dr. Himawan, dr. Cemara, dr.

Dini,
dr. Yusuf, dr. Ratna, dr. Anshari
1. Djenkolic Acid Intoxication
 Jengkol contains djenkolic acid & sulphur which can be crystallized in renal
tubules  obstructive uropathy, acute kidney injury, or chronic kidney
disease.
 Acute intoxication can occur 5-12 hours after eating jengkol.
 Clinical manifestation:
 Flank pain
 Colic abdomen
 Oliguria
 Hematuria
 Treatment:
 Aggressive hydration to increase urine flow
 Djenkolic acid crystals are more soluble in alkaline solutions, and
alkalinization of the urine may be of benefit.
2. Antihypertension Drugs
2. Antihypertensive Drugs
Some -sympatholytics possess higher affinity for cardiac  1-receptors than for
 2-receptors and thus display cardioselectivity (e.g., metoprolol, acebutolol,
bisoprolol). None of these blockers is sufficiently selective to permit its use in
asthma or DM
 3. Asthma: classification
 Measurements of lung function enhance
diagnostic confidence.
 Spirometry:
 Airway obstruction:
FEV1/FVC <75% or FEV 1 <80%
 Reversibility: improvement of FEV1
≥15% after bronchodilator inhalation.
 Classification of asthma severity
 Peak expiratory flow meter:
 Reversibility: improvement of PEF ≥15%
after bronchodilator inhalation
 Variability: daily PEF measured at night
after bronchodilator & morning before
bronchodilator >20%.

GINA 2005
PDPI. Asma: pedoman diagnosis & penatalaksanaan di Indonesia. 2004
3. Asthma: classification on treatment
4. GERD
 GERD
 A pathologic condition of symptoms & injury to the esophagus
caused by percolation of gastric or gastroduodenal contents into
the esophagus associated with ineffective clearance & defective
gastroesophageal barrier.
 Symptoms:
 Heartburn; midline retrosternal burning sensation that radiates to
the throat, occasionally to the intrascapular region.
 Others: regurgitation, dysphagia, waterbrash.

GI-Liver secrets
4. GERD

 Management:
 Aggressive lifestyle modification & pharmacologic therapy.
 Surgery is encouraged for the fit patient who requires chronic high doses of
pharmacologic therapy to control GERD or who dislikes taking medicines.
 Endoscopic treatments for GERD are very promising, but controlled long-
term comparative trials with proton pump inhibitors and/or surgery are
lacking.
5. TB-HIV
 TB is the most common cause of death in HIV & increase
progresivity of AIDS.
 The problems in TB-HIV:
 TB drugs & ARV have overlapping side effects
 Drug interaction between TB drugs & ARV
 Paradoxal therapy (immune reconstitution inflammatory
syndrome/IRIS): worsening symptoms (fever, lymph node
enlargement, infiltrate) after receive TB drugs /ARV/both
which are not caused by therapeutic failure, but caused by
reactivation of immune system to TB antigen.
5. TB-HIV
 Principles of medication
 TB medication is a priority
 Do not give TB drugs & ARV simultaneously because of drugs
interaction, toxicity, & IRIS
 In life threatening case (disseminated TB or CD4 <200/mm3),
ARV & TB drugs can be given concurrently with closed
monitoring.
 ARV that has been given is continued.
 In situation where there is no threat to life, ARV may be
delayed to prevent IRIS & drug interaction.
5. TB-HIV

Management of tuberculosis & HIV coinfection. WHO.

6. Oxygen Therapy
 Oxygen must be delivered with the simplest method &
the lowest FiO2 which can maintain PaO2 >60 mmHg &
SaO2 >90%.
 In this case, FiO2 ambient air gives PaO2 60 mmHg.
Additional O2 can be obtained by nasal cannula.

Terapi Oksigen. Perhimpunan Dokter Paru Indonesia.

6. Oxygen Therapy
 PAO2 = (713 x FiO2) – PaCO2/0,8
 A: alveolar. a: arterial
 FiO2 ambient air: 0,21 (21%)
 PAO2 = 150 – 40/0,8 = 100 mmHg
 PAO2-PaO2 = 100 - 60 = 40 mmHg
 Gradien PAO2-PaO2 :
 < 20 mmHg: normal
 20-40 mmHg: V/Q mismatch
 40-60 mmHG: shunt
 >60 mmHg: diffusion defect

Terapi Oksigen. Perhimpunan Dokter Paru Indonesia.

6. Oxygen Therapy
 PAO2awal/PAO2 akhir= PaO2awal/PaO2akhir
 Misalnya: target PaO2 akhir = 80 mmHg
 100 mmHg/PAO2 akhir = 60 mmHg/80 mmHg
PAO2 akhir = 133,3 mmHg
 Masukkan ke rumus: PAO2 = (713 x FiO2) – PaCO2/0,8
133,3 = (713 x FiO2) – 40/0,8
FiO2 = 0,25 atau 25%
6. Oxygen Therapy
Device Oxygen flow rate FiO2 range
(L/min)
Nasal Cannula 1 0,21-0,24
2 0,23-0,28
3 0,27-0,34
Simple mask 5-6 0,30-0,45
7-8 0,40-0,60
Rebreathing mask 7 0,35-0,75
15 0,65-1,00
Nonrebreathing mask 7-15 0,40-1,00

Clinical Anesthesiology, 4th Edition. G. Edward Morgan, Jr., Maged S. Mikhail, Michael J. Murray
7. Hepatitis Transmission

aPrimarily with HIV co-infection and high-level viremia in index case; risk 5%.
8. E.S. OAT Mayor
MAYOR Kemungkinan Penyebab HENTIKAN OBAT
Gatal & kemerahan Semua jenis OAT Antihistamin & evaluasi
ketat
Tuli Streptomisin Stop streptomisin
Vertigo & nistagmus Streptomisin Stop streptomisin
(n.VIII)
Ikterus Sebagian besar OAT Hentikan semua OAT
s.d. ikterik menghilang,
hepatoprotektor
Muntah & confusion Sebagian besar OAT Hentikan semua OAT &
uji fungsi hati
Gangguan penglihatan Etambutol Stop etambutol
Kelainan sistemik, syok Rifampisin Stop rifampisin
& purpura
Tatalaksana TB di Indonesia.
8. E.S. OAT Minor
Minor Kemungkinan Tata Laksana
Penyebab
Tidak nafsu makan, Rifampisin OAT diminum malam
mual, sakit perut sebelum tidur
Nyeri sendi Pyrazinamid Aspirin/allopurinol
Kesemutan s.d. rasa INH Vit B6 1 x 100 mg/hari
terbakar di kaki
Urine kemerahan Rifampisin Beri penjelasan

• Etambutol juga dapat menyebabkan nyeri sendi & presipitasi arthritis gout
akut.

1. Tatalaksana TB di Indonesia. 2. Physician drugs handbook

9. Renal Disorder
Diagnosis
Acute glomerulonephritis
Rapidly progressive
glomerulonephritis
Chronic glomerulonephritis
Nephrotic syndrome
Pathophysiology of disease: an introduction to clinical medicine. 5th ed.
Characteristic
an abrupt onset of hematuria & proteinuria with
reduced GFR & renal salt and water retention, followed
by full recovery of renal function.
recovery from the acute disorder does not occur.
Worsening renal function results in irreversible and
complete renal failure over weeks to months.
renal impairment after acute glomerulonephritis
progresses slowly over a period of years & eventually
results in chronic renal failure.
manifested as marked proteinuria, particularly
albuminuria (defined as 24-h urine protein excretion >
3.5 g), hypoalbuminemia, edema, hyperlipidemia, and
fat bodies in the urine.
9. Renal Disease
 Glomerulonephritis:
 Pathologically: intraglomerular inflammation
 Clinically: hematuria with RBC cast, subnephrotic proteinuria often with
renal failure, hypertension, edema.

 Nephrotic Syndrome:
 Noniflammatory injury to glomerular filtration barrier
 Proteinuria >3,5 g/24 hours, hypoalbuminemia <3,5 mg/dL, edema,
hypercholesterolemia, lipiduria

Pocket Medicine. 3rd ed. Lippincott Williams & Wilkins; 2008.

9. Renal Disease
Urinary Tract Infections
 At least 80% of the uncomplicated cystitis and pyelonephritis are due to
E. Coli. Other less common uropathogens include Klebsiella, Proteus,
and Enterobacter spp. & enterococci.

 Pyelonefritis:
 Inflammation of the kidney & renal pelvis
 fever, chilling, nausea, vomit, flank pain, diarrhe, leukocyte silinder.

 Cystitis:
 Inflammation of the bladder
 Dysuria, frequency, urgency, suprapubic discomfort, foul odor &
greyish urine.

 Urethritis:
 Inflammation of the urethra
 Dysuria, frequency, pyuria.

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.

10. Lung Disease
Diagnosis Characteristic
Atelectasis Collapse of lung, producing areas of relatively airless
pulmonary parenchyma. Causes: obstruction, compression,
or contraction (fibrotic changes)
Bronchiectasis Irreversible airway dilation that involves the lung arise from
infectious or noninfectious causes. Symptoms: a persistent
productive cough with ongoing production of thick,
tenacious sputum. Auscultation: rales & wheezing. Ro:
honeycomb appearance.
Pneumonia Infiltrates in CXR + 2 or more symptoms (progressive cough,
purulent sputum, fever, ronchi/bronchial,
leukocytosis/leukopenia.
Tuberculosis Respiratory symptoms: cough >2 weeks, hemoptoe,
dyspnea, chest pain. Systemic symptoms: fever, malaise,
night sweat, weight loss.
Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.
10. Lung Disease
 Bronchiectasis:
 Major causes: obstruction & infection
 Both are necessary for the development of full-fledged lesions,
although either may come first.
 Bronchial obstruction  impaired clearing mechanisms  pooling of
secretions distal to the obstruction & airway inflammation
 Severe infections of the bronchi  inflammation, often with necrosis,
fibrosis, and eventually dilation of airways.
 Bronchiectasis causes severe, persistent cough; expectoration of foul-
smelling, sometimes bloody sputum; dyspnea and orthopnea in severe
cases; and occasional life-threatening hemoptysis.
 Paroxysms of cough are particularly frequent when the patient rises in
the morning, when changes in position lead to drainage of collections
of pus and secretions into the bronchi.

Robbins & Cotran pathologic basis of disease. 8th ed. Philadelphia: Saunders; 2010.
10. Lung Disease
 Bronchiectasis
 Treatment of infectious bronchiectasis is directed at the control of active
infection and improvements in secretion clearance and bronchial hygiene so as
to decrease the microbial load within the airways and minimize the risk of
repeated infections.
 Antibiotic Treatment
 Antibiotics targeting the causative or presumptive pathogen (with
Haemophilus influenzae and P. aeruginosa isolated commonly) should be
administered in acute exacerbations, usually for a minimum of 7–10 days.
 Bronchial Hygiene
 The numerous approaches employed to enhance secretion clearance in
bronchiectasis include hydration and mucolytic administration,
aerosolization of bronchodilators and hyperosmolar agents (e.g., hypertonic
saline), and chest physiotherapy.

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.

10. Lung Disease

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.

10. Lung Disease
 Pneumonias may be classified as having lobar, bronchial, or interstitial
characteristics. Although the different histologic patterns are characteristic of
particular microorganisms, this is not invariable, and the same microorganism may
present with different histologic patterns
 Lobar pneumonia
 Characterized by the presence of neutrophilic infiltration in the alveoli. The
inflammation spreads through the pores of Khon and the Lambert channels, and
it consequently often affects a whole lobe.
 Characteristic of pneumonia due to S. pneumoniae, Klebsiella spp., and H.
influenzae.
 Bronchopneumonia
 Characterized by purulent exudate in terminal bronchioles and adjacent alveoli.
Endobronchial spread results in multiple foci of consolidation in lung segments,
subsegments, or smaller anatomic units.
 Characteristic of Staphylococcus aureus, Pseudomonas aeruginosa, Escherichia
coli, and other gram-negative bacilli.
 Intersitital
 Characterized by edema of the alveolar septum and infiltration by mononuclear
cells.
Murray & Nadel’s textbook of respiratory medicine.
 Characteristic of M. pneumoniae and virus. 4th ed. Philadelphia: Saunders; 2005.
 11. Organophosphate Intoxication
 Organophosphorus pesticides inhibit esterase enzymes,
especially acetylcholinesterase in synapses and on red-
cell membranes.
 Acetylcholinesterase inhibition  accumulation of
acetylcholine & overstimulation of acetylcholine
receptors in synapses of the autonomic nervous system,
CNS, and neuromuscular junctions  DUMBELS.
 DUMBELS: diarrhea, urination, miosis,
bradycardia/bronchorea/bronchospasm, emesis,
lacrimation, salivation.

Review article: Allergic rhinitis management pocket reference 2008. Journal compilation 2008 Blackwell Munksgaard. Allergy 2008:
63: 990–996.
11. Organophosphate Intoxication
 12. Diagnosis of Tuberculosis
 Several points of caution regarding
the algorithm.
 Completion of all of the steps
requires a substantial amount
of time; thus, it should not be
used for patients with an
illness that is worsening
rapidly.
 Patients with tuberculosis may
respond, at least transiently, to
broad spectrum antimicrobial
treatment.
 The approach outlined in the
algorithm may be quite costly
to the patient and deter
her/him from continuing with
the diagnostic evaluation.
International standards for tuberculosis care.
 Suspek TB paru

Pemeriksaan dahak sewaktu-pagi-sewaktu

BTA: + + + / + + - BTA: + - - BTA: - - -

Antibiotik nonOAT,
nonkuinolon
Pelatihan DOTS. Departemen Pulmonologi & Ilmu
Kedokteran Respirasi FKUI; 2008.

Tidak ada ada

perbaikan perbaikan

Foto toraks & Pemeriksaan dahak

pertimbangan dokter
mikroskopis

BTA: +++/ + + -/+ - - BTA: +++/ + + -/+ - -

Foto toraks &

pertimbangan dokter

TB Bukan TB
13. Malaria Complication
13. Malaria Complication

 Tatalaksana hipoglikemia (glukosa darah <40 mg/dL):

 Bolus glukosa 40% IV 40-100 mL
 Lanjutkan dengan infus glukosa 10% perlahan
 Pemantauan gula darah tiap 4-6 jam
Guidelines for the treatment of malaria, WHO 2010.
Pedoman penatalaksanaan kasus malaria di Indonesia, DEPKES 2003.
14. Lung Disease
 Diagnosis of pneumonia is established if there is new
infiltrate/progressive infiltrate with 2/> symptoms below:
 Progressive cough
 Change in sputum characteristic/purulent
 Fever
 Physical exam: bronchial breath sounds & crackles
 Leukocytes >10.000 or <4.500/mm3
14. Lung Disease
 Acute bronchitis
 Cough lasting more than 3 weeks. Fever, constitutional
symptoms, & a productive cough. No rales nor wheezing.
 Lobar pneumonia
 Characterized by the presence of neutrophilic infiltration in the
alveoli. The inflammation spreads through the pores of Khon and
the Lambert channels, and it consequently often affects a whole
lobe.
 Characteristic of pneumonia due to S. pneumoniae, Klebsiella
spp., and H. influenzae.
 Lung cancer
 Unresolved cough, dyspneu, hemoptysis weight loss in high risk
patient (smokers, age >40 years, exposure with industrial
substances.

Murray & Nadel’s textbook of respiratory medicine. 4th ed. Philadelphia: Saunders; 2005.
 15. Disorder of Calcium Balance
 Hypoparathyroidism may
occur as a complication of
thyroidectomy
 PTH released is inadequate
 hypocalcemia.
 Proximal tubular effect of
PTH to promote phosphate
excretion is lost 
hyperphosphatemia
 Low level of 1,25-(OH)2D
 Less PTH is available to act
in the distal nephron 
increase calcium excretion
 Less PTH  less Mg
reabsorption at ansa Henle.
McPhee SJ, et al. Pathophysiology of disease: an introduction to
clinical medicine. 5th ed. McGraw-Hill; 2006.
 15. Disorder of Calcium Balance
Organ Symptoms & Signs
Systemic Confusion
Weakness
Neuromuscular Paresthesias
Psychosis
Seizures
Carpopedal spasms
Chvostek's and Trousseau's signs
Depression
Muscle cramping
Parkinsonism
Irritability
Cardiac Prolonged QT interval Carpal spasm
T-wave changes
Congestive heart failure
Ocular Cataracts
Dental Enamel hypoplasia of teeth
McPhee SJ, et al. Pathophysiology
Respiratory Laryngospasm
of disease: an introduction to
Bronchospasm clinical medicine. 5th ed. McGraw-
Stridor Hill; 2006.
16. Thyroid Disease
 Anaplastic carcinoma
 Undifferentiated tumors , accounting for less than 5% of thyroid tumors,
with 100% mortality.
 Approximately a quarter of patients with anaplastic thyroid
carcinomas have a past history of a well-differentiated thyroid
carcinoma.
 Morphology. Microscopically, these neoplasms are composed of
highly anaplastic cells, with variable morphology, including:
 Large, pleomorphic giant cells, including occasional osteoclast-like
multinucleate giant cells;
 Spindle cells with a sarcomatous appearance;
 Mixed spindle and giant cells. The neoplastic cells express epithelial
markers like cytokeratin, but are usually negative for markers of thyroid
differentiation, like thyroglobulin.
16. Thyroid Disease
 Adenomas:
 Typically discrete, solitary masses, derived from follicular
epithelium, and hence they are also known as follicular
adenomas.
 The vast majority of adenomas are nonfunctional,
 A small proportion produces thyroid hormones and causes
clinically apparent thyrotoxicosis.
 Occasionally the neoplastic cells acquire brightly eosinophilic
granular cytoplasm (oxyphil or Hürthle cell change);
 The hallmark of all follicular adenomas is the presence of an
intact, well-formed capsule encircling the tumor.
16. Thyroid Disease
 Hashimoto’s thyroiditis: autoimmune destruction with
patchy lymphocytic infiltration, antithyroid peroxidase &
antithyroglobulin (+)  goitrous hypothyroidism.
 Therapy: levothyroxine

Hypothyroidism
16. Thyroid Disease
 Hashimoto’s thyroiditis
 The thyroid is often diffusely enlarged, although more
localized enlargement may be seen in some cases.
 Microscopic examination:
 Extensive infiltration of small lymphocytes, plasma cells, and well-
developed germinal centers.
 The thyroid follicles are atrophic and are lined in many areas by
epithelial cells distinguished by the presence of abundant
eosinophilic, granular cytoplasm, termed Hürthle cells.
16. Thyroid Disease
 Subacute thyroiditis or granulomatous thyroiditis or De Quervain
thyroiditis
 Subacute thyroiditis is believed to be triggered by a viral infection.
 This viral antigen stimulates cytotoxic T lymphocytes, which then
damage thyroid follicular cells.
 Histologically, the changes are patchy and depend on the stage of
the disease:
 Early stages: scattered follicles may be entirely disrupted and replaced
by neutrophils forming microabscesses.
 The more characteristic features: aggregates of lymphocytes, activated
macrophages, and plasma. Multinucleate giant cells enclose naked
pools or fragments of colloid (granulomatous thyroiditis).
 In later stages: chronic inflammatory infiltrate & fibrosis.
 17. Endocrine Disorder
Cushing's syndrome
(hyperadrenocorticalism/hypercortisolism)
 The clinical condition resulting from chronic
exposure to excessive circulating levels of
glucocorticoids
 The most common cause: excess ACTH secretion
from the anterior pituitary gland (Cushing's disease).
Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.
17. Kelainan Endokrinologi
 Hipertiroid: mudah marah, tremor, palpitasi, diare,
massa di leher.
 Cushing: moon face, buffalo hump, stria, resistensi
insulin, osteoporosis, imunokompromais, HT.
 Sindrom Conn (hiperaldosteron): HT, deplesi K,
retensi Na, ↓ akt. renin
 Feokromositoma : sakit kepala, HT, palpitasi, sudoris.
18. Renal Disorder
Causes of Nephrotic Syndrome
19. Diabetes Management

PERKENI 2011
19. Diabetes Management

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.

Diagnosisi & tatalaksana DM tipe 2 di Indonesia. PERKENI
19. Diabetes Management

PERKENI 2011
19. Diabetes Management
 Target terapi dislipidemia pada DM:
 Pada penyandang DM, target utamanya adalah penurunan
LDL
 Pada penyandang diabetes tanpa disertai penyakit
kardiovaskular: LDL <100 mg/dL (2,6 mmol/L)
 Pasien dengan usia >40 tahun, dianjurkan diberi terapi statin
untuk menurunkan LDL sebesar 30-40% dari kadar awal
 Pasien dengan usia <40 tahun dengan risiko penyakit
kardiovaskular yang gagal dengan perubahan gaya hidup,
dapat diberikan terapi farmakologis.

PERKENI 2011
 20. Hepatitis B
 HBsAg (the virus coat, s= surface)
 the earliest serological marker in the
serum.
 HBeAg
 Degradation product of HBcAg.
 It is a marker for replicating HBV.
 HBcAg (c = core)
 found in the nuclei of the hepatocytes.
 not present in the serum in its free form.
 Anti-HBs
 Sufficiently high titres of antibodies
ensure imunity.
 Anti-Hbe
 suggests cessation of infectivity.
 Anti-HBc
 the earliest immunological response to
HBV
 detectable even during serological gap.
Principle & practice of hepatology.
20. Acute
Hepatitis
21.GI Tract Disorder
 Irritable bowel syndrome (IBS) is a functional bowel disorder
characterized by:
 abdominal pain or discomfort
 altered bowel habits
 absence of detectable structural abnormalities.
 Most studies show a female predominance.
 No clear diagnostic markers exist for IBS, thus the diagnosis
of the disorder is based on clinical presentation.
21. GI Tract Disorder
aCriteria
fulfilled for the last 3 months with symptom onset at least 6 months prior to
diagnosis. Discomfort means an uncomfortable sensation not described as pain. “
21. GI tract Disorder
Diagnosis Characteristic
Crohn disease diarrhea; abdominal pain that is usually insidious in the
right lower quadrant, triggered or aggravated frequently
after meals; weight loss; & an association with a tender,
inflammatory mass in the right lower quadrant. The
diarrhea is usually nonbloody.
Somatization somatic symptoms without any abnormality found (4
disorder different location of pain, 2 GI tract symptom, 1 sexual
symptom, 1 pseudoneurological symptom)
Peptic ulcer epigastric burning, nausea, postprandial fullness, or
"bloating,“.
Colitis diarrhea, with or without blood in the stool. If inflammation
ulcerative is confined to the rectum (proctitis), blood may be seen on
the surface of the stool; other symptoms include tenesmus,
urgency, rectal pain, and passage of mucus, without
diarrhea.
22. Hypertensive Crisis
 Hypertensive crisis:
 Sudden elevated blood pressure (systole ≥180 mmHg or
diastole ≥120 mmHg) in hypertensive patient, which needs
immediate treatment.
 Emergency hypertension: target organ damage (+). BP
should be decreased in minutes/hours.
 Urgency hypertension: target organ damage (-). BP should
be decreased in 24-48 hours.

Ringkasan eksekutif krisis hipertensi. Perhimpunan hiperensi Indonesia.

