemia oc- Establishing the diagnosis of complications of pesti-
curred during the hospitalization. The drugs administered cides poisoning is very important for adequate treatment
to the patient before the installation of hyperglycemia, and to improve the patient’s outcome.
namely phenobarbital and atropine, don’t cause hypergly-
cemia as an adverse effect. We have excluded drug abuse Consent
because of the identification of illicit drugs and psycho- Written informed consent was obtained from the patient
tropic drugs was negative, and because of the improve- for publication of this Case Report. A copy of the writ-
ment of the patient after atropine therapy and supportive ten consent is available for review by the Editor-in-Chief
treatment. of this journal.
Badrane et al. BMC Research Notes 2014, 7:485 Page 4 of 4
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Abbreviations
OP: Organophosphates; MICU: Medical intensive care unit; IV: Intravenous;
CRP: C-reactive protein; PYR: Pyrethroids; CM: Cypermethrin; CPF: Chlorpyrifos;
ChE: Acetylcholine esterase.
Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
NB, TD, KB, KA, MA, AAZ handled the case in the MICU. NB, TD, KA, KB, AAZ
conceived the case report, and participated in its design. NB, TD, AAZ drafted
the manuscript and sequence alignment of the report. NB, KB, MA, AAZ
reviewed the literature. All authors read and approved the final manuscript.
Author details
1
Centre Anti Poison et de Pharmacovigilance du Maroc, Rabat, Morocco.
2
Service de Réanimation Médicale-CHU Ibn Sina, Rabat-Faculté de Médecine
et de Pharmacie de Rabat, Université Mohammed V Souissi, Rabat, Morocco.
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