22. Hypertensive Crisis
 Clinical manifestation of hypertension crisis:
 Neurology: headache, blurred vision, convulsion,
neurological deficit, unconsciousness.
 Eye: retinal hemorrhage, retinal exudate, edema papil.
 Cardiovascular: chest pain, lung edema.
 Renal: azotemia, proteinuria, oliguria.
 Obsteric: severe preeklampsia.
 Risk Factors:
 noncompliance, pregnancy, drug abuse, high sympathetic
stimulation (severe burn, pheochromocytoma, collagen
disease, vascular disease, trauma)
Ringkasan eksekutif krisis hipertensi. Perhimpunan hiperensi Indonesia.
22. Hypertensive Crisis
 Management:
 Management should be done in hospital, however primary
care service can give oral antihypertension as a first aid.
 Parenteral drug is given via bolus or infusion ASAP.
 Drugs:
 ACE-I (Captopril): sublingual 6,25-50 mg
 Nifedipin oral: only used as alternative if other drugs aren’t
available. Contraindicated in brain & heart ischemia.
 Nicardipine 10-30 mcg/kgBW bolus.
 Clonidine 900 mcg into 500 mL of 5% glucose infusion, given in 12
drops/minute.
 Nitroprusside infus 0,25-10,0 mcg/kg/menit

Ringkasan eksekutif krisis hipertensi. Perhimpunan hiperensi Indonesia.

22. Hypertensive Crisis
 Blood pressure target:
 First 5-120 minutes
 MAP is lowered by 20-25%
 2-6 hours after:
 Blood presssure is lowered to 160/100 mmHg
 6-24 hours:
 If there is no symptom of organ ischemia, blood pressure is
lowered until <140/90 mmHg.

Ringkasan eksekutif krisis hipertensi. Perhimpunan hiperensi Indonesia.

23. Fever
a) Fever continues
b) Fever continues to
abrupt onset and
remission
c) Fever remittent
d) Intermittent fever
e) Undulant fever
f) Relapsing fever
 23. Fever

 Saddleback
fever in dengue
infection
Shock
Bleeding
24. Hypertension
24.Hypertension
 If a drug is not tolerated
or is contraindicated,
then one of the other
classes proven to
reduce cardiovascular
events should be used
instead.
 Treating SBP and DBP to
targets that are <140/90
mmHg is associated
with a decrease in CVD
complications.
 In patients with
hypertension and
diabetes or renal
disease, the BP goal is
<130/80 mmHg.
25. Urinary Tract Infection
25. Urinary Tract Infection
25. Urinary Tract Infection

 Cystitis: dysuria, frequency, urgency, suprapubic discomfort,

foul odor & greyish urine.
 Pyelonefritis: fever, chilling, nausea, vomit, flank pain,
diarrhe, leukocyte silinder.
 Urethritis: dysuria, frequency, pyuria.

Harrison’s principles of internal medicine. 18th ed. McGraw-Hill; 2011.

25. Urinary Tract Infection
 Recurrent UTI
 2 uncomplicated UTIs in 6 months or 3 positive cultures within
the preceding 12 months
 Investigation:
 physical examination to evaluate urogenital anatomy &
estrogenization of vaginal tissues & to detect prolapse.
 Post-void residual urine volume should be measured.
 Diabetes screening in patients with other risk factors (family
history & obesity).
 Women who suffer infection with organisms that are not
common causes of UTI, such as Proteus, Pseudomonas,
Enterobacter, and Klebsiella may have structural abnormalities or
renal calculi  imaging & cystoscopy
25. Urinary Tract Infection
 Women who are felt to be in the early stages of a problem
with recurrent UTI should have documented cultures  gold
standard for diagnosis & provides information about the
uropathogen & antibiotic susceptibilities.
 The standard definition of a UTI on culture is >105 colony
forming units per HPF.
 In women with symptoms of a UTI > 103 colony forming units
per HPF is considered sufficient.
25. UTI
 Patients with 3 infections
annually should be offered
a regimen of:
 continuous, low-dose
prophylaxis or
 post-coital prophylaxis.
26. Tuberculosis
Tipe Pasien Definisi
Baru Belum pernah/sudah pernah OAT <1 bulan
Kambuh/relaps Pernah sembuh atau OAT lengkap, kembali BTA +
Defaulted/drop out OAT >1 bulan, tidak mengambil obat ≥2 bulan
Gagal Telah berobat tapi BTA tetap + pada akhir bulan ke-5
Kronik BTA + dengan OAT kategori 2
Bekas TB BTA -, Ro: tidak aktif

Paduan Obat Tipe Pasien

Kategori 1: Pasien baru, TB paru BTA (-), TB ekstra paru.
2RHZE/4(RH)3
Kategori 2 Pasien kambuh, Pasien gagal, Pasien default
2RHZES/RHZE/5(RHE)3
Kategori anak Anak dengan skor TB ≥6
2RHZ/4RH
Profilaksis anak Anak dengan kontak penderita TB BTA (+)
6INH 5-10 mg/kgBB
27. Burn Injury http://en.wikipedia.org/wiki/Burn

prick test (+)

• Berat luka bakar:
• Ringan: derajat 1 luas <
15% a/ derajat II < 2%
• Sedang: derajat II 10-
15% a/ derajat III 5-
10%
• Berat: derajat II > 20%
atau derajat III > 10%
atau mengenai wajah,
tangan-kaki, kelamin,
persendian,
pernapasan
 To estimate scattered burns:
patient's palm surface = 1%
total body surface area

Total Body
Surface Area

Parkland formula = baxter formula

http://www.traumaburn.org/referring/fluid.shtml
28. Trauma Uretra
 Suspect that a patient may
have injured his lower
urinary tract if:
 he has some injury which
makes this likely
(especially a fractured
pelvis)
 cannot pass urine after
an accident
 there is blood at the tip
of his urethra
  Don't pass a diagnostic
 Retrograde urethrography
catheter up the patient's
 Primary imaging modality
urethra because:
for evaluating traumatic
 The information it will injuries and inflammatory
give will be unreliable. and stricture diseases of
 May contaminate the the male urethra
haematoma round the
injury.
 May damage the slender
bridge of tissue that joins
the two halves of his
injured urethra

Posterior urethral rupture above the

intact urogenital diaphragm
following blunt trauma

http://ps.cnis.ca/wiki/index.php/68._Urinary
29. DVT
Virchow Triads:
(1) venous stasis
(2) activation of blood
coagulation
(3) vein damage

Crurales Vein is a
common and correct
terminology
Superficial vein
systems
  Signs and symptoms of DVT
include :
 Pain in the leg
 Tenderness in the calf ( this
is one of the most
improtant signs )
 Leg tenderness
 Swelling of the leg
 Increased warmth of the leg
 Redness in the leg
 Bluish skin discoloration
 Discomfort when the foot is
pulled upward (Homan’s)

http://www.medical-explorer.com/blood.php?022
30. Carpal Tunnel syndrome
 Carpal tunnel syndrome (CTS) is a collection of
characteristic symptoms and signs that occurs following
entrapment of the median nerve within the carpal
tunnel.
 Usual symptoms include numbness, paresthesias, and
pain in the median nerve distribution.
 These symptoms may or may not be accompanied by
objective changes in sensation and strength of median-
innervated structures in the hand
Symptoms
 Numbness and tingling
 Pain
 Autonomic symptoms
 Many patients also report sensitivity to changes in
temperature (particularly cold) and a difference in skin
color.
 Weakness/clumsiness - Loss of power in the hand
(particularly for precision grips involving the thumb)
If you can hold your hands in this
position for 30 seconds without pain,
numbness or tingling, then you
probably do not have Carpal Tunnel
31. Male Genital Disorder

Epispadiathe urethra ends

in an opening on the upper
aspect (the dorsum) of the
penis
• Penis typically broad,
shortened upward
curvature (dorsal chordee)
• Attached to the pelvic
bones, which are widely
separated
• Classification:
• the glans (glanular)
• along the shaft of the
penis (penile)
• near the pubic bone
(penopubic)

http://www.genitalsurgerybelgrade.com/uroge
nital_surgery_detail.php?Epispadias-4
 Hypospadia
• The urethral opening is ectopically
located on the ventrum of the
penis proximal to the tip of the
glans penis
• Three anatomical characteristics
• An ectopic urethral meatus
• An incompleteprepuce

http://emedicine.medscape.com/article/1015227
• Chordee ventral shortening and
curvature

Anorchia  the absence of both testes at birth

• Normal outside genitals before puberty
• Failure to start puberty at the correct time
• Empty scrotum
• Lack of secondary sex characteristics
• penis and pubic hair growth
• deepening of the voice
• increase in muscle mass
Phimosis Paraphimosis
 Inability to retract the  Entrapment of a
distal foreskin over the retracted foreskin
glans penis behind the coronal
 Physiologic in newborn sulcus
 Complications  Emergency
 Superficial vein
 Balanitis
obstruction  edema
 Postitis and pain  penile
 Balanopostitis glands necrosis
 Treatment  Treatment
 Dexamethasone 0.1% (6  Manual reposition
weeks) for spontaneous  Dorsum incision
retraction
32. Posterior Hip Dislocation
Symptoms
• knee pain
• pain in the back
hip
• difficulty moving
the lower
extremity
• The leg is
shortened and
internally rotated
with flexion and
adduction at the
hip

Risk Factor
• Accident
• Improper seating
adjustment
• sudden break in
the car
netterimages.com soundnet.cs.princeton.edu
Anterior Hip Dislocation
Symtomps
• pain in the hip
• inability to walk or
adduct the leg.
• The leg is externally
rotated, abducted,
and extended at the
hip

netterimages.com soundnet.cs.princeton.e
Treatment: Reposition
 If the patient has no other complications:
 Anesthetic or a sedative and manipulate the bones back
into their proper position (this is called a reduction)
 In some cases the reduction must be done in the
operating room with anesthesia. A formal procedure with
an incision may be required to reduce the hip.
 Following treatment, the surgeon will request another set
of X-rays and possibly a computed tomography (CT) scan
to make sure that the bones are in the proper position.
 Anterior reduction/reposition

Posterior reduction/reposition
http://orthoinfo.aaos.org/topic.cfm?topic=A00352
33.Rabies

http://www.cdc.gov/rabies/medical_care/index.html
Purified Chick Embryo Cell Vaccine (PCEC) Human Diploid Cell Vaccine (HDCV)
34. Ureterolithiasis
 Urinary tract stone disease
 Signs:
 Flank pain
 Irritative voiding symptom
 Nausea
 microscopic hematuria
 Urinary crystals of calcium
oxalate, uric acid, or cystine
may occasionally be found
upon urinalysis
 Diagnosis: IVP
Differential Diagnosis

 Nephrotic syndrome is
defined as the presence of
proteinuria (>3.5 g/24
hours), hypoalbuminaemia
(<30 g/L), oedema, and
hyperlipidaemia
 35. Posterior Hip Dislocation
Symptoms
• knee pain
• pain in the back
hip
• difficulty moving
the lower
extremity
• The leg is
shortened and
internally rotated
with flexion and
adduction at the
hip

Risk Factor
• Accident
• Improper seating
adjustment
• sudden break in
the car
netterimages.com soundnet.cs.princeton.edu
Hip Dislocation in Emergency
Medicine Workup
 AP pelvis radiograph should reveal most type hip
dislocations.
 Lateral views may further classify the type of
dislocation.
 If the AP pelvis film is nondiagnostic and a high index
of suspicion exists, a lateral hip film, dedicated hip
films, Judet views, or CT scan may be indicated

http://emedicine.medscape.com/article/823471-workup#a0720
36. Hemorrhoid
37. Compartment Syndrome
A condition in which
increased pressure within a
limited space compromises
the circulation and function
of the tissues within that
space.
 Elevated tissue pressure
within a closed fascial
space
 Reduces tissue perfusion -
ischemia
 Results in cell death -
necrosis

True Orthopaedic Emergency

Compartment Syndrome
Etiology
Compartment Size
 tight dressing; Bandage/Cast
 localised external pressure; lying on limb
 Closure of fascial defects

Compartment Content
 Bleeding; Fx, vas inj, bleeding disorders
 Capillary Permeability;
 Ischemia / Trauma / Burns / Exercise / Snake Bite
/ Drug Injection / IVF
optimized by optima
Compartment Syndrome
Etiology
 Fractures-closed and open
 Blunt trauma
 Temp vascular occlusion
 Cast/dressing
 Closure of fascial defects
 Burns/electrical
 Exertional states
 IV/A-lines
 Intraosseous IV(infant)
 Snake bite
 Arterial injury
Compartment Syndrome
Diagnosis
 Pain out of proportion
 Palpably tense compartment
 Pain with passive stretch
 Paresthesia/hypoesthesia
 Paralysis
 Pulselessness/pallor
Clinical Evaluation
“Pain and the aggravation of pain by passive stretching
of the muscles in the compartment in question are the
most sensitive (and generally the only) clinical finding
before the onset of ischemic dysfunction in the nerves
and muscles.”

Whitesides AAOS 1996

 Compartment Syndrome
Pressure Measurements
 Infusion  Arterial line
 manometer  16 - 18 ga. Needle
 saline (5-19 mm Hg higher)
 3-way stopcock  transducer
(Whitesides, CORR 1975)  monitor
 Catheter  Stryker device
 wick
 Side port needle
 slit wick
Compartment Syndrome
Emergent Treatment
 Remove cast or dressing
 Place at level of heart
(DO NOT ELEVATE to optimize perfusion)
 Alert OR and Anesthesia
 Bedside procedure
 Medical treatment
Surgical Treatment
 Fasciotomy
 Casts and tight
bandages
 remove or loosen
any constricting
bandages

All compartments !!!

38. Acute Appendicitis
 Gross Findings：
 Congested & swollen.
 Dilated lumen contain pus, or a fecalith, or both.
 Serosa coated with fibrin, fibrinopurulent exudate, or pus.
 Micro Findings：
 Mucosal ulceration & infiltration by PMNs, eosinophils,
plasma cells, &lymphocytes throughout all layers &
frequently into serosa.
 More advanced stage, the inflammatory process involved
the full thickness of wall,with partial necrosis or infarction
of wall (perforated areas).
Robbins Pathologic Basis of Disease, 6th ed. P.839-840.
Pseudomyxoma
 Rare form of peritoneal cancer.
 At its origin is a rather benign small tumor at the base of
the appendix which blocks the passage.
 Jelly accumulates in the appendix which eventually
bursts, releasing jelly and tumor cells in the abdominal
cavity.
 These tumor cells continue to produce jelly, which results
in a swollen abdomen and sticking together of parts of
the small bowel with obstruction
 A HIPEC is regarded in many centers as the first choice
treatment of this slowly growing tumor.
 http://en.wikipedia.org/wiki/Diverticulum

Diverticulum
Psoas abscess • an outpouching of a hollow (or a
 A is a collection of pus in fluid-filled) structure in the body
the iliopsoas muscle • Classification  depending upon
compartment the layers involved:
 It may arise via contiguous
spread from adjacent • True diverticula  all layers
structures or by the of the structure, including
hematogenous route from muscularis propria and
a distant site adventitia.
 Incidence is rare
• False diverticula do not
 Symptoms
 hip is flexed and has a
involve muscular layers or
limited and painful range adventitia. False diverticula,
of motion in the GI tract for instance,
 fever, flank pain, involve only the submucosa
abdominal pain, or limp
and mucosa.
http://www.uptodate.com/contents/psoas-abscess
 39.
Atresia
Anii

http://www.acssurgery.com/acssur
gery/secured/figTabPopup.action?
bookId=ACS&linkId=part09_ch02_
fig3&type=fig
 The steps in the stabilization of a critically ill neonate
before transport are similar to the ABCs of initial care in
an adult (airway, breathing, circulation).
 Establish vascular access. Appropriate fluids should be
infused to prevent dehydration and to correct any fluid
or electrolyte deficits
 A nasogastric or esophageal pouch suction tube should
be placed and decompression initiated
 Antibiotics as needed
40. Appendectomy
41. Kidney Stone
 Calcium oxalate stones
 the most common
 They tend to form when the urine is acidicit has a low pH
 Some of the oxalate in urine is produced by the body
 Calcium and oxalate in the diet play a part but are not the only
factors that affect the formation of calcium oxalate stones
 Dietary oxalate an organic molecule found in many vegetables,
fruits, and nuts
 Calcium from bone may also play a role in kidney stone
formation.
 Calcium phosphate stones
 less common
 tend to form when the urine is alkalineit has a high pH
 Struvite stones
 Found more often in women
 almost always the result of urinary tract infections
 Uric acid stones
 These are a byproduct of protein metabolism
 commonly seen with gout,and may result from certain genetic
factors and disorders of your blood-producing tissues
 fructose also elevates uric acid, and there is evidence that
fructose consumption is helping to drive up rates of kidney
disease
 Cystine stones
 Representing only a very small percentage
 these are the result of a hereditary disorder that causes kidneys
to excrete massive amounts of certain amino acids (cystinuria)
 42. Goiter
 Thyrotoxic storm (thyroid crisis)  an unusual
complication of thyroid surgery
 This condition may result from manipulation of the
thyroid gland during surgery in the patients with
hyperthyroidism.
 It can develop preoperatively, intraoperatively, or
postoperatively.

http://emedicine.medscape.com/article/
  Surgery in hyperthyroide condition generally
recommended only when:
 patients have Graves disease
 other treatment strategies fail
 when underlying thyroid cancer is suspected
 Hyperthyroide must be controlled before the surgery
done
 Thyrotoxic storm is potentially lethal and must be dealt
with astutely

http://emedicine.medscape.com/article/
43. Maxillofacial Trauma
44. Hospital admission criteria for
patients with thermal injury
 Partial-thickness burns greater than 20% total BSA (TBSA)
child < 10 or elderly >10%
 Full-thickness burns greater than 2% TBSA
 Burns involving the face, hands, genitalia, perineum, or
major joints
 Circumferential extremity burns
 All high-voltage electrical burns, including lightning injury
 Admission of low-voltage electrical burns is selective
  Chemical burns
 Inhalation injury
 Burn injuries in patients with preexisting medical
disorders that could complicate management, prolong
recovery, or affect mortality (eg, diabetes,
immunosuppression)
 Suspected child abuse
 Cases in which it is determined that it is in the best
interest to admit the child (ie, parental inability to care
for the burn)

http://emedicine.medscape.com/article/934173-treatment
45. Hypovolemic Shock
46. Osteoporosis
 Dual-energy radiographic absorptiometry (DXA) is the
standard study used to establish or confirm a diagnosis of
osteoporosis because it allows for quantification of bone
mineral density.
 Quantitative computed tomography (CT) can also
measure bone mineral density, but the cost and radiation
exposure limit its use.
 Ultrasonography is a low-cost screening modality for
asymptomatic women, but has not been proven as
effective as DXA.
 47. Intussusception
• age 6 to 12 months
• male gender
• abdominal pain
• vomiting
• lethargy/irritability
• blood per rectum
/currant jelly stool
• palpable abdominal mass
• Portio-like on DRE

http://bestpractice.bmj.com/best-practice/monograph/679/highlights/overview.html
Abdominal Ultrasound
48. Hernia

VENTRAL HERNIA
Hernia Location and Nomenclature

Additional:
Spigellian hernia: very rare, a hernia through the spigelian fascia and in most cases, it
has a small size
Ventral hernia: hernia in the abdominal wall, for example: incisional, umbilical and
paraumbilical hernia
49. Phimosis
Phimosis Paraphimosis
 Inability to retract the  Entrapment of a
distal foreskin over the retracted foreskin behind
glans penis the coronal sulcus
 Physiologic in newborn  Emergency
 Complications  Superficial vein
 Balanitis obstruction  edema
 Postitis and pain  penile
 Balanopostitis glands necrosis
 Treatment  Treatment
 Dexamethasone 0.1% (6
 Manual reposition
weeks) for spontaneous
retraction  Dorsum incision
50. BPH
The size of prostate enlarged microscopically since the age
of 40. Half of all men over the age of 60 will develop an
enlarged prostate
By the time men reach their 70’s and 80’s, 80% will
experience urinary symptoms
But only 25% of men aged 80 will be receiving BPH treatment
What is Benign Prostatic Hyperplasia?
• BPH is part of the natural
aging process, like
getting gray hair or
Peripheral zone
wearing glasses
Transition zone
Urethra • BPH cannot be
prevented
• BPH can be treated

Peripheral zone
Transition zone
Urethra
 Diagnosis of BPH
• Symptom assessment
– the International Prostate Symptom Score (IPSS) is recommended as it is used
worldwide
– IPSS is based on a survey and questionnaire developed by the American Urological
Association (AUA). It contains:
• seven questions about the severity of symptoms; total score 0–7 (mild), 8–19
(moderate), 20–35 (severe)
• Digital rectal examination(DRE)
– inaccurate for size but can detect shape and consistency
• PV determination- ultrasonography
• Urodynamic analysis
– Qmax >15mL/second is usual in asymptomatic men from 25 to more than 60 years of
age
• Measurement of prostate-specific antigen (PSA)
– high correlation between PSA and PV
– men with larger prostates have higher PSA levels
– PSA is a predictor of disease progression and screening tool for CaP
– PSA may be used as a prognostic marker for BPH
Management
 Lifestyle modification
 Reduce fluid intake
 Stop diuretics if poss
 Avoid xs night time fluid intake/caffeine
/alcohol
 Empty bladder before long trips/meetings
Management
 Drug therapy
 Alpha blockers
 Improve bladder and
prostate smooth muscle
tone
 More effective than 5
alpha reductase inhibitors
 All work equally well
 Tamsulosin and alfuzosin
require no dose titration
 Drug therapy
 5 alpha reductase inhibitors
 Reduce prostate volume
 Reduces risk of prostate
cancer, increases risk of
high grade disease
 Combined therapy
 Men with large prostate >
40g or PSA >4 or
moderate to severe
symptoms combined
therapy will prevent 2
episodes of clinical
progression per 100men
over 4yrs. Much less
effective for men with
smaller prostates
http://www.medscape.org/viewarticle/456664
http://www.medscape.org/viewarticle/541739_2
51. Prevention for Tetanus
 DTaP: diphtheria, tetanus, acellular pertussis
Tdap:tetanus, diphtheria, acellular pertussis
TIG:tetanus immune globulin

http://emergency.cdc.gov/disasters/disease/tetanus.asp
Tetanus - Pencegahan
 Imunisasi Aktif:
 Pencegahan pada luka:
1. Luka ringan & bersih:
 Imunisasi lengkap: ≠ ATS/imunoglobulin
 Tidak lengkap: imunisasi aktif DPT/DT
2. Luka sedang/berat & kotor:
 Imunisasi (-)/tidak jelas: ATS 3000-5000 U, Imunoglobulin 250-
500 U, toksoid tetanus.
 Imunisasi (+) >5 tahun: ulangan toksoid, ATS 3000-5000 U,
tetanus imunoglobulin 250-500 U.
 52.Labiognatopalatoshisis
 Celah pada bibir, gusi dan langitan
 RULE OF TEN :
 Berat badan 10 lb (5 kg)
 Usia 10 minggu
 Kadar hemoglobin darah
10 g/dL

http://en.wikipedia.org/wiki/Cleft_lip_and_palate
http://www.scribd.com/doc/55885689/labio-gnato-palatoschisis
• Cleft palate
• the two plates of the skull that form the hard
palate (roof of the mouth) are not completely
joined
• The soft palate is in these cases cleft as well
• Cleft lip
• formed in the top of the lip
• a small gap or an indentation in the lip
(partial or incomplete cleft)
• continues into the nose (complete
cleft)
• due to the failure of fusion of the
maxillary and medial nasal processes
(formation of the primary palate)
53. KATARAK
ANAMNESIS
MATA MERAH
VISUS NORMAL MATA
• struktur yang MATA MERAH MATA TENANG TENANG
bervaskuler  VISUS TURUN VISUS TURUN VISUS TURUN
sklera MENDADAK PERLAHAN
konjungtiva mengenai media
• tidak refraksi (kornea, • uveitis posterior • Katarak
menghalangi uvea, atau • perdarahan vitreous • Glaukoma
media refraksi seluruh mata) • Ablasio retina • retinopati
• oklusi arteri atau penyakit
• konjungtivitis vena retinal
• Keratitis sistemik
murni • neuritis optik
• Keratokonjung • neuropati optik akut • retinitis
• Trakoma
tivitis karena obat pigmentosa
• mata kering,
• Ulkus Kornea (misalnya • kelainan
xeroftalmia
• Uveitis etambutol), migrain, refraksi
• Pterigium
• glaukoma akut tumor otak
• Pinguekula
• Endoftalmitis
• Episkleritis
• panoftalmitis
• skleritis
 http://sdhawan.com/ophthalmology/lens&cataract.pdf E-mail: sdhawan@sdhawan.com

Cataract
 Any opacity of the lens or loss of transparency of the lens that causes
diminution or impairment of vision
 Classification : based on etiological, morphological, stage of maturity
 Etiological classification :
 Senile
 Traumatic (penetrating, concussion, infrared irradiation, electrocution)
 Metabolic (diabetes, hypoglicemia, galactosemia, galactokinase
deficiency, hypocalcemia)
 Toxic (corticosteroids, chlorpromazine, miotics, gold, amiodarone)
 Complicated (anterior uveitis, hereditary retinal and vitreoretinal
disorder, high myopia, intraocular neoplasia
 Maternal infections (rubella, toxoplasmosis, CMV)
 Maternal drug ingestion (thalidomide, corticosteroids)
 Presenile cataract (myotonic dystrophy, atopic dermatitis)
 Syndromes with cataract (down’s syndrome, werner’s syndrome, lowe’s
syndrome)
 Hereditary
 Secondary cataract
• Morphological classification :
 Juvenile (1-13years)
 Capsular
 Presenile (13-35 years)
 Subcapsular
 Senile
 Nuclear
• earlier than the other
 Cortical
– Shadow test +
 Lamellar
 Sutural
• Sign & symptoms:
• Stage of maturity classification:
– Near-sightedness (myopia
 Immature shift) Early in the
 Mature development of age-related
 Intumescent cataract, the power of the lens
 Hypermature may be increased
 Morgagnian – Reduce the perception of blue
colorsgradual yellowing and
• Chronological classification:
opacification of the lens
 Congenital (since birth)
– Gradual vision loss
 Infantile ( first year of life)
– Almost always one eye is
affected
Diabetic Cataract
• Cataracts are among the earliest complication of DM
• Aldose reductase, is an enzyme that is normally present in many
other parts of the body, and catalyzes one of the steps in the
sorbitol(polyol) pathway that is responsible for fructose formation
from glucose.
• Aldose reductase activity increases as the glucose concentration
rises in diabetes in those tissues that are not insulin sensitive, which
include the lenses, peripheral nerves and glomerulus.
• Sorbitol does not diffuse through cell membranes easily and
therefore accumulates, causing osmotic damage which leads to
retinopathy and neuropathy.
Polyol Pathway
Treatment
• Extracapsular cataract extraction (ECCE) and
– Removing the lens, but leaving the majority of the lens
capsule intact
– High frequency sound waves (phacoemulsification)break
up the lens before extraction
• Intracapsular cataract extraction (ICCE)
– Removing the lens and lens capsulerare
• The cataractous lens is removed and replaced with a
plastic lens (an intraocular lens implant) which stays in
the eye permanently.

www.wikipedia.org
54. GANGGUAN LAPANG PANDANG
HIPOFISE/PITUITARI  Pada dinding lateral dari
GLAND : sella terdapat dinding
medial dari sinus
• Terletak pada sella
kavernosus yang
turcica
 berisi N III, IV, VI, V1,V2
• Superior dari kelenjar dan A.karotis interna.
hipofisis terdapat
diaphragma sella,
• Diatas diaphragma ini
terletak nervus optikus,
chiasma dan traktus.
GANGGUAN LAPANG PANDANG
Gangguan Lapang Pandang
 www.wikipedia.org

55. Refraction Disorder

Disorders Feature Correction

Myopia the light that comes in does not directly focus on the Concave lens. The
retina but in front of itimage at a distant object to smallest Dioptri to
be out of focus but in focus when looking at a close corret the visual
objec. aquity to 6/6

Hypermetropia imperfection in the eye (often when the eyeball is too Convex lenses. The
short or the lens cannot become round enough). largest Dioptri to
Difficult focusing on near objects corret the visual
aquity to 6/6

Astigmatisma Unspherical corneal structure; distorted image Lens correction,

laser ceratotomy

Presbyopia the eye exhibits a progressively diminished ability to Correction lens

focus on near objects with age, eyestrain, difficulty
seeing in dim light, problems focusing on small
objects
Ambliopia Decrease of vision; disuse/inadequate
foveal/peripheral retinal stimulation and/or abnormal
binocular interaction that cause different visual input
 Presbiopia • Kekuatan lensa yang
• a condition in which the lens of the • biasa digunakan:
eye loses its ability to focus, making it
difficult to see objects up close.
+ 1.0 D  usia 40 tahun
• Symptoms : decreased focusing ability
+ 1.5 D  usia 45 tahun
for near objects, eyestrain, headache + 2.0 D  usia 50 tahun
• Test : examination of the retina, + 2.5 D  usia 55 tahun
muscle integrity test, refraction test, + 3.0 D  usia 60 tahun
slit-lamp test, visual acuity
• Treatment : corrected with
• converging lenses
Lensa:
• monofokal
• bifokal
• trifokal

http://www.ivo.gr/files/items/1/145/51044.jpg
http://en.wikipedia.org/wiki/ http://www.ncbi.nlm.nih.gov/pubmedhealth/

56. Eyelids Disorders

Pathology Feature

Chalazion Chronic inflamation of Zeis/Meibom gland; when acutely inflammed Painful,

(meibomian gland warm, swollen, and firm eyelids, granulomatous reaction, lipogranuloma, usually on
lipogranuloma) the upper eyelid and inside the lid, painless nodules, Increased tearing, Sensitivity to
light
Hordeolum Localized infection or inflammation of the eyelid margin involving hair follicles of the
eyelashes (external hordeolum) or meibomian glands (internal
hordeolum),Staphylococcal infection; painful, warm, swollen, and tender eyelids,
focal collection of PMN cells and necrotic tissue. erythematous, and
localized,Purulent material exudates
 Chalazion
• The result of obstruction of the duct of a meibomian gland, which is usually
idiopathic, with secondary lipogranulomatous inflammation
• Epidemiology : higher incidence in seborrheoc dermatitis, rosacea, and DM
• Clinical features : a pale, round, firm lesion of the lid.
Diagnosis : made clinically
• Treatment : incision of the cyst and removed by curetting. Steroid injection can
initiate remission
• Prognosis : ocacasionally recurrent

http://www.healblog.net/wp-content/uploads/Hordeolum-and-
Chalazion.jpg
57-58. LACRIMAL GLAND DISORDER
Evaluasi Sistem Lakrimal-Drainase Lakrimal :
Uji Anel : Dengan melakukan uji anel, dapat diketahui apakah fungsi
dari bagian eksresi baik atau tidak.
Cara melakukan uji anel :
Lebarkan pungtum lakrimal dengan dilator pungtum
Isi spuit dengan larutan garam fisiologis. Gunakan jarum lurus atau
bengkok tetapi tidak tajam
Masukkan jarum ke dalam pungtum lakrimal dan suntikkan cairan
melalui pungtum lakrimal ke dalam saluran eksresi , ke rongga hidung
Uji anel (+): terasa asin di tenggorok atau ada cairan yang masuk
hidung. Uji anel (-) jika tidak terasa asin  berarti ada kelainan di
dalam saluran eksresi.
Jika cairan keluar dari pungtum lakrimal superior, berarti ada
obstruksi di duktus nasolakrimalis. Jika cairan keluar lagi melalui
pungtum lakrimal inferior berarti obstruksi terdapat di ujung nasal
kanalikuli lakrimal inferior, maka coba lakukan uji anel pungtum
lakrimal superior.
Atlas of ophthalmology; Pedoman pelayanan medis RS Cicendo
 Tes Konfrontasi Pemeriksaan lapangan penglihatan perifer
Tes Fluoresensi Memulaskan fluoresens ke permukaan kornea untuk melihat
keteraturan dari permukaannya. Dilihat dengan slit lamp
Tes Ishihara Pemeriksaan buta warna
Tes Amsler Kisi-kisi amsler untuk menguji lapangan pandang sentral 20
derajat

Oftalmologi Umum
 Dacryocistitis Acute
• Partial or complete obstruction of the nasolacrimal duct with
inflammation due to infection (Staphylococcus aureus or
Streptococcus B-hemolyticus), tumor, foreign bodies, after
trauma or due to granulomatous diseases.
• Clinical features : epiphora, acute, unilateral, painful
inflammation of lacrimal sac, pus from lacrimal punctum, fever,
general malaise, pain radiates to forehead and teeth
• Diagnosis : Anel test  (+) :not dacryocystitis, probably skin
abcess; (-) or regurgitation (+) : dacryocystitis. Swab and culture
• Treatment : Systemic and topical antibiotic, irrigation of lacrimal
sac, Dacryocystorhinotomy

Atlas of ophthalmology; Pedoman pelayanan medis RS Cicendo

Konjungtivitis Inflammation of conjunctiva due to infection or allergy. itching and
burning or a gritty, foreign-body sensation, mucopurulent discharge,
visual acuity is normal
Uveitis Swelling and irritation of the uvea (middle layer of the eye). Pain,
redness, photophoia, excessive tearing, decreased vision, limbic
injection, miosis, might be followed by glaucoma
Hordeolum Localized infection or inflammation of the eyelid margin involving
hair follicles of the eyelashes (external hordeolum) or meibomian
glands (internal hordeolum),Staphylococcal infection; painful, warm,
swollen, and tender eyelids, focal collection of PMN cells and
necrotic tissue. erythematous, and localized,Purulent material
exudates
Glaukoma A group of eye conditions that leads to optic nerve damage. Acute
onset of ocular pain, nausea, headache, vomitting, blurred vision,
haloes (+), palpable increased of IOP(>21 mm Hg), conjunctival
injection, corneal epithelial edema, mid-dilated nonreactive pupil
59. KERATITIS
 Keratitis : inflammation of the cornea
Types Etiology Epidemiology Clinical Feature
Bacterial Staphylococcus aureus, Contact lens wearer, Corneal ulcer, hypopion,
Staphylococcus disease of the corneal infiltrate,
epidermidis, Streptococcus corneal surface reduce vision
pneumoniae, Pseudomonas
aeruginosa, Moraxella.

Viral Herpes simpleks, herpes Elderly, Dendritic keratitis

zooster immunosuppressed
person
Fungal Aspergillus fusarium After ocular trauma Satellite lesions,
due to introduction hypopion
of plant material
Fungal Keratitis
 Etiology :after ocular trauma due to the introduction of plant
materials into the eye, usually Aspergillus fusarium and
Cephalosporium species.
 Epidemiology :rare
 Clinical features :resembles bacterial keratitis. A gray-white
infiltrate with fine “outliers” in the stroma (satellite lesions).
Hypopion. Condition worsens when steroid is given.
 Diagnosis :the history. No response to antibiotics  fungal
should be considered.Scrapings from the margin to examined
histologically. Corneal sensitivity
 Treatment : local natamycin eye ointment. Mydriatics if there is
anterior chamber irritation. Systemic treatment with
ketoconazole.
 Prognosis :show healing process
Opthalmology; Color Atlas of Ophthalmology
 www.wikipedia.org

60. Refraction Disorder

Refraction error, is an error in the focusing of light by the eye and a frequent reason for
reduced visual acuity.
Disorders Feature Correction
Myopia the light that comes in does not directly focus on Concave lens. The
the retina but in front of itimage at a distant smallest Dioptri to
object to be out of focus but in focus when looking corret the visual
at a close objec. aquity to 6/6
Hypermetropi imperfection in the eye (often when the eyeball is Convex lenses. The
a too short or the lens cannot become round enough). largest Dioptri to
Difficult focusing on near objects corret the visual
aquity to 6/6
Astigmatisma Unspherical corneal structure; distorted image Lens correction,
laser ceratotomy
Presbyopia the eye exhibits a progressively diminished Correction lens
ability to focus on near objects with age,
eyestrain, difficulty seeing in dim light,
problems focusing on small objects
Ambliopia Decrease of vision; disuse/inadequate
foveal/peripheral retinal stimulation and/or
abnormal binocular interaction that cause different
Refraction Test
 an eye exam that measures a person’s prescription for
eyeglasses or contact lenses
 This test can be done as part of a routine eye exam. The
purpose is to determine whether the person have a
refractive error (a need for glasses or contact lenses).
 Pinhole Test
 a test performed on a person who has diminished visual acuity
to distinguish a refractive error from organic disease.
 A refractive error may be corrected with glasses, whereas
organic disease may signal the development of preventable
blindness.
 Several pinholes, 0.5 to 2 mm in diameter, are punched in a
card. The patient selects one and looks through it with one eye
at a time, without wearing corrective lenses.
 If visual acuity is improved, the defect is refractive; if not, it is
organic.
 The pinhole effect results from blocking peripheral light waves,
which are most distorted by refractive error.

http://medical-dictionary.thefreedictionary.com/pinhole+test
Siklopegik dan refraksi ulang
IOP (intraocular pressure)
Pinhole
Funduskopi
Using cyclopegic drugs (to paralyze the ciliary muscle
in order to determine the true refractive error of the
lens)
Measured by tonometry to measure the outflow and
resistance to outflow of the aqueous humour from
the eye
pinhole testing device can determine if a problem
with acuity is the result of refractive error (and thus
correctable with glasses) or due to another process. If
the deficit corrects with the pinholes in place, the
acuity issue is related to a refractive problem.
a test that allows a health professional to see inside
the fundus of the eye and other structures using an
ophthalmoscope (or funduscope).
 61. KONJUNGTIVITIS
Conjunctivitis is swelling (inflammation) or infection of
the membrane lining the eyelids (conjunctiva)

Pathology Etiology Feature Treatment

Bacterial staphylococci Acute onset of redness, grittiness, topical antibiotics
streptococci, burning sensation, usually bilateral Artificial tears
gonocci eyelids difficult to open on waking,
Corynebacter diffuse conjungtival injection,
ium strains mucopurulent discharge, Papillae +
Viral Adenovirus Unilateral watery eye, redness, Days 3-5 of  worst, clear
herpes discomfort, photophobia, eyelid up in 7–14 days without
simplex virus edema & pre-auricular treatment
or varicella- lymphadenopathy, follicular Artificial tears relieve
zoster virus conjungtivitis, pseudomembrane dryness and inflammation
(+/-) (swelling)
Antiviral herpes simplex
virus or varicella-zoster virus

http://www.cdc.gov/conjunctivitis/about/treatment.html
Pathology Etiology Feature Treatment
Fungal Candida spp. can Not common, mostly occur in Topical antifungal
cause immunocompromised patient,
conjunctivitis after topical corticosteroid and
Blastomyces antibacterial therapy to an
dermatitidis inflamed eye
Sporothrix
schenckii
Vernal Allergy Chronic conjungtival bilateral Removal allergen
inflammation, associated atopic Topical antihistamine
family history, itching, Vasoconstrictors
photophobia, foreign body
sensation, blepharospasm,
cobblestone pappilae, Horner-
trantas dots
Inclusion Chlamydia several weeks/months of red, Doxycycline 100 mg PO
trachomatis irritable eye with mucopurulent bid for 21 days OR
sticky discharge, acute or Erythromycin 250 mg
subacute onset, ocular irritation, PO qid for 21 days
foreign body sensation, watering, Topical antibiotics
unilateral ,swollen lids,chemosis
,Follicles
 X-linked recessive
62. Color Blindness

http://en.wikipedia.org/wiki/Color_blindness
63. CHEMICAL EYE INJURY
 Etiology : acids, alkalis, detergents, solvents,
adhesives, irritants (like tear gas)
 Symptoms : epiphora, blepharosapm, severe pain
 Acid burns less dangerous than alkali burns
 Acids  cause immediate coagulation necrosis in the
superficial tissue  preventing the acid from penetrating
deeper  self-limiting process
 Alkalis  can penetrate by hydrolizing structural proteins
and dissolving cells  liquefactive necrosis
Chemical Eye Injury
Treatment :
• Restrain blepharospasm by holding the eyelids open
• Irrigate the eye within seconds of the injury using any
watery solution of neutral pH, such as tap water, mineral
water, soft drinks, coffee, tea, or similar liquids. Milk
should be avoided  increases penetration of the burn
by opening the epithelial barrier
• Remove any coarse particles from the conjunctival sac
• Transport the patient to the nearest ophthalmologist or
eye clinic

Opthalmology; Color Atlas of Ophthalmology

http://calsprogram.org/manual/volume1/section1/ophthalmology/acute_care_38.html
64. REFRACTIVE DISORDER
 Refractive Disorder
Myopia Concave lens. The smallest
Dioptri to corret the visual
aquity to 6/6
Minus lenses to be used to
correct myopia should be
no stronger than abso-
lutely necessary.
Accommodative
asthenopia
(rapid ocular fatigue)
results from the excessive
stress caused by chronic
con-
traction of the atrophic
ciliary muscle.
65. SARAF AUTONOM

Efek Saraf Autonom terhadap fungsi organ

Neurotransmiter Saraf Autonom
 66. SPONDILITIS TB
• A presentation of extrapulmonary tuberculosis that affects the spine
• Neurologic abnormalities : 50% of cases
• Compression of spinal cord  paraplegia, paresis, impaired sensation, nerve
root pain, and/or cauda equina syndrome.
• Spondilitis TBC in cervical : rare but the complication is serious,
– Pain and stiffness.
– Patients with lower cervical spine disease can present with dysphagia or
stridor.
– Symptoms can also include torticollis and hoarseness,
– neurologic deficits.
• Physical exam. : vertebral deformity (kiphosis), abcess, neurological deficit
• Diagnosis : Imaging (CT/MRI), biopsy, tuberkulin skin test GIBBUS

ABCESS
67. MULTIPLE SCLEROSIS
• A slowly progressive CNS disease characterized by
patches of demyelination in the brain and spinal cord,
resulting in multiple neurological symptoms.
• an Auto Immune Disease which is when the body starts to
destroy itself.
• the body attacks and destroys the fatty tissue called
myelin that insulates an axon/nerve, and is called
demyelination.
MS-Symptoms
• Weakness and clumsiness
• Stiffness and gait
disturbances
• Visual disturbances
• Mental disturbances,
including lack of judgment,
emotional liability, sudden
weeping or laughter
• MRI is a sensitive test for
making the diagnosis of MS
68. Meningeal Irritation
• Meningism : the triad of nuchal rigidity (neck
stiffness), photophobia, headache  signs of
meninges irritation
• Caused by:
– Meningitis
– Subarachnoid hemorrhage
– Drugs
– Increased intracranial pressure
Causes abnormal contraction of various muscle groups, which
are identified on physical examination
Nuchal Rigidity
 Ask the patient to touch his chest with his chin (sitting) or
the examiner passively flexes the head on the chest
(supine)
 (+) Nuchal Rigidity – the patient cannot place the chin on
the chest. Passive flexion of the neck is limited by
involuntary muscle spasm, while passive extension and
rotation are normal
Brudzinski Sign
 With the patient supine, passively flex his head on his
chest
 (+) flexion of the patient’s hips and knees
 Note: in doing nuchal rigidity and brudzinski sign, first
make sure there is no injury to the cervical vertebrae or
cervical cord
Kernig Sign
 With the patient supine, flex his thigh at the hip level and
extend the leg
 With the hip kept in flexion, attempts to extend the knee
produce pain in the hamstrings and resistance to further
extension
 (+) Kernig Sign: back pain or sciatic pain
 Severe stiffness of the hamstrings causes an inability to
straighten the leg when the hip is flexed to 90 degrees.
 Reliable signs of meningitis, herniated disk, or tumors of the
cauda equina
69-70. HEAD INJURY
• Brain hematoma : a collection of blood within brain
tissue.
• Hematoma inside the cranium is named according to its
location:
– Subdural hematoma: blood collection between brain and
dura
– Epidural hematoma: blood collection between dura and the
skull
– Subarachnoid Hemorrhage: beneath the arachnoid
membrane
– Intracerebral hematoma: blood collection within the brain
Epidural Hematomas
• 70%-80% located in
temporoparietal region where
skull fractures cross the path of
middle meningeal artery or its
dural branches
• May present with lucid period
immediately after trauma and a
delay before symptoms evident
• on CT : Lens shaped (biconvex
lens) hematomas that do not
cross suture lines
Subdural hematomas : crescent shaped
density that may run length of the skull

 Crescent shaped density that may run length of skull

Subarachnoid
Hemorrhage

Intracranial Hemorrhage
HEAD INJURY

www.kalbemed.com/portals/6/05_193PenatalaksanaanKedaruratan.pdf
TATALAKSANA
CKR :
• Dilakukan PF, perawatan luka, foto
kepala, isitirahat baring dengan
mobilisasi bertahap sesuai kondisi
pasien disertai terapi simptomatis.
• Observasi 24 jam di RS untuk
menilai kemungkinan hematoma
intrakranial, misalnya riwayat lucid
interval, nyeri kepala, muntah-
muntah, kesadaran menurun,
gejala lateralisasi (pupil anisokor,
refleks patologis positif)
 Tidak perlu dirawat jika:
 Orientasi (waktu dan tempat
baik)
 Gejala fokal neurologik (-)
 Muntah/sakit kepala (-)
 Fraktur tulang kepala (-)
 Tempat tinggal dalam kota
 Ada yang bisa mengawasi
dengan baik di rumah, dan bila
dicurigai ada perubahan
kesadaran dibawa kembali ke
RS
 TATALAKSANA
CKS :
 Bisa mengalami gangguan
kardiopulmoner
 Periksa dan atasi gangguan jalan
napas (ABC)
 Periksa singkat tingkat kesadaran,
pupil, tanda fokal serebral, cedera
organ lain. Jika curiga adanya fraktur,
lakukan fiksasi pada tulang tersebut.
 Foto kepala, bila perlu foto bagian
tubuh lainnya
 CT scan otak bila curiga hematoma
intrakranial
 Observasi fungsi vital, kesadaran,
pupil, dan defisit fokal serebral
lainnya
CKB :
 Biasanya disertai cedera multipel
 Bila didapatkan fraktur servikal,
segera pasang kerah fiksasi leher,
bila ada luka terbuka dan ada
perdarahn, dihentikan dengan
balut tekan untuk pertolongan
pertama.
 Tindakan sama dengan CKS
dengan pengawasan lebih ketat
dan dirawat di ICU
 Sering berada dalam keadaan
hipoksi, hipotensi, dan
hiperkapni akibat gangguan
kardiopulmoner
71. EPILEPSI
72. MENINGITIS
 Meningitis: radang pada selaput otak yang melapisi otak dan
sumsum tulang belakang
 Manifestasi klinis : nyeri kepala, dapat menjalar ke tengkuk
dan punggung, kaku kuduk, kernig (+), brudzinsky (+)
 Klasifikasi (berdasarkan perubahan pada cairan otak) :
 Meningitis serosa : cairan otak jernih, paling sering disebabkan
oleh Mycobacterium tuberculosa, penyebab lain: virus,
toxoplasma gondhii, ricketsia
 Meningitis purulenta : cairan mengandung pus, penyebabnya
antara lain diplococcus pneumoniae, neisseria meningitidis,
streptococcus haemolyticus, staphylococcus aureus,
haemophilus influenza, pseudomonas aeruginosa
Meningitis Bacterialis
 An acute infection of subarachnoid space and
meninges characterised by polymorphonuclear cells
in the CSF.
 Bacteria may invade the subarachnoid space by
spread from contiguous structures,e.g sinuses or
indirectly from bloodstream
 Etiology : gram –ve bacilli (e.coli, klebsiella,
haemophilus influenza), neisseria meningitis,
pneumococcus
Meningitis Bacterialis
Clinical Feature :
 Classical clinical triad: fever,
headache, neck stiffness
 Prodromal features (variable): a
respiratory infection (otitis media
or pneumonia) associated with
muscle pain, backache, lethargy
 Meningitic symptoms: severe
frontal/occipital headache, stiff
neck, photophobia
Diagnosis:
 CSF analysis
 CT scan to exclude an intracranial
mass if patient in coma or has
papilloedema
 Blood culture
 Serum electrolytes
 Detect source of infection: chest
x-ray, sinus x-ray (sinusitis), skull x-
ray (fracture), petrous views
(mastoiditis)
Neurology Illustrated

Meningitis Bacterialis
CSF Findings in Meningitis
 73. Glasgow Coma Scale
 The Glasgow Coma Scale is a neurological scale  to give a
reliable, objective way of recording the conscious state of a person,
for initial as well as continuing assessment
 A patient is assessed against the criteria and the resulting points
give the Glasgow Coma Score
Generally, comas are classified as:
1. Severe, with GCS ≤ 8
2. Moderate, GCS 9 - 12
3. Minor, GCS ≥ 13.
 Highest score is 15/15.the person in this case is alert and oriented to
person, place and time
 Lowest score is 3/15 there’s no 0.The patient is in deep coma and is
considered brain dead if he can’t breath without a ventilator

Neurology and Neurosurgery Illustrated

Glasgow Coma Scale
Eye opening Motor Response Verbal Response

Spontaneously Obeys Commands Oriented when speaking to

=4 Points =6 Points person, place and time)
=5 Points
To speech and Unconscious but can localize Confused Disoriented to
commands pain person, place and time)
=3 Points =5 Points =4 Points
To pain Withdrawal Response to pain Words only unconscious but
=2 Points (but can’t localize pain) responds to painful stimuli by
= 4 Points words)
=3 Points
No Response Decortication(spastic flexion Sounds Only
= 1 Point of the upper limbs and =2 Points
extension of the lower
limbs)+Rigidiy
= 3 Points
Decerebration(extension and No Response
outwards turning of the arms =1 Point
and legs)+ Rigidity
= 2 Points
No Response
=1 Point
Posturing
 74. STROKE
Menurut Penyebab Stroke dibagi :
1. Stroke Hemoragik
a. Intra cerebral hemoragik (ICH)
OK : Hypertensi, Aneurysma dan arterioveneus Malformasi (AVM)
b. Sub Arachnoid Hemoragik (SAH)
 diagnosis medis : CT brain scan
2. Stroke Non Hemoragik (Iskemik)
OK : Arteriosklerosis & sering dikaitkan dengan : DM,
Hypercolesterolemia, Asam urat, hyperagregasi trombosit
3. Emboli  Sumber dari tronkus di arteria carotis communis di jantung 
Lepas  trombus embolus  otak.
Stroke
Manifestasi Klinis : Faktor Resiko :
• Kelumpuhan wajah atau anggota  Usia
badan (biasanya hemiparese),  Riw. TIA atau stroke
timbul mendadak
 Peny. Jantung koroner
• Gangguan hemisensorik
• Perubahan mendadak status  Hipertensi
mental  DM
• Afasia; disartria  Merokok
• Gangguan penglihatan atau  Dislipidemia
diplopia
• Ataksia
• Vertigo, mual, muntah, nyeri
kepala
Intracerebral Hemorrhage
• Bleeding into brain tissue Hemorrhage:
• Usually caused by chronic Symptoms only suggestive of
hypertension hemorrhage.
• Non-hypertension cause
CT or LP needed for definitive
more likely if: diagnosis
– No past history of
• Headache
hypertension • Neck stiffness
– Lobar (i.e., peripheral, not • Neck pain
subcortical) • Light intolerance
• May require emergency • Nausea, vomiting
surgery
• Decreased consciousness
• Accounts for  10% of
strokes
 75. MENINGITIS
 Meningitis: radang pada selaput otak yang melapisi otak dan
sumsum tulang belakang
 Manifestasi klinis : nyeri kepala, dapat menjalar ke tengkuk dan
punggung, kaku kuduk, kernig (+), brudzinsky (+)
 Klasifikasi (berdasarkan perubahan pada cairan otak) :
 Meningitis serosa : cairan otak jernih, paling sering disebabkan oleh
Mycobacterium tuberculosa, penyebab lain: virus, toxoplasma gondhii,
ricketsia
 Meningitis purulenta : cairan mengandung pus, penyebabnya antara
lain diplococcus pneumoniae, neisseria meningitidis, streptococcus
haemolyticus, staphylococcus aureus, haemophilus influenza,
pseudomonas aeruginosa

Kapita Selekta
Meningitis TB
Diagnosis
 CSF Examination
 Usually lymphocytic pleocytosis
 Paradoxic change from lymphocytic to neutrophilic
predominance over 48 hr pathognomonic for TB meningitis
 Elevated protein with severely depressed glucose
 Repeated specimens for AFB culture necessary
 Other Studies
 Brain imaging – demonstrates hydrocephalus, basilar exudates
and inflammation, tuberculoma, cerebral edema, cerebral
infarction
 CXR
 Abnormal, sometimes miliary pattern
Treatment
CSF Findings in Meningitis
76. POLYNEUROPATHY
 a neurological disorder that occurs when many nerves throughout the
body malfunction simultaneously.
 It may be acute and appear without warning, or chronic and develop
gradually over a longer period of time.
 Many polyneuropathies have both motor and sensory involvement;
some also involve dysfunction of the autonomic nervous system.
 These disorders are often symmetric and frequently affect the feet and
hands, causing weakness, loss of sensation, pins-and-needle sensations
or burning pain.
 Damage may occur to axon, myelin sheath, cell body, supporting
connective tissue and nutrient blood supply to nerves. 3 basic
pathological process occurs : wallerian degeneration, segmental
demyelination, distal axon degeneration
Guillaine Barre Syndrome
 Acute immune-mediated polyneuropathies
 Peripheral nerve myelin is target of an immune attack
 Starts at level of nerve root  conduction blocks muscle
weakness. Eventually get widespread patchy demyelination 
increased paralysis
 Usually postinfection
 Immune-mediated: infectious agents thought to induce Ab
production against specific gangliosides/glycolipids
 Lymphocytic infiltration of spinal roots/peripheral nerves & then
macrophage-mediated, multifocal stripping of myelin
 Result: defects in the propagation of electrical nerve impulses, with
eventual conduction block and flaccid paralysis
 GBS
Clinical Feature :
Progressive, fairly symmetric muscle
weakness, typically starts in proximal
legs, weakness in face arm, severe
respiratory muscle weakness
Absent or depressed DTR
Often prominent severe pain in lower
back
Common to have paresthesias in
hands and feet
Dysautonomia is very common:
tachycardia, urinary retention,
hypertenison alternating w/
hypotension, ileus
Diagnosis :
• CSF : protein elevated
• Nerve conduction studies: findings of
multifocal demyelination with slowing
of motor conduction, conduction
block, prolonged distal motor
latencies
Treatment:
Supportive, with management of the
paralyzed patient and with elective
ventilation for impending respiratory
failure

Neurology Illustrated
77. Waham
Diagnosis Karakteristik
Gangguan cemas Ansietas berlebih terus menerus tidak terbatas pada situasi
menyeluruh tertentu, disertai ketegangan motorik (gemetar, sulit berdiam diri,
sakit kepala), hiperaktivitas otonomik, kewaspadaan mental.
Gangguan waham Waham adalah satu-satunya ciri khas klinis yang menonjol.
menetap Sedikitnya 3 bulan lamanya & tidak ada gejala skizofrenia.
Obsesif kompulsif Gejala obsesif atau tindakan impulsif harus ada hampir setiap hari
sedikitnya 2 minggu berturut-turut. Obsesi atau impuls tersebut
merupakan pengulangan yang tidak menyenangkan.
Gangguan Ansietas terjadi dalam 1 bulan setelah terjadinya kejadian yang
penyesuaian stressful & biasanya tidak bertahan >6 bulan.

PPDGJ
78. Generalized Anxiety Disorder
 The two major schools of thought about psychosocial
factors leading to the development of generalized anxiety
disorder are:
 the cognitive-behavioral school: patients with generalized
anxiety disorder respond to incorrectly and inaccurately
perceived dangers. The inaccuracy is generated by selective
attention to negative details in the environment, by
distortions in information processing, and by an overly
negative view of the person's own ability to cope
 the psychoanalytic school hypothesizes that anxiety is a
symptom of unresolved, unconscious conflicts

Kaplan & Sadock synopsis of psychiatry.

 79. Defense Mechanism
 In patients with phobias, the primary defense involved is
displacement; that is, the conflict is displaced from the person who
evokes the conflict to a seemingly unimportant, irrelevant object or
Kaplan & Sadock synopsis of psychiatry.

situation, which then has the power to arouse a constellation of

affects, one of which is called signal anxiety. The phobic object or
situation may have a direct associative connection with the primary
source of the conflict and thus symbolizes it (the defense
mechanism of symbolization).
80. Gangguan Somatoform
Diagnosis Karakteristik
Gangguan somatisasi Banyak keluhan fisik (4 tempat nyeri, 2 GI tract, 1
seksual, 1 pseudoneurologis).
Hipokondriasis Keyakinan ada penyakit fisik.
Disfungsi otonomik Bangkitan otonomik: palpitasi, berkeringat,
somatoform tremor, flushing.
Nyeri somatoform Nyeri menetap yang tidak terjelaskan.

PPDGJ
 81. Drug Abuse
Zat Intoksikasi
Alkohol Cadel, inkoordinasi, unsteady gait, nistagmus,
gangguan memori/perhatian, stupor/koma
Heroin Euforia, analgesia, ngantuk, mual, muntah,
napas pendek, konstipasi, midriasis, gangguan
jiwa
Kanabis/ganja Injeksi konjungtiva, peningkatan nafsu makan,
/marijuana mulut kering, takikardia
Kokain Taki/bradikardia, dilatasi pupil,
peningkatan/penurunan TD,
perspirasi/menggigil, mual/muntah, turun BB,
agitasi/retardasi psikomotor, kelemahan otot.
Depresi napas, nyeri dada, aritmia, bingung,
kejang, distonia, koma
Amfetamin Taki/bradikardia, dilatasi pupil,
peningkatan/penurunan TD,
perspirasi/menggigil, mual/muntah, turun BB,
agitasi/retardasi psikomotor, kelemahan otot.
Depresi napas, nyeri dada, aritmia
Benzodiazepin Cadel, inkoordinasi, gangguan berjalan,
nistagmus, gangguan perhatian/memori,
stupor/koma.
Withdrawal
Hiperaktivitas otonom, tremor, insomnia,
mual/muntah, halusinasi, agitasi,
ansietas, kejang.
Miosis/midriasis, mengantuk/koma,
cadel, gangguan perhatian/memori
Disforik mood, fatigue, mimpi buruk,
insomnia/hipersomnia, peningkatan
nafsu makan, agitasi/retardasi psikomotor
Disforik mood, fatigue, mimpi buruk,
insomnia/hipersomnia, peningkatan
nafsu makan, agitasi/retardasi psikomotor
Hiperaktivitas otonom, tremor, insomnia,
mual/muntah, halusinasi
visual/taktil/auditorik, agitasi psikomotor,
ansietas, bangkitan grand mal.
81. Drug Abuse
 Phencyclidine (PCP)
 synthetic dissociative drug originally developed as a general
anesthetic. The effects of dissociative drugs like PCP include
feelings of detatchment from the environment and self.
 PCP is ingested orally, snorted, smoked, or injected.

 Symptoms: Mild to intense euphoria, Relaxation or drowsiness,

Feelings of unreality and dissociation with the environment,
Distorted sense of one’s body, including a feeling of weightlessness ,
Anxiety, Agitation, Paranoid thoughts, Confusion and disorientation,
Depression, Grandiose delusions, Panic.

 Signs: Impaired motor skills , Blurred vision and constricted pupils ,

painful reaction to sound , Speech disturbances, decreased
sensitivity and awareness of pain, touch, and position, Stupor or
coma, Irregular heartbeat.
 82. Delirium

Delirium. Ondria C, Gleason MD., University of Oklahoma College of Medicine, Tulsa, Oklahoma. Am Fam
Physician. 2003 Mar 1;67(5):1027-1034.
 82. Delirium
 Subtypes of Delirium
 Hyperactive subtype
may be agitated, disoriented, and delusional, and may
experience hallucinations. This presentation can be confused
with that of schizophrenia, agitated dementia, or a psychotic
disorder.
 Hypoactive subtype
Subdued, quietly confused, disoriented, & apathetic. Delirium in
these patients may go unrecognized or be confused with
depression or dementia.
 Mixed subtype
Fluctuating between the hyperactive &hypoactive.
Delirium. Ondria C, Gleason MD., University of Oklahoma College of Medicine, Tulsa, Oklahoma. Am Fam Physician. 2003 Mar 1;67(5):1027-
1034.
 82. Delirium

Delirium. Ondria C, Gleason MD., University of Oklahoma College of Medicine, Tulsa, Oklahoma. Am Fam
Physician. 2003 Mar 1;67(5):1027-1034.
 82. Delirium
 During the search for an underlying medical condition,
symptomatic treatment for delirium may include the use
of antipsychotic drugs to control agitation &
hallucinations, and to clear the sensorium (i.e., improve
attention abilities and level of orientation).
 Haloperidol: 1-2 mg twice daily, IV/IM/oral repeated
every four hours as needed.
 Elderly patients should be started at lower drug dosages:
haloperidol 0.25 - 1.0 mg

Delirium. Ondria C, Gleason MD., University of Oklahoma College of Medicine, Tulsa, Oklahoma. Am Fam Physician. 2003 Mar 1;67(5):1027-
1034.
83. Sign & Symptom
Diagnosis Karakteristik
Illusion Perceptual misinterpretation of a real external
stimulus.
Hallucination False sensory perception occurring in the
absence of any relevant external stimulation of
the sensory modality involved.
Depersonaliz Sensation of unreality concerning oneself, parts
ation of oneself, or one's environment that occurs
under extreme stress or fatigue. Seen in
schizophrenia, depersonalization disorder, and
schizotypal personality disorder.
Kaplan & Sadock synopsis of psychiatry.
84. Depresi
• Gejala utama:  Gejala lainnya:
1. konsentrasi menurun,
1. afek depresif,
2. harga diri & kepercayaan diri
2. hilang minat & berkurang,
kegembiraan, 3. rasa bersalah & tidak berguna
3. mudah lelah & yang tidak beralasan,
menurunnya 4. merasa masa depan suram &
aktivitas. pesimistis,
5. gagasan atau perbuatan
membahayakan diri atau bunuh
diri,
6. tidur terganggu,
7. perubahan nafsu makan (naik
atau turun).
PPDGJ
84. Depresi
 Episode depresif ringan: 2 gejala utama + 2 gejala lain > 2
minggu

 Episode depresif sedang: 2 gejala utama + 3 gejala lain, >2

minggu.

 Episode depresif berat: 3 gejala utama + 4 gejala lain > 2

minggu. Jika gejala amat berat & awitannya cepat, diagnosis
boleh ditegakkan meski kurang dari 2 minggu.

 Episode depresif berat dengan gejala psikotik: episode

depresif berat + waham, halusinasi, atau stupor depresif.

PPDGJ
84. Depresi
 A review of the use of antidepressants (Anderson, ‘01):
 The different antidepressant class adverse effect profiles
make the SSRIs more tolerable than the TCAs  SSRI is
commonly used as first line drug for major depression.
85. Gangguan Disosiatif
• Gejala utama adalah adanya kehilangan dari integrasi
normal, antara:
• ingatan masa lalu,
• kesadaran identitas dan penginderaan segera, &
• kontrol terhadap gerakan tubuh
• Terdapat bukti adanya penyebab psikologis, kejadian yang
stressful atau hubungan interpersonal yang terganggu
• Tidak ada bukti adanya gangguan fisik.

PPDGJ
85. Gangguan Disosiatif
Diagnosis Karakteristik
Amnesia Hilang daya ingat mengenai kejadian stressful atau traumatik yang
baru terjadi (selektif)
Fugue Melakukan perjalanan tertentu ke tempat di luar kebiasaan, tapi
tidak mengingat perjalanan tersebut.
Stupor Sangat berkurangnya atau hilangnya gerakan volunter & respons
normal terhadap rangsangan luar (cahay, suara, raba)
Trans Kehilangan sementara penghayatan akan identitias diri &
kesadaran, berperilaku seakan-akan dikuasai kepribadian lain.
Motorik Tidak mampu menggerakkan seluruh/sebagian anggota gerak.
Konvulsi Sangat mirip kejang epileptik, tapi tidak dijumpai kehilangan
kesadaran, mengompol, atau jatuh.
Anestesi & Anestesi pada kulit yang tidak sesuai dermatom.
kehilangan Penurunan tajam penglihatan atau tunnel vision (area lapang
sensorik pandang sama, tidak tergantung jarak).
PPDGJ
86. Sexual Dysfunction
 Sexual desire disorders
 Hypoactive Sexual Desire Disorder (HSDD);
Persistently or recurrently deficient (or absent) sexual fantasies
and desire for sexual activity
 Sexual Aversion Disorder (SAD)
 Persistent or recurrent extreme aversion to, and avoidance of, all
(or almost all) genital sexual contact with a sexual partner.
 Sexual arousal disorders
 Female Sexual Arousal Disorder (FSAD)
Persistent or recurrent inability to attain, or to maintain until
completion of the sexual activity, an adequate lubrication-
swelling response of sexual excitement.
 Male Erectile Disorder
 Persistent or recurrent inability to attain, or to maintain until
completion of the sexual activity, an adequate erection.

(APA, 2000)
86. Sexual Dysfunction
 Orgasmic disorders
 Female Orgasmic Disorder (Inhibited Female Orgasm)
 Male Orgasmic Disorder (Inhibited Male Orgasm)
 Premature Ejaculation
 Sexual pain disorders
 Dyspareunia: recurrent or persistent genital pain associated with
sexual intercourse.
 Vaginismus: involuntary muscle constriction of the outer third of the
vagina that interferes with penile insertion and intercourse.
 Sexual dysfunction due to general medical condition
 Substance-Induced Sexual Dysfunction
 With impaired desire/With impaired arousal/With impaired
orgasm/With sexual pain/With onset during intoxication
 Sexual Dysfunction Not Otherwise Specified (NOS)
87. Skizofrenia
Diagnosis Gangguan isi pikir, waham, halusinasi
Paranoid merasa terancam/dikendalikan
Hebefrenik 15-25 tahun, afek tidak wajar, tidak dapat
diramalkan, senyum sendiri
Katatonik stupor, rigid, gaduh, fleksibilitas cerea
Skizotipal perilaku/penampilan aneh, kepercayaan aneh,
bersifat magik, pikiran obsesif berulang
Waham menetap hanya waham
Psikotik akut gejala psikotik <2 minggu.
Skizoafektif gejala skizofrenia & afektif bersamaan
88. Reaksi Terhadap Stres Berat
 Gangguan stres pascatrauma
 kondisi yang ditandai oleh munculnya gejala (gangguan
otonomik, afek, & tingkah laku) setelah melihat,
mengalami, atau mendengar peristiwa traumatis dalam
kurun waktu 6 bulan.

 Gangguan stres akut

 Gangguan yang serupa dengan gangguan stres
pascatrauma, yang muncul segera setelah kejadian
88. Reaksi Terhadap Stres Berat
 Kriteria Diagnosis reaksi stres pascatrauma
 Individu terpajan situasi (melihat, mengalami, menghadapi) yang
melibatkan ancaman kematian atau cedera serius atau ancaman lain
yang serupa.
 Adanya bayang-bayang kejadian yang persisten, berupa gambaran,
pikiran, persepsi, atau mimpi buruk. Individu mengalami gejala
penderitaan bila terpajan pada ingatan akan trauma aslinya.
 perilaku menghindar dari bayang-bayang dan pikiran tentang kejadian
traumatis (termasuk orang, tempat, dan aktivitas), dan dapat tidak
ingat aspek tertentu dari kejadian.
 Adanya gejala peningkatan kesiagaan yang berlebih seperti insomnia,
iritabililta, sulit konsentrasi, waspada berlebih.
 Gejala menyababkan hendaya pada fungsi sosial atau pekerjaan.
 89. Keganasan pada kulit
 Karsinoma sel basal  Karsinoma sel skuamosa
 Berasal dari sel epidermal  Berasal dari sel epidermis.
pluripoten. Faktor predisposisi: Etiologi: sinar matahari, genetik,
lingkungan (radiasi, arsen, herediter, arsen, radiasi,
paparan sinar matahari, trauma, hidrokarbon, ulkus sikatrik
ulkus sikatriks), genetik  Usia tersering 40-50 tahun
 Usia di atas 40 tahun
 Dapat bentuk intraepidermal
 Biasanya di daerah berambut,
 Dapat bentuk invasif: mula-mula
invasif, jarang metastasis berbentuk nodus keras, licin,
 Bentuk paling sering adalah kemudian berkembang menjadi
nodulus: menyerupai kutil, tidak verukosa/papiloma. Fase lanjut
berambut, berwarna tumor menjadi keras, bertambah
coklat/hitam, berkilat (pearly), bila besar, invasif, dapat terjadi
melebar pinggirannya meninggi di ulserasi. Metastasis biasanya
tengah menjadi ulkus (ulcus melalui KGB.
rodent) kadang disertai
talangiektasis, teraba keras
Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
 Melanoma maligna SCC
 Etiologi belum pasti. Mungkin
faktor herediter atau iritasi
berulang pada tahi lalat
 Usia 30-60 tahun
 Bentuk:
 Superfisial: Bercak dengan warna
bervariasi, tidak teratur, berbatas
tegas, sedikit penonjolan BCC
 Nodular: nodus berwarna biru
kehitaman dengan batas tegas
 Lentigo melanoma maligna:
plakat berbatas tegas, coklat
kehitaman, meliputi muka
 Warna kehitaman akibat
peningkatan jumlah melanosit
 Prognosis buruk MM
 90. Psoriasis vulgaris
 Bercak eritema berbatas tegas dengan skuama kasar berlapis-lapis
dan transparan
 Predileksi: skalp, perbatasan skalp-muka, ekstremitas ekstensor (siku
& lutut), lumbosakral
 Khas: fenomena tetesan lilin, Auspitz sign, Kobner sign
 Patofisiologi:
 Genetik: berkaitan dengan HLA
 Imunologik: diekspresikan oleh limfosit T, sel penyaji antigen dermal,
dan keratinosit
 Pencetus: stress, infeksi fokal, trauma, endokrin, gangguan
metabolisme, obat, alkohol, dan merokok
 Tata laksana:
 Sistemik: KS, sitostatik (metotreksat), levodopa, etretinat, dll
 Topikal: preparat ter, KS, ditranol, tazaroen, emolien, dll
 PUVA (UVA + psoralen)

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
91. Psoriasis
 Although most cases of psoriasis are diagnosed clinically,
some, particularly the pustular forms, can be difficult to
recognize.
 In these cases, dermatologic biopsy can be used to make
diagnosis.
 Biopsy of the skin lesion may reveal basal cell hyperplasia,
proliferation of subepidermal vasculature, absence of normal
cell maturation, and keratinization.
 A large number of activated T cells are present in the
epidermis.
92. Urtikaria
 Reaksi vaskular di kulit akibat
bermacam-macam sebab, biasanya
ditandai dengan edema setempat
yang cepat timbul dan menghilang
perlahan-lahan berwarna pucat dan
kemerahan, meninggi di permukaan
kulit, sekitarnya dapat dikelilingi halo
 Etiologi: obat, makanan, gigitan
serangga, bahan fotosensitizer,
inhalan, kontaktan, trauma fisik,
infeksi, psikis, genetik, atau penyakit
sistemik
Klasifikasi urtikaria
 Berdasarkan waktu
 Akut: Kurang dari 6 minggu
 Kronik: lebih dari 6 minggu
 Berdasarkan morfologi
 Papular: berbentuk papul
 Gutata: sebesar tetesan air
 Girata: ukurannya besar-
besar
 Berdasarkan luas:
 Lokal
 Generalisata
 Angioedema: terkena
lapisan yang lebih dalam
daripada dermis
• Berdasarkan penyebab
– Karena reaksi imunologik
• Bergantung pada IgE (atopi,
karena antigen spesifik)
• Ikut sertanya komplemen
(reaksi sitotoksik, reaksi
kompleks imun, defisiensi C1
esterase inhibitor)
• Reaksi alergi tipe IV
– Reaksi nonimunologik
• Langsung memicu sel mast
• Bahan yang menyebabkan
perubahan metabolisme
asam arakidonat
• Trauma fisik
– Idiopatik
 Gejala:
 Gatal, rasa terbakar, atau tertusuk
 Eritema atau edema berbatas tegas, kadang bagian tengah
tampak lebih pucat
 Besarnya dapat lentikular, numular, plakat
 Pengobatan:
 Menghindari penyebab
 Antihistamin
 Betaadrenergik (untuk urtikaria kronik)
Jenis Keterangan
Urtikaria adrenergik Urtikaria yang berhubungan dengan kenaikan konsentrasi
noradrenalin dan adrenalin plasma. Dapat dipicu dengan
pemberian adrenalin atau noradrenalin
Urtikaria kolinergik Urtikaria yang dipicu karena kenaikan suhu tubuh sendiri dan
(bagian dari keringat
urtikaria fisik)
Urtikaria dingin Urtikaria yang dipicu karena rangsangan dingin
Urtikaria fisik Kelompok urtikaria yang dipicu oleh rangsangan fisik dari luar.
Gejala khas: dermografisme
Urtikaria idiopatik Urtikaria yang tidak jelas penyebabnya
 93. Eritroderma
 Kelainan kulit yang ditandai dengan adanya eritema universalis
biasanya disertai skuama
 Patofisiologi: belum jelas, kemungkinan karena peranan sitokin
 Gejala:
 Eritroderma akibat alergi obat
 Eritroderma akibat oerluasan penyakit kulit: psoriasis
eritrodermik, penyakit Leiner
 Eritroderma akibat penyakit sistemik: sindrom Sezary
 Pengobatan:
 Kortikosteroid
 Diet tinggi protein (pada edema karena protein loss)
 Emolien: untuk mengurangi radiasi akibat vasodilatasi

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
94. Skabies
 Penyakit kulit yang disebabkan oleh infestasi dan sensitisasi terhadap
Sarcoptes scabiei var. hominis
 Transmisi: kontak langsung (skin to skin), tidak langsung
 Kelainan kulit akibat terowongan tungau atau karena garukan penderita
 Gejala:
 Pruritus nokturna
 Menyerang manusia secara kelompok
 Adanya terowongan (kunikulus) yang berwarna putih/keabuan,
lurus/berkelok, panjang 1 cm, pada ujung didapatkan papul/vesikel.
Predileksi: sela jari tangan, pergelangan tangan bag volar, siku luar, lipat
ketiak depan, areola mammae, umbilikus, bokong, genitalia eksterna,
perut bawah
 Ditemukan tungau
 Obat: sulfur presipitat 4-20%, benzil benzoat 20-25%, gameksan 1%,
krotamiton 10%, permetrin 5%
Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
95. Vaginitis
 Usually characterized by:
 Vaginal discharge
 Vulvar itching
 Irritation
 Odor
 Common types
 Bacterial vaginosis (40%-45%)
 Vulvovaginal candidiasis (20%-25%)
 Trichomoniasis (15%-20%)

www2a.cdc.gov
Vaginitis Differentiation
Normal Bacterial Vaginosis Candidiasis Trichomoniasis

Itch, discomfort,
Symptom Itch, discharge, 50%
Odor, discharge, itch dysuria, thick
presentation asymptomatic
discharge
Homogenous,
Frothy, gray or
Clear to adherent, thin, milky Thick, clumpy, white
Vaginal discharge yellow-green;
white white; malodorous “cottage cheese”
malodorous
“foul fishy”
Inflammation and Cervical petechiae
Clinical findings
erythema “strawberry cervix”

Vaginal pH 3.8 - 4.2 > 4.5 Usually < 4.5 > 4.5

KOH “whiff” test Negative Positive Negative Often positive

Motile flagellated
Clue cells (> 20%),
NaCl wet mount Lacto-bacilli Few WBCs protozoa, many
no/few WBCs
WBCs
Pseudohyphae or
KOH wet mount spores if non-
268
albicans species
96. Pedikulosis pubis
 Infeksi rambut di daerah pubis dan sekitarnya
 Menyerang dewasa (tergolong PMS), dapat menyerang
jenggot/kumis
 Dapat menyerang anak-anak, seperti di alis/bulu mata
dan pada tepi batas rambut kepala
 Gejala: Gatal di daerah pubis dan sekitarnya, dapat
meluas ke abdomen/dada, makula serulae (sky blue spot),
black dot pada celana dalam
 Pengobatan: gameksan 1%, benzil benzoat 25%
 97. Pitiriasis versikolor
 Penyakit jamur superfisial yang kronik disebabkan
Malassezia furfur
 Gejala:
 Bercak berskuama halus yang berwarna putih sampai coklat
hitam, meliputi badan, ketiak, lipat paha, lengan, tungkai
atas, leher, muka, kulit kepala yang berambut
 Asimtomatik – gatal ringan, berfluoresensi
 Pemeriksaan: lampu Wood (kuning keemasan), KOH 20%
(hifa pendek, spora bulat: meatball & spaghetti
appearance)
 Obat: selenium sulfida, azole, sulfur presipitat

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
Lampu Wood
 Tinea kapitis (M. canis, M. audouinii, M. rivalieri, M.
distortum, M. ferrugineum dan M. gypseum): hijau terang
 Pitiriasis versikolor : putih kekuningan, orange tembaga,
kuning keemasan, atau putih kebiruan (metabolit
koproporfirin)
 Tinea favosa (Trichophyton schoenleinii): biru suram/hijau
suram (akibat metabolit pteridin)
 Eritrasma (Corynebacterium minutissimum): merah koral
(metabolit porfirin)
 Infeksi pseudomonas: hijau (metabolit pioverdin atau
fluoresein)
 Hasil positif palsu:
 Salep dan krim di kulit atau eksudat: biru – jingga
 Tetrasiklin, asam salisilat dan petrolatum: kuning
98. Dermatitis kontak
 Dermatitis kontak alergi
 Reaksi peradangan kulit imunologik, diperantarai cell-mediated
immune response (hipersensitivitas tipe IV)
 Mengenai orang yang kulitnya hipersensitif
 Penyebab: hapten (alergen yang belum diproses, lipofilik,
sangat reaktif, mampu menembus stratum korneum)
 Fase: sensitisasi & elitisasi
 Gejala:
 Akut: gatal, eritema, edema, papulovesikel, vesikel, bula
 Kronik: kulit kering, skuama, papul, likenifikasi, fisur
 DD: DKI
 Pemeriksaan: uji tempel
 Pengobatan: menghindari pajanan, KS

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
  Uji tempel digunakan untuk membedakan DKA dengan DKI
 Antigen dibiarkan menempel selama 48 jam
 Pembacaan dilakukan 2 kali: pertama dilakukan 15-30 menit setelah
dilepas; kedua dilakukan 72-96 jam setelah dilepas
 Bila reaksi bertambah (crescendo) di antara kedua pembacaan, cenderung
ke respons alergi. Disesuaikan juga dengan keadaan klinis.

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
99. Sifilis
 Penyakit infeksi yang disebabkan Treponema pallidum,
kronik, bersifat sistemik
 Dapat menyerang hampir semua organ, dapat
menyerupai banyak penyakit (the great imitator),
mempunyai masa laten, dapat ditularkan dari ibu ke janin
Stadium sifilis
 Stadium dini (menular)
 Stadium I (sifilis primer): papul lentikular yang kemudian menjadi
ulkus dinding tidak bergaung, indolen, teraba indurasi, tidak
ada radang akut (ulkus durum) biasanya di genitalia eksterna.
Seminggu setelah afek primer terdapat pembesaran KGB inguinal
 Stadium II (sifilis sekunder): 6-8 minggu sejak S I, dapat
menyerupai berbagai kelainan kulit (the great imitator), dapat
memberi kelainan pada mukosa, KGB, mata, hepar, tulang, saraf.
Kelainan biasanya tidak gatal, sering disertai limfadenitis
generalisata
 Sifilis laten dini: tidak ada gejala klinis, tetapi infeksi masih aktif.
Tes serologi darah (VDRL, TPHA) positif
 Stadium rekuren: relaps dapat terjadi berupa kelainan kulit mirip
sifilis sekunder
 Stadium sifilis (cont’d)
 Stadium lanjut (tidak menular)
 Sifilis laten lanjut: lama bertahun-tahun, tidak menular,
diagnosis dengan tes serologik
 Stadium III (sifilis tersier): 3-10 tahun sejak S I, kelainan khas
adalah guma (infiltrat sirkumskrip, kronis, biasanya
melunak, destruktif), nodus, dapat menyerang mukosa,
tulang, hepar, jantung & aorta (sifilis kardiovaskular), otak
(neurosifilis)

 Tata laksana: penisilin G prokain/penisilin G benzatin

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
 100. Varicella (chicken pox)
 Infeksi akut oleh virus varicella-zoster yang menyerang kulit
dan mukosa
 Transmisi secara aerogen
 Gejala
 Masa inkubasi 14-21 hari
 Gejala prodromal: demam subfebris, malaise, nyeri kepala
 Disusul erupsi berupa papul eritematosa yang kemudian berubah
menjadi vesikel berupa tetesan air (tear drops)  mejadi pustula
 menjadi krusta. Bisa menimbulkan gejala polimorfik karena
timbul vesikel baru. Predileksi: daerah badan kemudian
menyebar secara sentrifugal
 Pemeriksaan: percobaan Tzanck
 Pengobatan: simtomatik (antipiretik, analgesik, antipruritus)

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
 Penyakit Karakteristik
Variola (small pox) Makula eritematosa  papul  vesikel  pustula 
krusta. Sifat lesi monomorfik. Sudah tereradikasi.
Herpes zoster Reaktivasi dari varicella. Gejala prodromal  vesikel
jernih  vesikel keruh  pustula  krusta. Predileksi
unilateral dan sesuai dermatom.
Herpes simpleks Vesikel yang berkelompok di atas kulit yang sembab dan
eritematosa pada daerah dekat mukokutan
•HSV tipe I: predileksi di daerah pinggang ke atas
terutama daerah mulut dan hidung
•HSV tipe II: predileksi di daerah pinggang ke bawah
terutama daerah genital
Impetigo vesikobulosa Disebabkan S. aureus. Predileksi di ketiak, dada,
punggung. Berupa eritema, bula, dan bula hipopion.
 101. Pitiriasis rosea
 Dermatitis eritroskuamosa yang disebabkan oleh infeksi
virus (self-limiting disease)
 Bentuk klinis:
 Dimulai dengan lesi inisial berbentuk eritema berskuama
halus dengan kolaret (herald patch)
 Disusul dengan lesi yang lebih kecil di badan, paha dan
lengan atas, tersusun sesuai lipatan kulit (inverted christmas
tree appearance)
 Pengobatan: simtomatik

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
Herald patch
 102. Dermatitis seboroik
 Segolongan kelainan kulit yang didasari oleh faktor konstitusi dan berpredileksi
di tempat-tempat seboroik
 Etiologi: belum diketahui pasti
 Kelainan konstitusi berupa status seboroik yang diturunkan
 Pertumbuhan Pityrosporum ovale yang berlebihan
 Proliferasi epidermis yang meningkat
 Faktor predisposisi: kelelahan, stres emosional, infeksi, defisiensi imun
 Gejala: eritema, skuama agak kekuningan yang berminyak
 Pitiriasis sika (ketombe): dermatitis seboroik ringan ditandai skuama halus yang
kemudian mengenai seluruh kulit kepala
 Predileksi: kepala, scalp, dahi, postaurikular, leher, lipat nasolabial, liang telinga
luar, dada, areola mammae, lipatan mammae, interskapular, umbilikus, lipat
paha, anogenital
 Pengobatan:
 Sistemik: KS, isotretinoin, UVB
 Topikal: selenium sulfida shampoo (pitiriasis sika), emolien, ter, sulfur presipitat,
KS, ketokonazol (pada infeksi P. ovale)
 Hindari faktor predisposisi, diet rendah lemak

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
 103. Moluskum kontagiosum
 Penyakit yang disebabkan oleh poxvirus berupa papul-papul, pada
permukaannya terdapat lekukan, berisi massa yang mengandung badan
moluskum
 Transmisi: kontak langsung, autoinokulasi
 Gejala:
 Masa inkubasi: satu hingga beberapa minggu
 Papul miliar, kadang-kadang lentikular dan berwarna putih seperti lilin,
berbentuk kubah yang ditengahnya terdapat lekukan, jika dipijat keluar
massa yang berwarna putih seperti nasi
 Predileksi: muka, badan, ekstremitas, pubis (hanya pada dewasa)
 Pemeriksaan:
 Sebagian besar berdasarkan klinis
 Pemeriksaan mikroskopik badan moluskum (Henderson-Paterson bodies) –
menggunakan pewarnaan Giemsa atau gram
 Diagnosis pasti: biopsi kulit menggunakan pewarnaan HE
 Tata laksana: mengeluarkan massa (manual, elektrokauterisasi, bedah beku)

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
Bhatia AC. Molluscum contagiosum. http://emedicine.medscape.com/article/910570-overview
 104. Veruka
 Hiperplasia epidermis disebabkan oleh HPV
 Transmisi: kontak kulit, autoinokulasi
 Bentuk klinis:
 Veruka vulgaris (common wart): predileksi di ekstremitas ekstensor,
muka & kulit kepala, kutil bulat berwarna abu-abu/sewarna kulit,
lentikular, dapat berkonfluensi, permukaan kasar
 Veruka plana juvenilis: kutil miliar/lentikular, sewarna
kulit/kecoklatan, permukaan licin dan rata, predileksi di muka, leher,
dorsum manus/pedis, pergelangan tangan, lutut
 Veruka plantaris (plantar wart): predileksi di telapak kaki terutama
daerah yang mengalami tekanan, berupa cincin keras di tengahnya
agak lunak dan berwarna kekuningan, nyeri
 Kondiloma akuminata
 Pemeriksaan penunjang: biopsi kulit

Djuanda A. Ilmu penyakit kulit dan kelamin, 5th ed. Balai Penerbit FKUI; 2007.
Wolff K. Fitzpatrick’s color atlas & synopsis of clinical dermatology, 5th ed. McGraw-Hill; 2007.
105. Chlamydia conjunctivitis
 Conjunctival erythema,
 mucoid discharge,
 periorbital swelling,
 often bilateral
Clinical Manifestations
Clinical Syndromes Caused by C. trachomatis
Local Infection Complication Sequelae
Conjunctivitis Chronic arthritis
Men Reiter’s syndrome
Urethritis (rare)
Epididymitis
Prostatitis Infertility (rare)
Infertility
Conjunctivitis Endometritis
Ectopic pregnancy
Women Urethritis Salpingitis
Chronic pelvic pain
Cervicitis Perihepatitis
Chronic arthritis
Proctitis Reiter’s syndrome
(rare)
Conjunctivitis
Infants Chronic lung
Pneumonitis Rare, if any
Pharyngitis disease?
Rhinitis
288
Chlamydia trachomatis
 Infection is through the birth canal
 40% of infants will develop conjunctivitis, 10% will
develop pneumonia
 Treatment is by erythromycin or azithromycin
 Cytology is used mainly for diagnosing infant inclusion
conjunctivitis and ocular trachoma through the
demonstration of intracytoplasmic C trachomatis
inclusions
 Intracytoplasmic inclusions can be detected either by
Giemsa stains or by immunofluorescent staining with
monoclonal antibodies
106. Amoebiasis
Immature Entamoeba histolytica Trophozoites of Entamoeba histolytica with
cyst (mature cysts have 4 nuclei) ingested erythrocytes
107. Gonococcal conjunctivitis
 Symptoms in a newborn with gonococcal conjunctivitis
usually include red eyes, thick pus in the eyes, and
swelling of the eyelids. This type of conjunctivitis usually
begins about 2 to 4 days after birth
• Diagnosis:
– Gram Stain : negative gram
diplococcus
– Culture : Thayer-Martin agar
108. Corynebacterium diphtheriae
 Aerobic gram-positive bacillus
 Toxin production occurs only
when C. diphtheriae infected by virus (phage) carrying tox
gene
 If isolated, must be distinguished from normal diphtheroid
 Toxoid developed in 1920s
Diphtheria Clinical Features
 Incubation period 2-5 days
(range, 1-10 days)
 May involve any mucous membrane
 Classified based on site of infection
 anterior nasal
 pharyngeal and tonsillar
 laryngeal
 cutaneous
 ocular
 genital
Pharyngeal and Tonsillar Diphtheria
 Insidious onset
 Exudate spreads within 2-3 days and may form adherent
membrane
 Membrane may cause respiratory obstruction
 Pseudomembrane: fibrin, bacteria, and inflammatory
cells, no lipid
 Fever usually not high but patient appears toxic
Chinese letter/palisade appearance
109. Cryptococcosis
 Encapsulated yeast
 4 serotypes
 A (C. neoformans v grubii)
 B and C ( C. gatti)
 D (C. neoformans v neoformans)
 All types can cause human disease
 Life cycle
 Asexual: yeast that reproduce by budding
 Human infections

 Sexual: only seen in the laboratory

Ecology and Epidemiology
 World wide
 C. neoformans associated with bird droppings
 C. gatti not associated with birds, associated with
eucalyptus trees
 Generally an infection of immunocompromised but
can cause clinical disease in healthy persons
 Decreased Cell-mediated immunity
 AIDS – CD 4 usually < 100
 Prolonged corticosteroids
 Organ transplant
Ecology and Epidemiology
 15-30% of AIDS patients in Sub-Saharan Africa*
 Much less common in children
 No person to person transmission

*Powderly, WG Clin Infect Dis 1993

Clinical Presentations
 Pulmonary
 Asymptomatic nodule
 Symptomatic: not distinguishable from other causes
 History, PE, routine laboratory testing does not produce
features peculiarly suggestive of cryptococcal infection
 Diagnosis
 Staining of biopsy specimen
 Culture of sputum and/or blood
 Serum cryptococcal antigen (CRAG)
 All patients with pulmonary disease need a CSF
examination to r/o sub clinical meningitis
Silver Stain
110. The Malarial Parasite
 The periodicity of fever associated with each species (ie,
48 h for P falciparum, P vivax, and P ovale [or tertian
fever] ; 72 h for P malariae [or quartan fever]
 P. vivax schizonts are large, have 12 to 24 merozoites,
yellowish-brown, coalesced pigment, and may fill the rbc.
 111. Filariasis
 Penyakit yang disebabkan cacing Filariidae, dibagi menjadi 3
berdasarkan habitat cacing dewasa di hospes:
 Kutaneus: Loa loa, Onchocerca volvulus, Mansonella streptocerca
 Limfatik: Wuchereria bancroftii, Brugia malayi, Brugia timori
 Kavitas tubuh: Mansonella perstans, Mansonella ozzardi
 Fase gejala filariasis limfatik:
 Mikrofilaremia asimtomatik
 Adenolimfangitis akut: limfadenopati yang nyeri, limfangitis retrograde,
demam, tropical pulmonary eosinophilia (batuk, mengi, anoreksia,
malaise, sesak)
 Limfedema ireversibel kronik
 Grading limfedema (WHO, 1992):
 Grade 1 - Pitting edema reversible with limb elevation
 Grade 2 - Nonpitting edema irreversible with limb elevation
 Grade 3 - Severe swelling with sclerosis and skin changes

Wayangankar S. Filariasis. http://emedicine.medscape.com/article/217776-overview

WHO. World Health Organization global programme to eliminate lymphatic filariasis. WHO Press; 2010.
Pemeriksaan & tatalaksana filariasis
limfatik
 Pemeriksaan penunjang:
 Deteksi mikrofilaria di darah
 Deteksi mikrofilaria di kiluria dan cairan hidrokel
 Antibodi filaria, eosinofilia
 Biopsi KGB
 Pengobatan:
 Tirah baring, elevasi tungkai, kompres
 Antihelmintik (ivermectin, DEC, albendazole)
 Suportif
 Pengobatan massal dengan albendazole+ivermectin (untuk
endemik Onchocerca volvulus) atau albendazole+DEC (untuk
nonendemik Onchocerca volvulus) guna mencegah transmisi
 Bedah (untuk kasus hidrokel/elefantiasis skrotal)
 Diet rendah lemak dalam kasus kiluria
Wuchereria bancroftii
Panjang:lebar kepala sama
Inti teratur
Tidak terdapat inti di ekor

Perbandingan panjang:lebar
Brugia malayi kepala 2:1
Inti tidak teratur
Inti di ekor 2-5 buah

Perbandingan panjang:lebar
Brugia timori kepala 3:1
Inti tidak teratur
Inti di ekor 5-8 buah
 112. Infeksi cacing tambang
 Disebabkan Ancylostoma
duodenale & Necator
americanus
 Gejala:
 Pruritus lokal pada tempat
yang mengalami invasi
 Nyeri abdomen, diare,
muntah
 Anemia defisiensi besi
 Infeksi berat menyebabkan
pneumonitis (Loefflerlike
syndrome)

Haburchak DR. Hookworms. http://emedicine.medscape.com/article/218805-overview#showall

Necator Americanus Clinical
 Local irritation; pruritus, papular
 Infect exposed skin
erythematous lesion/vesicular
 Agricultural/mining workers are rash around lesion.
often infected
 Gastrointestinal symptoms;
Nausea, IDA
 Anemia
 No. 113 Sepsis Neonatorum
 Sindrom klinik penyakit sistemik akibat infeksi yang
terjadi pada satu bulan pertama kehidupan. Mortalitas
mencapai 13-25%
 Jenis :
 Early Onset = Dalam 3 hari pertama, awitan tiba-tiba, cepat
berkembang menjadi syok septik
 Late Onset = setelah usia 3 hari, sering diatas 1 minggu, ada
fokus infeksi, sering disertai meningitis
 Tanda awal sepsis pada bayi baru lahir tidak spesifik →
diperlukan skrining dan pengelolaan faktor risiko

Sepsis Neonatal. Pedoman Pelayanan Medis. Ikatan Dokter Anak Indonesia 2010.
Skrining
 Kecurigaan besar sepsis bila :
 Bayi umur sampai dengan usia 3 hari
 Riwayat ibu dengan infeksi rahim, demam dengan
kecurigaan infeksi berat, atau ketuban pecah dini
 Bayi memiliki dua atau lebih gejala yang tergolong dalam
kategori A, atau tiga atau lebih gejala pada kategori B
 Bayi usia lebih dari 3 hari
 Bayi memiliki dua atau lebih temuan Kategori A atau tiga
atau lebih temuan Kategori B
Kelompok Temuan berhubungan dengan Sepsis
Kategori A Kategori B
Kesulitan Bernapas (>60x/menit, retraksi Tremor
dinding dada, grunting, sianosis sentral,
apnea)
Kejang Letargi atau lunglai, malas minum padahal
sebelumnya minum dengan baik
Tidak sadar Mengantuk atau aktivitas berkurang
Suhu tubuh tidak normal (sejak lahir dan Iritabel, muntah, perut kembung
tidak memberi respons terhadap terapi)
atau suhu tidak stabil sesudah
pengukuran suhu selama tiga kali atau
lebih
Persalinan di lingkungan yang kurang Tanda-tanda mulai muncul setelah hari
higienis ke-empat
Kondisi memburuk secara cepat dan Air ketuban bercampur mekonium
dramatis
 Kriteria SIRS - Sepsis

Goldstein B. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit
Care Med 2005; 6(1).
 Tatalaksana Awal
 Tata laksana:
 Dini: stabilisasi pernafasan, hemodinamik, hipoglikemia
 Pemberian inotropik dan vasoaktif (atas indikasi)
 Hidrokortison (pada insufisiensi adrenal)
 Target terapi: CRT<2 detik, kualitas nadi baik pada
sentral/perifer, akral hangat, urin > 1cc/kg/jam, kesadaran
baik, anion gap turun, saturasi vena kava superior >70%

Anderson-Berry AL. Neonatal sepsis. http://emedicine.medscape.com/article/978352-overview

Pudjiadi AH. Pediatric sepsis management.
No. 114 Dengue
Demam dengue
 Demam akut 2-7 hari dengan 2
atau lebih gejala berikut:
 Nyeri kepala
 Nyeri retroorbita
 Myalgia/arthralgia
 Ruam
 Manifestasi perdarahan
 Leukopenia
DBD
 Infeksi dengue yang ditambah 1
atau lebih gejala:
 Uji bendung positif
 Petekie, ekimosis, purpura
 Perdarahan mukosa
 Hematemesis/melena
 Trombositopenia (<100.000)
 Adanya kebocoran plasma
(kenaikan >20% Ht normal;
adanya bukti kebocoran seperti
efusi pleura, asites,
hipoproteinemia)
WHO. SEARO. Guidelines for treatment of dengue fever/dengue hemorrhagic fever in small hospitals. 1999.
No. 115 Pneumonia
 Signs and symptoms :
 Non respiratory: fever, headache, fatigue, anorexia, lethargy,
vomiting and diarrhea, abdominal pain
 Respiratory: cough, chest pain, tachypnea , grunting, nasal
flaring, subcostal retraction (chest indrawing), cyanosis, crackles
and rales (ronchi)

Fast breathing (tachypnea)

Respiratory thresholds
Age Breaths/minute
< 2 months 60
2 - 12 months 50
1 - 5 years 40
Etiology
Neonatal (< 28 days of age)
 Virus: Rubella, Cytomegalovirus (CMV), Herpes, Varicella-zoster
 Bacteria: Streptococci G or D, S pneumoniae (Pneumococci), Coliform
bacteria
Post Neonatal ( > 28 days to < 2 months of age)
 Virus: Adenovirus, Coxsackie, Parainfluenza, Influenza A or B,
Respiratory Syncytial Virus (RSV)
 Bacteria: Streptococci B, E coli, P aeruginosa, Klebsiella, S pneumoniae
(Pneumococci), S aureus, Chlamydia spp
Infants and preschool children (2 months to < 5 years of age)
 Virus: Adenovirus, Parainfluenza, Influenza A or B
 Bacteria: S pneumoniae (Pneumococci), H influenzae, Streptococci A, S
aureus, Chlamydia spp
School age and adolescents (> 5 years)
 Virus: Adenovirus, Parainfluenza, Influenza A or B
 Bacteria: S pneumoniae (Pneumococci), Streptococci A, M. pneumoniae
 WHO recommendations for treatment of children aged 2 months to
4 years who have cough or difficulty breathing using clinical
classifications of pneumonia
No • No tachypnea, no chest indrawing
• Do not administer an antibiotic
pneumonia

• Tachypnea, no chest indrawing

Pneumonia • Home tratment with cotrimoxazole or amoxicillin or
procaine penicillin

Severe • Chest indrawing, no cyanosis, and able to feed

• Admit, administer benzyl penicillin IM every 6 hour
pneumonia

Very severe • Chest indrawing with cyanosis and not able to feed
• Admit, administer chloramphenicol IM every 6 hour
pneumonia and oxygen

Said M. Acute respiratory infection.

No. 116 Malaria
  Gejala:
 Prodromal: sakit kepala, malaise, mual, nyeri otot, diare ringan,
demam ringan
 Demam akut paroksismal
 Setiap 48 jam untuk Plasmodium ovale, Plasmodium vivax,
Plasmodium falciparum
 Setiap 72 jam untuk Plasmodium malariae

 Plasmodium falciparum biasanya demam persisten/ setiap hari

 Interval antar demam asimtomatik

 Gejala lain: anemia, trombositopenia, ikterus,

hepatosplenomegali
 Pemeriksaan penunjang: morfologi darah tepi (pewarnaan Giemsa)
 Tebal : Ada tidaknya plasmodium
 Tipis : Identifikasi spesies Plasmoodium/tingkat parasitemia

Behrman RE. Nelson’s textbook of pediatrics, 19th ed. McGraw-Hill; 2011.

 Morfologi
Plasmodium

Brooks GF. Jawetz, Melnick & Adelberg’s medical microbiology, 23rd ed. McGraw-Hill; 2004.
 Tatalaksana  Sulfadoksin-pirimetamin
sebaiknya dihindari di
usia beberapa minggu
pertama karena
menyebabkan
hiperbilirubinemia
neonatal
 Primakuin sebaiknya
dihindari di usia < 1 bulan
karena menyebabkan
anemia hemolitik pada
defisiensi G6PD
 Tetrasiklin sebaiknya
dihindari di usia < 8
tahun karena
menyebabkan perubahan
warna gigi dan hipoplasia
enamel

World Health Organization. Guidelines for the treatment of malaria, 2nd ed. WHO Press; 2011.
No. 117 Tetanus
 Penyakit spastik paralitik akut akibat toksin tetanus (tetanospasmin) yang
dihasilkan Clostridium tetani. Tanda utama : spasme tanpa gangguan
kesadaran
 Toksin masuk melalui neuromuscular junction → endositosis ke neuron
motorik → transport retrograde → interneuron di spinal → menghambat
pelepasan GABA (neurotransmiter inhibitor → Eksitasi terus menerus
 Gejala khas generalized tetanus: spasme (dipicu oleh rangsang cahaya,
suara, atau sentuhan)
 Trismus (spasme m. masseter)
 Risus sardonicus (spasme otot wajah dan buccal)
 Opisthotonos (hiperekstensi tubuh)
 Boardlike rigidity (rigiditas spastik pada dinding abdomen)
 Pada neonatus : sulit menyusu, mulut mencucu
 Kesadaran dan fungsi sensorik tidak terganggu
 Gejala lain: demam, retensi uri, defekasi yang tidak terkontrol, takikardia,
asfiksia, dll
 Trismus

Opisthotonos
Risus sardonicus
Tatalaksana Dasar
 Antibiotik
 Penisilin Prokain 50.000 IU/kg/kali IM, per 12 jam
 Ampisilin 150 mg/kg/hari IV dibagi 4 dosis
 Metronidazole loading dose 15 mg/kg, selanjutnya 7,5 mg/kg/6 jam
 Netralisasi toksin
 Anti Tetanus Serum 50.000-100.000 IU
 Human Tetanis Immunoglobulin 3.000-6.000 IU
 Anti konvulsan
 Diazepam 0.1-0.3 mg/kg/kali IV tiap 2-4 jam
 Perawatan luka (port d’entre) : Eksisi dan debridement luka
 Terapi Suportif
 Bebaskan jalan napas, hindari aspirasi
 Oksigen
 Minimalisir stimulasi
 Cairan dan nutrisi per NGT
Pencegahan
 Imunisasi Aktif
 Imunisasi dasar DPT diberikan tiga kali sejak usia 2 bulan dengan
interval 4-6 minggu, ulangan pada umur 18 bulan dan 5 tahun
 Pencegahan pada luka
 Luka ringan dan bersih
 Imunisasi lengkap : tidak perlu ATS/Imunoglobulin
 Imunisasi tidak lengkap : Imunisasi aktif DPT/DT
 Luka sedang/berat dan kotor
 Imunisasi (-) : ATS 3.000-5.000 IU. TT pada sisi lain
 Imunisasi (+) : Jika lebih dari 5 tahun, Ulangan TT dan ATS 3.000-5.000 IU
 No. 118 Penyakit jantung kongenital
 Asianotik: L-R shunt
 ASD: fixed splitting S2, murmur
ejeksi sistolik
 VSD: murmur pansistolik
 PDA: continuous murmur
 Sianotik: R-L shunt
 TOF: AS, VSD, overriding aorta,
RVH. Boot like heart pada
radiografi
 TGA

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002103 /
Park MK. Pediatric cardiology for practitioners. Mosby; 2008.
VSD
ASD
PDA
TOF
No. 119 Developmental Milestone
No. 120 APGAR Score
No. 121 Bronkiolitis
Infection (inflammation) at bronchioli
 Etiology: predominantly RSV (Respiratory Syncytial
Virus), adenovirus etc
 Clinical syndromes: fast breathing, retractions,
wheezing (Episode pertama wheezing pada anak
<2 tahun)
 Predominantly < 2 years of age (2-6 months)
 Difficult to differentiate with pneumonia and
asthma
Bronchiolitis:
Clinical manifestastion
 Clinical Symptoms
Cough, cold, fever, fast breathing, irritable,
vomitus, poor intake
 Physical Examinations
Tachypnea, tachycardia, retraction, prolonged expiration,
wheezing, pharyngitis, conjunctivitis, otitis media.
Bronchiolitis:
Management
Mild disease
• Symptomatic therapy
Moderate to Severe diseases
 Life Support Treatment : O2, IVFD
 Etiological Treatment
 Anti viral therapy (rare)
 Antibiotic (if etiology bacteria)
 Symptomatic Therapy
 Bronchodilator: controversial
 Corticosteroid: controversial (not effective)
 122. Defisiensi vitamin A
 Vitamin A meliputi retinol, retinil ester, retinal dan asam
retinoat. Provitamin A adalah semua karotenoid yang memiliki
aktivitas biologi β-karoten
 Fungsi: penglihatan, diferensiasi sel, keratinisasi, kornifikasi,
metabolisme tulang, perkembangan plasenta, pertumbuhan,
spermatogenesis, pembentukan mukus
 Gejala defisiensi:
 Okular (xeroftalmia): rabun senja, xerosis konjungtiva & kornea,
keratomalasia, bercak Bitot, hiperkeratosis folikular, fotofobia
 Retardasi mental, gangguan pertumbuhan, anemia,
hiperkeratosis folikular di kulit
 Sumber vitamin A: hati, minyak ikan, susu & produk derivat,
kuning telur, margarin, sayuran hijau, buah & sayuran kuning

Kliegman RM. Nelson’s textbook of pediatrics, 19th ed. McGraw-Hill; 2011

Deficiency
Vitamin A Beta carotene - Night blindness due to retinal injury, B

No. 122 Defisiensi vitamin

Vitamin B1 Beriberi - a disease whose symptoms include weight loss, body weakness and pain,
brain damage, irregular heart rate, heart failure, and death if left untreated
Vitamin B2 Ariboflavinosis - it causes distinctive bright pink tongues, although other symptoms
are cracked lips, throat swelling, bloodshot eyes, and low red blood cell count
Vitamin B3 Pellagra - symptoms included diarrhea, dermatitis, dementia, and finally death
Vitamin B5 Chronic paresthesia
Vitamin B7 Biotin deficiency - it causes rashes, hair loss, anaemia, and mental conditions
including hallucinations, drowsiness, and depression
Vitamin B12 Hypocobalaminemia - it causes gradual deterioration of the spinal cord and very
gradual brain deterioration, resulting in sensory or motor deficiencies
Vitamin C Scurvy – it causes lethargy, skin spots, bleeding gums, loss of teeth, fever, and
death
Vitamin D Rickets - muscles and bones to become soft, which can cause permanent
deformities in children
Vitamin E Neurological problems due to poor nerve conduction
Vitamin K Uncontrolled bleeding and underdeveloped faces and bones
Bitot’s Spot Xerophtalmi
a

Follicular hyperkeratosis
World Health Organization. Control of vitamin A deficiency and xerophthalmia. WHO; 1982.
 No. 123 Sindrom Nefrotik
 Spektrum gejala yang ditandai dengan protein loss
yang masif dari ginjal
 Gejala klasik: proteinuria, edema, hiperlipidemia,
hipoalbuminemia
 Gejala lain : hipertensi, hematuria, dan penurunan
fungsi ginjal
 Primer vs sekunder
 Terapi: kortikosteroid (prednison, prednisolon)

Lane JC. Pediatric nephrotic syndrome. http://emedicine.medscape.com/article/982920-

overview
Diagnosis
 Anamnesis : Bengkak di kedua kelopak mata, perut,
tungkai atau seluruh tubuh. Penurunan jumlah urin. Urin
dapat keruh/kemerahan
 Pemeriksaan Fisik : Edema palpebra, tungkai, ascites,
edema skrotum/labia. Terkadang ditemukan hipertensi
 Pemeriksaan Penunjang : Proteinuria masif ≥ 2+, rasio
albumin kreatinin urin > 2, dapat disertai hematuria.
Hipoalbumin (<2.5g/dl), hiperkolesterolemia (>200
mg/dl). Penurunan fungsi ginjal dapat ditemukan.
Nefrotik vs Nefritik
No. 124. Algoritme Penanganan Kejang
ALGORITME PENANGANAN KEJANG AKUT & STATUS KONVULSIF 3
Diazepam 5-
Prehospital 10mg/rekt max 2x 0-10 mnt
jarak 5 menit

Hospital/ED Diazepam 0,25-0,5mg/kg/iv/io Monitor

Airway 10-20 mnt
(kec 2mg/mnt, max dosis 20mg) Tanda vital
Breathing, O2
Circulation atau EKG
Midazolam 0,2mg/kg/iv bolus Gula darah
atau Elektrolit serum
NOTE : JIKA DIAZ RECTAL 1X PRE
HOSPITAL BOLEH RECTAL 1X Lorazepam 0,05-0,1mg/kg/iv (Na, K, Ca, Mg, Cl)
(rate <2mg/mnt) Analisa Gas Darah
KEJANG (-) Koreksi kelainan
5 – 7 mg/kg
12 jam kemudian Fenitoin Pulse oxymetri
20mg/kg/iv
20-30 mnt Kadar obat darah
ICU/ED Note : Aditional (20mnt /50ml NS)
5-10mg/kg/iv Max 1000mg

KEJANG (-) Phenobarbitone

4 – 5 mg/kg 30-60 mnt
20mg/kg/iv
12 jam kemudian
(rate >5-10min; max 1g)

ICU Refrakter

Midazolam 0,2mg/kg/iv bolus Pentotal - Tiopental Propofol 3-5mg/kg/infusion

Dilanjut infus 0,02-0,4 mg/kg/jam 5 – 8 mg/kg/iv
 No. 125 Kejang demam
 Kejang yang terjadi akibat kenaikan suhu tubuh di atas 38,4° C tanpa
adanya infeksi SSP atau gangguan elektrolit pada anak di atas usia 1
bulan tanpa riwayat kejang tanpa demam sebelumnya (ILAE, 1993)
 Umumnya berusia 6 bulan – 5 tahun
 Kejang demam sederhana (simpleks)
 Berlangsung singkat, tonik klonik, umum, tidak berulang dalam 24 jam
 Kejang demam kompleks
 Lama kejang > 15 menit
 Kejang fokal atau parsial menjadi umum
 Berulang dalam 24 jam
 Pungsi lumbal sangat dianjurkan untuk usia < 12 bulan dan
dianjurkan untuk usia 12-18 bulan

Mangunatmadja I. Kejang demam: diagnosis dan tata laksananya.

Tata

laksana
Intermiten
 Parasetamol 10-15 mg/kg diberikan 4 kali/hari
 Diazepam 0,5 mg/kg/hari dibagi 4 dosis
 Rumatan
 Fenobarbital 3-6 mg/kg/hari atau asam valproat 15-40 mg/kg/hari
 Dianjurkan profilaksis terus menerus:
 Kelainan neurologis nyata sebelum atau sesudah kejang (paresis Tod’s,
CP, hidrosefalus)
 Kejang lama > 15 menit
 Kejang fokal
 Dipertimbangkan:
 Kejang berulang dalam 24 jam
 Bayi usia < 12 bulan
 Kejang demam kompleks berulang > 4 kali
 Lama pengobatan 1 tahun bebas kejang
Mangunatmadja I. Kejang demam:
diagnosis dan tata laksananya.
No. 126 Epilepsi
 An epilepsy is defined
as a neurological
condition characterised
by recurrent epileptic
seizures unprovoked
by any immediately
identifiable cause
 Partial-onset seizures
begin in a focal area of
the cerebral cortex
 Generalized-onset
seizures have an onset
recorded
simultaneously in both
cerebral hemispheres
 Diagnosis
 A detailed history should be taken from the child, young person or adult
and an eyewitness to the attack, where possible, to determine whether or
not an epileptic seizure is likely to have occurred.
 In a child, young person or adult presenting with an attack, a physical
examination should be carried out. This should address their cardiac,
neurological and mental status, and should include a developmental
assessment where appropriate.
 An EEG should be performed only to support a diagnosis of epilepsy in
children and young people. If an EEG is considered necessary, it should be
performed after the second epileptic seizure but may, in certain
circumstances, as evaluated by the specialist, be considered after a first
epileptic seizure.
 The EEG should not be used in isolation to make a diagnosis of epilepsy.
 Neuroimaging should be used to identify structural abnormalities that
cause certain epilepsies.
 In children and young people, other investigations, including blood and
urine biochemistry, should be undertaken at the discretion of the
specialist to exclude other diagnoses, and to determine an underlying
cause of the epilepsy.

National Institute of Health and Clinical Excellence. The diagnosis and management of the epilepsies in adults and children in
primary and secondary care. 2012.
 Treatment
 It is recommended that children, young people and adults should be
treated with a single AED (monotherapy) wherever possible. If the initial
treatment is unsuccessful, then monotherapy using another drug can be
tried.
 It is recommended that combination therapy (adjunctive or ‘add-on’
therapy) should only be considered when attempts at monotherapy with
AEDs have not resulted in seizure freedom. If Treatment with AED therapy
is generally recommended after a second epileptic seizure.
 Offer carbamazepine or lamotrigine as first-line treatment to children,
young people and adults with newly diagnosed focal seizures.
 Offer sodium valproate as first-line treatment to children, young people
and adults with newly diagnosed generalized tonic-clonic seizures.
 Offer ethosuximide or sodium valproate as first-line treatment to children,
young people and adults with absence seizures.
 If complete seizure control is accomplished by an anticonvulsant, a
minimum of 2 seizure-free years is an adequate and safe period of
treatment for a patient with no risk factors
 When the decision is made to discontinue the drug, the weaning process
should occur for 3–6 mo, because abrupt withdrawal may cause status
epilepticus
National Institute of Health and Clinical Excellence. The diagnosis and management of the epilepsies in adults and children in primary and
secondary care. 2012.
No. 127 Ikterus Neonatorum
 Ikterus neonatorum: fisiologis vs non fisiologis.
 Ikterus fisiologis:
 Awitan terjadi setelah 24 jam
 Memuncak dalam 3-5 hari, menurun dalam 7 hari (pada NCB)
 Ikterus fisiologis berlebihan → ketika bilirubin serum puncak adalah 7-15 mg/dl
pada NCB
 Ikterus non fisiologis:
 Awitan terjadi sebelum usia 24 jam
 Tingkat kenaikan > 0,5 mg/dl/jam
 Tingkat cutoff > 15 mg/dl pada NCB
 Ikterus bertahan > 8 hari pada NCB, > 14 hari pada NKB
 Tanda penyakit lain
 Gangguan obstruktif menyebabkan hiperbilirubinemia direk. Ditandai bilirubin
direk > 2 mg/dl. Penyebab: kolestasis, atresia bilier, kista duktus koledokus.

Indrasanto E. Hiperbilirubinemia pada neonatus.

20
18
16
14
12
fisiologis
10
non- fisiologis
8
6
4
2
0
hari 1 hari 2 hari 3 hari 4 hari 5 hari 6 hari 7

 Ikterus yang berkembang cepat pada hari ke-1

 Kemungkinan besar: inkompatibilitas ABO, Rh, penyakit hemolitik,
atau sferositosis. Penyebab lebih jarang: infeksi kongenital,
defisiensi G6PD
 Ikterus yang berkembang cepat setelah usia 48 jam
 Kemungkinan besar: infeksi, defisiensi G6PD. Penyebab lebih
jarang: inkompatibilitas ABO, Rh, sferositosis.
Penyebab Hemolisis
Penyakit Keterangan
Inkompatibilitas ABO Adanya aglutinin ibu yang bersirkulasi di darah anak
terhadap aglutinogen ABO anak. Ibu dengan golongan darah
O, memproduksi antibodi IgG Anti-A/B terhadap gol. Darah
anak
Inkompatibilitas Rh Adanya antibodi ibu yang bersirkulasi di darah anak
terhadap antigen Rh anak. Jarang pada anak pertama.
Hematoma darah Akibat proses persalinan.
ekstravaskuler
Defisiensi G6PD Penyakit terkait kromosom X. Enzim G6PD berfungsi untuk
melindungi eritrosit dari kerusakan oksidatif.
Sferositosis herediter Terdapat defek protein membran yang menyebabkan
instabilitas eksoskeleton eritrosit
Polisitemia Peningkatan pembentukan eritrosit yang menyebabkan
peningkatan destruksi eritrosit
Daerah tubu Kadarbilirubin (mg/dl)
Muka 4 -8
Dada/punggung 5 -12
Perut dan paha 8 -16
Tangan dan kaki 11-18
Telapak tangan/kaki >15
Panduan foto terapi

AAP, 2004
Panduan transfusi tukar

AAP, 2004
 No. 128 Kretinisme
 Hipotiroid kongenital (kretinisme) ditandai produksi hormon
tiroid yang inadekuat pada neonatus
 Penyebab:
 Defek anatomis kelenjar tiroid atau jalur metabolisme hormon
tiroid
 Inborn error of metabolism
 Defisiensi iodin
 Merupakan salah satu penyebab retardasi mental yang dapat
dicegah. Bila terdeteksi setelah usia 3 bulan, akan terjadi
penurunan IQ bermakna.
 Tata laksana tergantung penyebab. Sebaiknya diagnosis
etiologi ditegakkan sebelum usia 2 minggu dan normalisasi
hormon tiroid (levotiroksin)sebelum usia 3 minggu.

Postellon DC. Congenital hypothyroidism. http://emedicine.medscape.com/article/919758-overview

 Most affected infants have few or no symptoms,
because their thyroid hormone level is only
slightly low. However, infants with severe
hypothyroidism often have a unique
appearance, including:
 Dull look
 Puffy face
 Thick tongue that sticks out
 This appearance usually develops as the disease
gets worse. The child may also have:
 Choking episodes
 Constipation
 Dry, brittle hair
 Jaundice
 Lack of muscle tone (floppy infant)
 Low hairline
 Poor feeding
 Short height (failure to thrive)
 Sleepiness
 Sluggishness
Neonatal hypothyroidism. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002174/
Longo DL. Harrison’s principles of internal medicine, 18th ed. McGraw-Hill; 2012.
No. 129 Vanillylmandelic acid (VMA)
 VMA adalah metabolit hasil akhir dari metabolisme
katekolamin (epinefrin & norepinefrin)
 Kadar VMA urin digunakan untuk pemeriksaan pada
feokromositoma (tumor sel kromafin pada kelenjar adrenal),
neuroblastoma, atau tumor lain yang berasal dari krista
neuralis
 The reference range in persons aged 15 years and older is 2-7
mg/24 hours.
The main pathways of catecholamine metabolism. The end products of noradrenaline (NA) and
adrenaline (ADR) metabolism in effector cells are 3-methoxy-4-hydroxyphenylglycol (MHPG) and
vanillylmandelic acid (VMA), and of dopamine metabolism homovanillic acid (HVA). In sympathetic nerve
terminals, the end product of NA and ADR metabolism is 3,4-dihydroxyphenylglycol (DHPG), and 3,4-
dihydoxyphenylacetic acid (DOPAC) is the end product of the dopamine metabolism. The aldehyde
intermediates exist only transiently and are rapidly metabolized to corresponding glycols by the enzyme
aldehyde reductase (AR) or to acids by the enzyme aldehyde dehydrogenase (AD). The majority of the
metabolites are conjugated at the position of phenolic hydroxyl group with sulfate or glucuronide. MAO,
monoamine oxidase; COMT, catechol-O-methyltransferase; DHMA, 3,4-dihydroxymandelic acid.
Enzim yang Terlibat
 Tyrosine hydroxylase → catalyzing the conversion of the amino acid L-tyrosine to L-3,4-
dihydroxyphenylalanine (L-DOPA). L-DOPA is a precursor for dopamine.
 Dopamine β – hydroxylase (DBH) → converts dopamine to norepinephrine
 Monoamine oxidase (MAO)
 Adrenaline or noradrenaline to 3,4-Dihydroxymandelic acid
 Metanephrine or normetanephrine to vanillylmandelic acid (VMA)
 Dopamine to dihydroxyphenylacetic acid
 3-Methoxytyramine to homovanillic acid
 Catechol-O-methyltransferase (COMT) → degrade catecholamines such as dopamine,
epinephrine, and norepinephrine
 DOPAC → HVA (homovanillic acid)
 Norepinephrine → Normetanephrine
 Epinephrine → Metanephrine
 Dihydroxyphenylethylene glycol (DOPEG) → Methoxyhydroxyphenylglycol (MOPEG)
 3,4-Dihydroxymandelic acid (DOMA) → Vanillylmandelic acid (VMA)
 Phenylethanolamine N-methyltransferase (PNMT) → catalyzes the synthesis of
epinephrine from norepinephrine
 Choline acetyltransferase → join Acetyl-CoA to choline, resulting in the formation of
the neurotransmitter acetylcholine
No. 130 Approach to
Bleeding Disorder in Children
History :
 Bleeding into the skin and mucous membranes : disorders of platelets and
blood vessels (purpuric disorders) and may be manifested as petechiae
and/or ecchymoses.
 Bleeding into soft tissue, muscle, and joints : hemophilia or other disorders
of coagulation
 Typical Presentation

male infant who is starting to walk and presents Hemofilia

with a painful swollen joint after a fall
adolescent girl who presents with excessive von Willebrand Disease
menstrual bleeding, recurrent nosebleeds, and (vWD)
pallor
five-year-old child who is not clinically ill but acute post-infectious
presents with moderate mucocutaneous purpura immune
in the wake of a viral infection thrombocytopenia
ten-day-old infant with bleeding from the umbilical factor XIII deficiency
stump
Abnormal Coagulation Test
Normal PT and prolonged aPTT
Prolonged PT and normal aPTT
Prolonged PT and aPTT
Prolonged thrombin time
characteristic of intrinsic pathway coagulation
factor (factors VIII, IX, XI, and XII) deficiency
characteristic of inherited or acquired factor VII
deficiency
Well child — inherited disorder within the
common pathway or an acquired disorder
involving multiple pathways (vitamin K-dependent
coagulation factors)
Sick child — disorders to consider are
disseminated intravascular coagulation (DIC),
severe hepatocellular dysfunction, and severe
vitamin K deficiency. Because the production of
factor V is independent of the status of vitamin K,
the factor V level can be used to distinguish
between vitamin K deficiency (in which factor V is
normal) and liver disease or DIC (in which factor V
is decreased)
hypofibrinogenemia, structurally abnormal
fibrinogens (dysfibrinogenemias)
Normal
Coagulation
Test
 No. 131 Anemia hemolitik
 Anemia
 Penurunan produksi eritrosit
 Aplasia: anemia aplastik, leukemia
 Eritropoiesis yang tidak efektif: defisiensi Fe, defisiensi asam folat,
penyakit kronik, CKD
 Peningkatan destruksi eritrosit (anemia hemolitik)
 Korpuskular: sferositosis, defisiensi G6PD, hemoglobinopati
(thalassemia)
 Ekstrakorpuskular: autoimun, idiopatik

 Perdarahan
 Berdasarkan morfologi eritrosit
 Mikrositik (<80 fl)
 Normositik (80-100 fl)
 Makrositik (>100 fl)

Windiastuti E. Anemia in children.

  Hypochromic Microcytic  Normocytic

◦ Iron deficiency anemia ◦ Acute blood loss

◦ Thalassemia ◦ Infection
◦ Sideroblastic anemia ◦ Renal failure
◦ Chronic infection ◦ Liver disease
◦ Lead poisoning ◦ Malignancy
◦ Hemoglobin E trait ◦ Early iron deficiency
◦ Severe Malnutrition ◦ Aplastic anemia
◦ Dyserythropoietic anemia
 Macrocytic

◦ Normal newborn Usia Kadar Hb normal

◦ Post-splenectomy (g/dl)
◦ Liver disease 1-3 hari 14,5-22,5
◦ Obstructive jaundice
◦ Aplastic anemia 2 bulan 9,0-14,0
◦ Hypothyroidism 6-12 tahun 11,5-15,5
◦ Megaloblastic anemia
12-18 tahun 13,0-16,0 (laki-laki)
12,0-16,0
(perempuan)
Windiastuti E. Anemia in children.
Behrman RE. Nelson’s textbook of pediatrics, 19th ed. McGraw-Hill; 2011.
 132. Resusitasi Neonatus

PPV : Positive
Pressure
Ventilation
Kattwinkel J, Perlman JM. Part 15: neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(suppl 3):S909 –S919
No. 133 Hipotermia pada Neonatus
 Definisi : Temperatur inti < 35 to 35.5° C
 Neonatus rentan terhadap hipotermi karena besarnya rasio luas
permukaan tubuh terhadap volume, terutama pada neonatus
dengan BBLR.
 Heat loss :
 Radiant heat loss occurs (akibat suhu lingkungan yang lebih
rendah)
 Evaporative heat loss (melalui cairan amnion yang masih melekat
di tubuh)
 Conductive heat loss (kontak dengan benda atau permukaan
dengan suhu rendah)
 Hipotermi juga dapat terjadi akibat kondisi patologis yang
mempengaruhi termoregulasi (sepsis, intracranial hemorrhage).
 Patofisiologi
 Hipotermia → Pengaktifan saraf simpatis, ↑Norepinefrin di
jaringan brown fat → Lipolisis dan oksidasi/re-esterifikasi
asam lemak → Menghasilkan energi panas lokal, dan supply
aliran darah → Meningkatnya metabolic rate dan konsumsi
O2 → respiratory insufficiency, hipoksia jaringan, kerusakan
neurologis, hipoglikemia, metabolik asidosis, dan kematian
 Pencegahan
 Menggunakan kain kering dan hangat saat melahirkan
 Metode Kanguru
 Hindari memandikan bayi di hari I
 Memakaikan pakaian yang menutupi seluruh tubuh,
termasuk kepala
 Menjaga temperatur saat transport
Gejala hipotermia
 Vasokonstriksi perifer  Peningkatan metabolisme
 Hipoglikemia
 Akrosianosis
 Hipoksia
 Ekstremitas dingin
 Asidosis metabolik
 Perfusi perifer ↓
 Peningkatan tekanan
 Depresi SSP arteri pulmonal
 Letargi  Respiratory distress
 Bradikardia  Takipnea
 Apnea  Tanda kronik
 Penurunan BB
 Poor feeding
 BB tidak bertambah
No. 134: Dehidrasi
 Evaluasi Diare dan Dehidrasi
 Anamnesis
Frekuensi BAB
 Lamanya diare

 Adanya darah dalam tinja

 Muntah

 Pengobatan yang baru diminum (antibiotik dan obat lainnya)

 Pemeriksaan Fisik
 Evaluasi tanda dehidrasi (rewel/gelisah, kesadaran, mata cekung,
turgor kulit, kehausan/malas minum)
 Darah dalam tinja

 Tanda-tanda gizi buruk

 Perut kembung

 Tanda invaginasi (massa intraabdomen, tinja lendir dan darah)

Scoring System
Degree of dehydration
Score 0 1 2
General condition Healthy Irritability, Delirium, coma
sleepy, apathy or shock
Skin elasticity Normal Decreased Very decreased
Eye Normal Sunken Very sunken
Fontanel Normal Sunken Very sunken
Mouth Normal Dry Dry & cyanotic
Pulse Normal 120-140 > 140

Amount of score: 0- 2 Mild dehydration

3- 6 Moderate dehydration
7-12 Severe dehydration

Maurice King, 1974

Penanganan
 Rehidrasi: dapat diberikan oral/parenteral tergantung
status dehidrasinya
 Tanpa dehidrasi
 5 cc/kg ORS setiap habis muntah
 10cc/kg ORS setiap habis mencret

 Dehidrasi ringan sedang

 75 cc/kg ORS dalam 3 jam
 Bila per oral tidak memungkinkan, dapat diberikan parenteral
tergantung kebutuhan maintenance cairan + defisit cairan
 Dehidrasi berat (parenteral)
Pemberian Pemberian Berikut
Golongan Umur Pertama 30 70 ml/kgbb selama :
ml/kgbb selama :
Bayi ( < umur 12 bulan ) 1 jam 5 jam
Anak ( 12 bln – 5 tahun ) 30 menit 2.5 jam
No. 135 Generalized Edema Approach
• Haematuria, oliguria, hypertension, pulmonary oedema to
Renal Disease suggest acute glomerulonephritis. Frothy urine suggests
nephrotic syndrome.

• Stigmata of chronic liver disease such as jaundice, palmar

erythema, clubbing, pruritic rash, hepatosplenomegaly
Liver Disease with gross ascites in the absence of jaundice to exclude
portal vein thrombosis

Allergic • Edema usually mild, commonly periorbital. History of

Reaction allergen exposure

• Decreased effort tolerance, orthopnoea, paroxysmal

Cardiac Disease nocturnal dyspnoea and signs such as cardiomegaly, gallop
rhythm, lung crepitations and turgid liver
Evaluasi
Pemeriksaan
 Urine dipstick and microscopy
 Proteinuria, haematuria and casts are indicative of renal disease
 Renal function test
 Raised serum urea and creatinine are indicative of renal disease
 Full blood count
 Liver function test
 hypoalbuminaemia in the absence of circulatory overload
suggests hypoproteinaemic states
 hyperbilirubinaemia and transaminitis suggest liver disease
 Chest X-ray and electrocardiogram
 No. 136 Infeksi Saluran Kemih dan Sepsis
 Sering terjadi pada bayi/anak perempuan.
 Tanda dan Gejala :
 Demam, BB sukar naik, anoreksia
 Disuria, poliuria, nyeri perut/pinggang, mengompol
 Urin berbau menyengat
 Nyeri ketok CVA, nyeri suprasimfisis
 Kelainan pada genitalia eksterna/kelainan pada tulang belakang
 Neonatus : suhu tidak stabil, irritable, napas tidak teratur, ikterik,
gejala sepsis
 Pemeriksaan Penunjang :
 Urinalisis : Proteinuria, leukosituria (>5/LPB), Hematuria
(Eritrosit>5/LPB)
 Biakan urin dan uji sensitivitas
 Kreatinin dan Ureum
 Diagnosa pasti : Bakteriuria bermakna pada biakan urin (>105 koloni
kuman per mm2)
Pelayanan Kesehatan Anak di Rumah Sakit. WHO.
Tatalaksana
 Medikamentosa
 Sebelum ada hasil biakan urin dan uji kepekaan, antibiotik
diberikan secara empirik selama 7-10 hari
 Obat rawat jalan : kotrimoksazol oral 24 mg/kgBB setiap 12 jam,
alternatif ampisilin, amoksisilin, kecuali jika :
 Terdapat demam tinggi dan gangguan sistemik
 Terdapat tanda pyelonefritis (nyeri pinggang/bengkak)
 Pada bayi muda
 Jika respon klinis kurang baik, atau kondisi anak memburuk
berikan gentamisin (7.5 mg/kg IV sekali sehari) + ampisilin (50
mg/kg IV setiap 6 jam) atau sefalosporin gen-3 parenteral.
 Pertimbangkan komplikasi pielonefritis atau sepsis.
 Kriteria SIRS - Sepsis

Goldstein B. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit
Care Med 2005; 6(1).
Sepsis Work-Up
 Pemeriksaan darah perifer lengkap
 Fungsi pembekuan dan koagulasi
 Elektrolit, fungsi hati dan ginjal
 Urinalisis
 Kultur
 Jika memungkinkan, ambil sediaan darah dan urin untuk
kultur sebelum memulai terapi antibiotik. Sediaan CSF
dapat diambil jika infeksi SSP tidak dapat disingkirkan.
No. 137 Imunisasi

BCG sudah dapat

diberikan sejak
lahir
Rekomendasi bila Vaksinasi
Terlambat
 BCG : Pada usia < 12 bulan, boleh diberikan kapan saja,
jika > 3 bulan uji tuberkulis terlebih dahulu
 DPaT, Polio, dan Hepatitis B : Bila terlambat, jangan
mengulang pemberian dari awal, tetapi lanjutkan dan
lengkapi imunisasi seperti jadwal, tidak peduli berapapun
jarak waktu/interval keterlambatan dari pemberian
sebelumnya. Bila belum pernah imunisasi dasar, diberikan
sesuai imunisasi dasar baik jumlah maupun intervalnya
 No. 138 Eksantema akut

Hadinegoro SRS. Acute exanthema. PPT presentation.

Morbili/Rubeola/Campak
 Pre-eruptive Stage
 Demam
 Catarrhal Symptoms – coryza,
conjunctivitis
 Respiratory Symptoms – cough
 Eruptive Stage/Stage of Skin Rashes
 Exanthem sign
 Maculopapular Rashes – Muncul 2-7
hari setelah onset
 Demam tinggi yang menetap
 Anoreksia dan iritabilitas
 Diare, pruritis, letargi dan
limfadenopati oksipital
 Stage of Convalescence
 Rash – menghilang sama dengan urutan
munculnya (muka lalu ke tubuh bag
bawah)  membekas kecoklatan
 Demam akan perlahan menghilang saat
erupsi di tangan dan kaki memudar

 Tindakan Pencegahan :
 Imunisasi Campak pada usia 9 bulan
 Mencegah terjadinya komplikasi berat
 Scarlet Fever
 Sindrom yang memiliki karakteristik: faringitis eksudatif, demam, dan
rash.
 Disebabkan oleh group A beta-hemolytic streptococci (GABHS)
 Manifestasi pada kulit diawali oleh infeksi streptokokus (umumnya pada
tonsillopharynx) dengan gejala nyeri tenggorokan dan demam tinggi.
Masa inkubasi 1-4 hari. Disertai gejala : nyeri kepala, mual, muntah, nyeri
perut, myalgia, dan malaise.

• Rash : Timbul 12-48 jam setelah onset demam.

Dimulai dari leher kemudian menyebar ke badan
dan ekstremitas.
• Pemeriksaan : Throat culture positive for group A
strep
• Tatalaksana : Antibiotik antistreptokokal minimal
10 hari (Eritromisin atau Penicillin G)

Scarlet Fever. http://emedicine.medscape.com/article/1053253-overview

139. HYPOPITUITARY
• The pituitary gland is located at the base of the brain, and intimately
connected with the hypothalamus.
• Consists of two lobes:
 Posterior pituitary secretes antidiuretic hormone (ADH): regulates osmolarity of
the blood ; and oxytocin: causes contractions of the uterus in childbirth and
participates in breastfeeding.
 Anterior pituitary secretes thyrotropin-releasing hormone, corticotropin-
releasing hormone, gonadotropin-releasing hormone and growth hormone-
releasing hormone
• Hypopituitarism is a condition in which the pituitary gland does not
produce one or more of its hormones or not enough of them.
• This condition may occur because of disease in the pituitary or
hypothalamus (a part of the brain that contains hormones that control the
pituitary gland).
• Causes : tumor, infection, inflammation, vascular problem, traumatic brain
injury, subarachnoid hemorrhage, radiation, congenital hypopituitarism
HYPOPITUITARY
Symptoms depend on the cause, rapidity of onset, and the hormone that is
involved :
ACTH deficiency: fatigue, low blood pressure, weight loss, weakness,
depression, nausea, or vomiting
TSH deficiency: constipation, weight gain, sensitivity to cold, decreased
energy, and muscle weakness or aching.
FSH and LH deficiency: In women, symptoms include irregular or stopped
menstrual periods and infertility. In men, symptoms include loss of body and
facial hair, weakness, lack of interest in sexual activity, erectile dysfunction,
and infertility
GH deficiency: In children, symptoms include short height, fat around the
waist and in the face, and poor overall growth. In adults, symptoms include
low energy, decreased strength and exercise tolerance, weight gain,
decreased muscle mass, and feelings of anxiety or depression.
Prolactin deficiency: In women, symptoms include lack of milk production,
fatigue, and loss of underarm and pubic hair. No symptoms are seen in men.
ADH deficiency: Symptoms include increased thirst and urination.
SHEEHAN SYNDROME
• Sheehan syndrome, is hypopituitarism, caused by necrosis
due to blood loss and hypovolemic shock during and after
childbirth
• Most common initial symptoms of Sheehan's syndrome are
agalactorrhea and/or difficulties with lactation.
• Many women also report amenorrhea or oligomenorrhea after
delivery
• Secondly, the anterior pituitary is supplied by a low pressure
portal venous system.
• These vulnerabilities, when affected by major hemorrhage or
hypotension during the peripartum period, can result in
ischemia of the affected pituitary regions leading to necrosis.
• The posterior pituitary is usually not affected due to its direct
arterial supply.
140. HIPERTENSI DALAM KEHAMILAN
Criteria for Preeclampsia
 Previously normotensive
woman
 > 140 mmHg systolic
 > 90 mmHg diastolic
 Proteinuria > 300 mg in 24
hour collection or > +1 on
dipstick
 Nondependent edema
Criteria for Severe Preclampsia
 BP > 160 systolic or >110 diastolic
 > 5 gr of protein in 24 hour urine
or > 3+ on 2 dipstick urines
greater than 4 hours apart
 Oliguria < 500 mL in 24 hours
 Cerebral or visual distrubances
(headache, scotomata)
 Pulmonary edema or cyanosis
 Epigastric or RUQ pain
 Evidence of hepatic dysfunction
 Thrombocytopenia
 Intrauterine growth restriciton
(IUGR)
 Pengelolaan Preeklampsia Berat

a. Terapi Medikamentosa terhadap penyulit

• Segera masuk rumah sakit

• Tirah baring miring ke kiri secara intermiten
• Infus Ringer Laktat atau Ringer Dekstrose 5%
• Pemberian anti kejang MgSO4 sebagai pencegahan dan terapi kejang.
• Pemberian MgSO4 dibagi :
Loading dose (initial dose) : dosis awal
Maintenance dose : dosis lanjutan

b. Terapi terhadap kehamilan

a. Ekspektatif/konservatif : umur kehamilan < 37 minggu, artinya : kehamilan

dipertahankan selama mungkin sambil memberikan terapi medikamentosa

b. Aktif/agresif : umur kehamilan ≥ 37 minggu, artinya kehamilan diakhiri

setelah
mendapat terapi medikamentosa untuk stabilisasi ibu.
Preeklampsia Berat
Syarat pemberian MgSO4. 7H2O :
Refleks patella normal
Respirasi > 16 menit
Produksi urine dalam 4 jam sebelumnya > 100 cc ; 0,5 cc/kg BB/jam
Siapkan ampul Kalsium Glukonat 10% dalam 10 cc

Antidotum : Bila timbul gejala dan tanda intoksikasi MgSO4. 7H2O ,

maka diberikan injeksi Kalsium Glukonat 10% dalam 10 cc dalam 3
menit

Tanda-tanda keracunan : kelemahan otot, hipotensi, refleks

fisiologis
menurun, fungsi jantung terganggu, depresi SSP,
kelumpuhan dan selanjutnya dapat menyebabkan kematian karena
kelumpuhan otot-otot pernapasan
141. PERDARAHAN POST PARTUM
• Kehilangan darah > 500 mL setelah persalinan pervaginam
ATONIA UTERI
• Kegagalan serabut-serabut otot miometrium uterus untuk
berkontraksi dan memendek
• Biasa terjadi segera setelah bayi lahir hingga 4 jam setelah
persalinan.
• Faktor resiko : overdistensi uterus (gemeli, makrosomia,
polihidramnion, paritas tinggi), umur terlalu muda/tua, multipara
dengan jarak kelahiran pendek, partus lama, malnutrisi,
penanganan salah dalam melahirkan plasenta
• Gejala :
 Kontraksi uterus lemah/tidak berkontraksi, lunak
 Perdarahan per vaginam warna merah tua
 Fundus uteri tinggi
 Tanda-tanda syok
• Pencegahan : manajemen aktif kala III dengan oksitosin injeksi
10U IM
 142. PREGNANCY AND MALIGNANCY
• Symptoms :abd.pain, distention, nausea and vomiting, constipation,
rectal bleeding
• Diagnosis: DRE, tests for occult blood, sigmoidoscopy, colonoscopy
• Management: follow the same guidelines as for nonpregnant, when
there is no evidence for metastase  surgery
• During the first half of pregnancy, hysterectomy is not necessary in
order to perform colon or rectal resection  therapeutic abortion is
not mandated
• During later pregnancy, delaying therapy to allow fetal maturation is
considered.
• Vaginal delivery is usually permitted if obstetrical conditions are
favorable, but rectal lesions below the pelvic brim may cause
dystocia
• The prognosis is similar with nonpregnant.

Williams Obstetrics 21st ed.

Challenges to diagnosing colorectal cancer during pregnancy
VOL 55: SEPTEMBER SEPTEMBRE 2009 Canadian Family Physician Le Médecin de famille canadien
Challenges to diagnosing colorectal cancer during pregnancy
VOL 55: SEPTEMBER SEPTEMBRE 2009 Canadian Family Physician Le Médecin de famille canadien
 Colorectalcancer in Pregnancy
 In patients in the 2nd and 3rd trimesters of their
pregnancy, they should be allowed to proceed to a full
term pregnancy with vaginal/c-section delivery without
interference or delay in their treatment.
 In cancers discovered during the1st trimester of
pregnancy, treatment may either be delayed to the 2nd
trimester or termination of the pregnancy should be
considered.
 In this setting, the patient’s willingness to keep the
pregnancy plays a major role in the treatment decision.

Colon Cancer during Pregnancy Pan Arab Journal of Oncology | vol 4; issue 2 | June 2011 22
143. DIABETES DALAM KEHAMILAN
Diabetes in pregnancy

Pre-existing diabetes Gestational diabetes

IDDM NIDDM
(Type1) (Type2)
Pre-existing diabetes True GDM

Diabetes pragestasional atau overt diabetes atau preexisting : ibu hamil yang sudah
diketahui mengidap diabetes sebelum kehamilan
 Riwayat kadar gula tinggi dengan glukouri atau ketoasidosis
 Kadar gula sewaktu ˃ 200 mg / dl dengan gejala trias (polidipsi, poliuri dan berat
badan turun yang tidak bisa dijelaskan )
 Kadar gula puasa ˃ 125 mg/dl
 Tergantung Insulin
Diabetes gestasional : Adanya intoleransi karbohidrat dengan derajat bervariasi yang
terjadi atau diketahui pertama kali pada saat kehamilan tanpa memandang apakah insulin
dipergunakan atau tidak dalam penanganannya.
Maternal hyperglycemia
|
Fetal hyperglycemia
|
Fetal pancreatic beta-cell
hyperplasia
|
Fetal hyperinsulinaemia
|
Macrosomia,organomegaly,
polycythaemia, hypoglycemia, RDS
Complications of pregnancy in Pre-existing DM
Maternal: Fetal:
Increase insulin requirment Congenital abnormalities
Hypoglycemia Increased neonatal and perinatal mortality
Infection Macrosomia
Ketoacidosis Late stillbirth
Deterioration in retinopathy’ Neonatal hypoglycemia
Increased proteinuria+edema Polycythemia
Miscarriage jaundice
Polyhydramnion
Shoulder dystocia
Preeclampsia
Increased caesarean rate
 Pre-existing Diabetes
 Management Aim: Achieve maternal near normoglycemic
level to prevent adverse perinatal outcomes
 Low-carbohydrate diet , high fibre with caloric restriction
 Frequent small snacks may be needed between meals
 Avoid starvation
 For Type 2 DM patients, to stop oral hypoglycemic agents and
change to insulin
 Oral Hypoglicemic  teratogenic in animal studies esp first
generation sulfonyureas
 3 pre-meal short acting insulin (actrapid) +/- intermediate-
acting insulin (protophane) as it allows maximum flexibility
 Target blood glucose:
 fasting < 5mmol/L
 2 hr <7 mmol/L
144. ANALGESICS IN PREGNANCY
• 2 main categories : non-opioid (acetaminophen, aspirin,
NSAIDs) and opioid (morphine, codeine, meperidine)
• Acetaminophen: demonstrated efficacy and apparent
safety in all stages of pregnancy in standard therapeutic
doses.
• Aspirin: has potential risks  inhibits platelet function
and can contibute to maternal and fetal bleeding. But
overall low dose aspirin is relatively safe.
Analgesics in Pregnancy
 NSAIDs: short-term use of NSAIDs in late pregnancy is
associated with a substantial increase risk of premature
ductal closure.
 Opioids: no congenital anomalies. Chronic maternal
ingestion is associated with neonatal withdrawal
syndrome, even with therapeutic doses in nonaddicted
mothers, especially in late pregancy.
 Analgesics in Pregnancy
Recommendations :
Medications used in therapeutic doses for acute and chronic pain appear to
be relatively safe in pregnancy.
To minimize fetal risk, initiate drug interventions at the lowest effective
dose, especially in late pregnancy, and select analgesics only after careful
review of a woman’s medical or medication history.
Women should avoid using NSAIDs after 30 weeks’ gestation, owing to the
possibility of antiplatelet or prolonged bleeding effects.
Opioids should also be used with caution, especially in higher doses in late
pregnancy  observed carefully for any signs of withdrawal (neonatal
abstinence syndrome).
Paracetamol as first-line treatment of fever and pain during pregnancy.

Analgesics and pain relief in pregnancy and breastfeeding | VOLUME 34 | NUMBER 1 | FEBRUARY 2011 www.australianprescriber.com
Williams Obstetrics 21st ed.
Treating pain during pregnancy VOL 56: JANUARY JANVIER 2010 Canadian Family Physician Le Médecin de famille canadien
 145. TUMOR JINAK VULVOVAGINAL-
Bartholin’s Duct Cyst
 Bartholin’s gland :glands deep in the perineum;
Located at the entrance of the vagina at 5
o’clock and 7 o’clock; not palpable; Its duct is
approximately 2 cm long, and open in a groove
between the hymen and labia minora in the
posterior lateral wall of the vagina
 Most common large cyst of the vulva
 Caused by obstruction of the duct secondary to
nonspecific inflammation or trauma.
 Mostly are asymptomatic, swelling of the labia.
If infected pus, painfull, fever.
 Treatment not necessary in women less than
40 unless infected or symptomatic
 Treatment of choice of symptomatic or infected
cases is “marsupialization”.
 In women older than 40, biopsy is performed
to exclude adenocarcinoma of Bartholin’s gland
Treatment
• Marsupialization is the surgical technique of cutting a slit into
a cyst and suturing the edges of the slit to form a continuous
surface from the exterior surface to the interior of the cyst 
the cyst remains open and drain freely.
• Used to treat a cyst when a single draining would not be
effective and complete removal of the surrounding structure
would not be desirable.
Carcinoma Vulva Malignant invasive growth in the vulva. Symptoms :A lump or
ulceration in the vulva, associated with itching, irritation, local
bleeding, discharge, dyspareunia, pain
Gartner cyst Vaginal cyst develop from gartner’s duct. The cyst: soliter,
unilateral, usually located in the anterolateral wall of the proximal
third of the vagina. Symptoms : asymptomatic, soft lump in the
vaginal wall or protruding from the vagina, discomfort during
sex/dyspareunia
Polip Abnormal growth of tissue projecting from a mucous membrane.
Vaginal polyp :develop inside the vagina. Asymptomatic, may cause
discomfort or pain
Papilloma A benign epithelial tumor growing exophytically (outwardly
projecting) in finger-like fronds
 146. PREGNANCY TEST
• Human chorionic gonadotropin (hCG) is a glycopeptide hormone
produced by the placenta during pregnancy.
• Usually, concentration of hCG in urine is at least 25 mIU/ml as
early as 7th to 10th days after conception.
• The concentration increases steadily and reaches its maximum
between 8th and 11th weeks of pregnancy.
• First morning urine usually contains the highest concentration of
hCG and is therefore the best sample when performing the urine
test. However, randomly collected urine specimens may be used.
Causes of Invalid Results :
• The directions may not have been followed correctly.
• Inadequate amount of sample has been exposed to the test
system.
• The test may have deteriorated.
 Limitations of the Procedure
 Besides pregnancy, elevated concentrations of hCG may be found in patients
with both gestational and non-gestational trophoblastic diseases. These
conditions should be ruled out in the interpretation of hCG levels to establish a
diagnosis of pregnancy.
 A low incidence of false results can occur. Consult with a physician if
unexpected or inconsistent results.
 A normal pregnancy cannot be distinguished from an ectopic pregnancy based
on hCG levels alone.
 A spontaneous miscarriage may cause confusion in interpreting the test results.
 A definitive diagnosis should not be based on the results of a single test, but
should only be made by the physician after all clinical and laboratory findings
have been evaluated.
 A negative result from a specimen collected from a woman in very early
pregnancy may be due to an unusually low concentration of hCG. In such
cases, the test should be repeated on a fresh specimen obtained
approximately two days later.
 A urine sample may be too diluted and thus may not contain a representative
concentration of hCG. If a negative result is obtained with a urine specimen
and pregnancy is still suspected, obtain a first morning urine specimen and re-
test.
147. TINGGI FUNDUS dan USIA GESTASI
 148. RUBELLA
INFECTION
 “ German Measles”:
Maculopapular rash illness with
fever caused by rubella virus
 Diagnosis :
 A 4x rise in rubella IgG antibody
titre between acute and
convalesence serum spesimen.
 A positive serologic test for
rubella-specific IgM antibody
 A positive rubella culture
(isolation of rubella virus in a
clinical specimen from the
patient).

THELANCET• Vol 363 • April 3, 2004 •www.thelancet.com

 Rubella Infection
• IgG is indicative of infection in the past - it takes some time to be
produced by the body. Therefore IgG POSITIVE means previous
infection or immunisation, and usually adequate protection against
getting the disease.
• IgM indicates current or very recent infection; IgM NEGATIVE means
that the patient does not have a new infection. IgM POSITIVE usually
means a new or recent infection with the Rubella virus, although in rare
cases IgM may persist for years after a previous infection or
immunisation.

Manual for the laboratory diagnosis of measles and rubella virus infection - Second edition
149. HIPERTENSI DALAM KEHAMILAN
Hipertensi Kronik
 Ditemukannya desakan darah ≥ 140/ 90 mmHg,
sebelum kehamilan atau sebelum kehamilan 20
minggu dan tidak menghilang setelah 12 minggu
pasca persalinan.
 Dibagi menjadi :
1 Risiko rendah : hipertensi ringan tanpa disertai
kerusakan organ
2 Risiko tinggi : hipertensi berat atau hipertensi ringan
disertai dengan perubahan patologis, klinis maupun
biologis, sebagai tanda kerusakan organ.
Diagnosis
Kriteria risiko tinggi pada hipertensi kronik dalam
kehamilan
 Hipertensi berat :
 desakan sistolik ≥ 160 mmHg dan / atau
 desakan diastolic ≥ 110 mmHg, sebelum 20 minggu kehamilan
 Hipertensi ringan < 20 minggu kehamilan dengan
 pernah preeklamsi
 kardiomiopati
 umur ibu > 40 tahun
 hipertensi ≥ 4 tahun
 adanya kelainan ginjal
 adanya diabetes mellitus (klas B – klas F)
 meminum obat anti hipertensi sebelum hamil
 Hipertensi Kronik Pengobatan Medikamentosa :
Tujuan pengobatan hipertensi kronik
dalam kehamilan :
• Menekan risiko pada ibu terhadap
kenaikan desakan darah
• Menghindari pemberian obat-obat
yang membahayakan janin
Pemeriksaan Kesejahteraan
Janin :
• Ultrasonografi :
Hipertensi kronik dalam
kehamilan dengan penyulit
kardiovaskuler atau penyakit
ginjal perlu mendapat perhatian
khusus.
• CTG
 Indikasi pemberian
antihipertensi adalah :
Risiko rendah hipertensi :
Ibu sehat dengan desakan
diastolik menetap ≥ 100 mmHg
Dengan disfungsi organ dan
desakan diastolik ≥ 90 mmHg
Obat antihipertensi :
 1) Pilihan pertama :
Methyldopa : 0,5 – 3,0 g/hari,
dibagi dalam 2-3 dosis.
 2) Pilihan kedua : Nifedipine :
30 – 120 g/hari, dalam slow-
release tablet (Nifedipine
harus diberikan per oral)
 Pengelolaan terhadap Kehamilannya
1 Sikap terhadap kehamilannya pada hipertensi kronik
ringan : konservatif yaitu dilahirkan sedapat mungkin
pervaginam pada kehamilan aterm
2 Sikap terhadap kehamilan pada hipertensi kronik berat :
Aktif, yaitu segera kehamilan diakhiri (diterminasi)
3 Anestesi : regional anestesi.

Konsensus POGI, Hipertensi dalam Kehamilan

150. Hiperemesis Gravidarum
 Definisi, keluhan mual,muntah pada ibu hamil yang
berat hingga mengganggu aktivitas sehari-hari.
 Biasanya mulai setelah minggu ke-6 dan baik dengan
sendirinya sekitar minggu ke-12
 Etiologi : Kemungkinan kadar BhCG yang tinggi atau
faktor psikologik
 Predisposisi :primigravida, mola hidatidosa dan
kehamilan ganda.
 Akibat mual muntah  dehidrasi  elektrolit
berkurang, hemokonsentrasi, aseton darah
meningkat  kerusakan liver
Grade
 Tingkat 1 :
lemah,napsu makan↓, BB↓,nyeri epigastrium,
nadi↑,turgor kulit berkurang,TD sistolik↓, lidah kering,
mata cekung.
 Tingkat 2 :
apatis, nadi cepat dan kecil, lidah kering dan kotor, mata
sedikit ikterik, kadang suhu sedikit ↑, oliguria, aseton
tercium dalam hawa pernafasan.
 Tingkat 3 :
KU lebih lemah lagi, muntah-muntah berhenti, kesadaran
menurun dari somnolen sampai koma, nadi lebih cepat,
TD lebih turun. Komplikasi fatal ensefalopati Wernicke :
nystagmus, diplopia, perubahan mental.Ikterik
 Hiperemesis Gravidarum
Diagnosis :
 Gejala : muntah hebat,
haus, dehidrasi, BB turun,
keadaan umum turun,
kenaikan suhu, ikterus,
gangguan serebral
(kesadaran menurun,
delirium)
 Lab. : proteinuri, ketonuri,
urobilinogen (+), porphyrin
(+), silinder (+) dalam
urine
Obstetri Patologi FK Unpad
Tatalaksana :
 Edukasi tentang kehamilan
 Makan porsi kecil tapi sering
 Bangun pagi : makan ditempat tidur dengan
roti atau biskuit dengan teh hangat.
 Makanan berminyak dan berbau dihindari,
diusahakan tinggi glukosa
 Berikan sedativa seperti phenobarbital dan
vitamin B complex
 Terkadang diperlukan terapi psikologik
 Jika dirawat di RS, berikan rehidrasi parenteral
glukosa 5% dalam NaCl sebanyak 2-3 liter/24
jam
 Antasida jika ada keluhan gastritis dan kontrol
asam lambung
 Jika kesadaran baik pasien tidak perlu
dipuasakan
Emesis Gravidarum Nausea and vomiting of pregnancy, “morning sickness”,
usually present in early hours of the morning and reduce as
the day progress
Ketoasidosis Diabetik Complication of diabetes mellitus. Nausea, vomiting, thirst,
excessive urine production, abdominal pain, “kussmaul
respiration”
Dismenore Pain during menstruation that interferes with daily
activities. “menstrual pain”
Gastritis Inflammation of the lining of the stomach. Symptoms:loss of
appetite, nausea, vomiting, pain in the upper abdomen
151. PERDARAHAN POST PARTUM
• Kehilangan darah > 500 mL setelah persalinan pervaginam
• Penanganan awal :
Minta bantuan, periksa seksama KU ibu & td vital; ABC :
 Jaga jalan napas, berbaring miring kiri, beri O2 5-6
L/mnt
 Infus 2 buah dengan kanula jarum besar nomor 16
sambil diambil contoh darah untuk cross darah
 Berikan paling sedikit 2000 cc cairan dalam 1 jam
pertama.
 Setelah kehilangan cairan terkoreksi berikan infus
rumatan 500-1000 cc per-6-8 jam
 Kateterisasi, ukur urin
 Pantau tanda-tanda vital tiap 5’  15’  30’ 1 jam
• Penanganan khusus :
 Identifikasi dan atasi penyebab syok
 Dalam obstetri  syok ec perdarahan
 Diagnosis – Apa penyebab?
 Nilai fundus

 Periksa saluran genitalia bawah

 Eksplorasi uterus
Sisa plasenta
 Ruptur uterus

 Inversio uterus

 Nilai faktor perdarahan

152. TUMOR JINAK ORGAN REPRODUKSI
MYOMA/UTERINE OVARIAN CYST
FIBROID
 Common among reproductive age  May develop at any time
 Associated with female hormons  Mostly asymptomatic
and drugs or herbs containing  Abdominal swelling (if large)
estrogen trace
 Severe pain if ruptured or torsion
 Mostly asymptomatic
 Urinary symptoms, rectal
 Irreguler enlargement of uterus symptoms, bloatedness
 Hypermenorrhea/metrorrhagia/d
ysmenorrhea
 Pain if there’s torsion or
degeneration
 Urinary symptoms, rectal
symptoms, backache, bloatedness

http://www.sgih.com.sg/technology-Introduction%20Fibroid%20&%20Cyst.pdf
KISTA OVARIUM
 Kista berarti kantung yang
berisi cairan. Kista ovarium
(atau kista indung telur)
berarti kantung berisi cairan,
normalnya berukuran kecil,
yang terletak di indung telur
(ovarium).
 Kista indung telur dapat
terbentuk kapan saja, pada
masa pubertas sampai
menopause, juga selama
masa kehamilan.
Kista Ovarium
 Etiologi : beberapa teori
menyebutkan adanya
gangguan dalam pembentukan
estrogen dan dalam
mekanisme umpan balik
ovarium-hipotalamus; gagalnya
sel telur (folikel) untuk
berovulasi.
 Terdiri dari :
 Kista Fungsional / Normal
 Kista Non-Fungsional
Manifestasi Klinis :
1. Sering tanpa gejala.
2. Nyeri saat menstruasi.
3. Nyeri pada saat berhubungan
badan.
4. Nyeri pada punggung terkadang
menjalar sampai ke kaki.
5. Terkadang disertai nyeri saat
buang air kecil dan/atau buang
air besar.
6. Terkadang dapat juga siklus
menstruasi tidak teratur
7. Perut terasa penuh, berat,
kembung
8. Tekanan pada dubur dan
kandung kemih (sulit BAK)
Kista Ovarium-Penegakan
Diagnosis
 Pemeriksaan dengan ultrasonografi atau USG (abdomen
atau transvaginal), kolposkopi screening, dan
pemeriksaan darah (tumor marker atau petanda
tumor) bila curiga ganas.
 Tatalaksana : Observasi atau Operasi (bila membesar)
153. ABORTUS
Definisi :
 Perdarahan dari uterus yang disertai dengan keluarnya
sebagian atau seluruh hasil konsepsi pada usia kehamilan
< 20-24 minggu dan atau Berat janin < 500gr
Patofisiologi :
 Pada awal abortus terjadi perdarahan dalam desidua
basalis + nekrosis jaringan sekitarnya  hasil konsepsi
terlepas sebagian atau seluruhnya (benda asing dalam
uterus)  uterus berkontraksi untuk mengeluarkannya.
 DERAJAT ABORTUS

Diagnosis Perdarahan Serviks Besar uterus Gejala lain

Abortus Sedikit  Tertutup Sesuai usia · Pt positif

iminens sedang Lunak kehamilan · Kram ringan
· Uterus lunak

Abortus Sedang  Terbuka Sesuai atau · Kram sedang/kuat

insipiens banyak Lunak lebih kecil · Uterus lunak

Abortus Sedikit  Terbuka  usia •Kram kuat

inkomplit banyak Lunak kehamilan . Keluar jaringan
•Uterus lunak

Abortus Sedikit  Tertutup  usia · Sedikit/tanpa kram

komplit tidak ada Lunak kehamilan · Massa kehamilan (+/-)
· Uterus agak kenyal
 Abortus Inkompletus
 Pengeluaran sebagian hasil konsepsi pada kehamilan < 20
minggu, dengan sisa yang tertinggal dalam uterus.
Diagnosis :
 Gejala :Pengeluaran jaringan, perdarahan berlangsung terus,
cervix terbuka dan kontraksi (+)
 Kanalis servikalis terbuka, jaringan dapat teraba dalam kavum
uteri/ menonjol dari OUE, perdarahan bisa banyak sekali, tak
akan berhenti sebelum sisa konsepsi dikeluarkan  syok.
Terapi
 Penanganan syok  infus NaCl/RL, transfusi bila perlu
 Pembersihan sisa konsepsi  Kuretase atau digital

Obstetri Patologi FK Unpad

 154. KELAINAN TELUR
Mola Hidatidosa : Kehamilan abnormal dimana hampir
seluruh villi chorialis degenerasi hidropik; kelainan dalam
proses fertilisasi
“hamil anggur”
2 tipe :
 Komplit : tidak ada janin/bagian janin
 Partial : ada janin/bagian janin

Obstetri Patologi Buku Ajar FK Unpad

Mola Hidatidosa
Gejala Diagnosis :
 Amenorrhea  B-hCG tinggi dalam darah dan
urin
 Perdarahan (banyak/sedikit) 
anemia  Percobaan sonde : masuk
 Rahim lebih besar dari usia mudah ke cavum uteri, tanpa
kehamilan tahanan
 Lahirnya gelembung-
 Hyperemesis
gelembung mola
 Dapat disertai
 USG : gambaran badai
preeklampsia/eklampsia;
hipertiroid salju/snowstorm
 Tidak ada tanda janin :
ballotement (-), DJJ (-)
Mola Hidatidosa
Tatalaksana :
• Perhatikan keadaan umum ibu
• Evakuasi jaringan : dengan vakum kuret, diberikan
oxytocin sebelumnya  harus yakin bersih
• Bila fungsi reproduksi cukup : dapat dianjurkan
histerektomi
• Follow up rutin : untuk evaluasi kemungkinan menjadi
choriocarcinoma
Abortus Inkomplit Pengeluaran sebagian hasil Kanalis servikalis terbuka,
konsepsi pada kehamilan < 20 teraba jaringan, perdarahan
minggu, dengan sisa yang sedang s/d banyak  syok
tertinggal dalam uterus.

Hiperplasia Endometrium Endometrium tumbuh secara Perdarahan uterus abnormal.

berlebihan. Bersifat jinak. Diagnosis: biopsi kuretase
Blighted Ovum An anembryonic gestation. A USG: a normal-appearing
fertilized egg attaches itself to gestational sac but the
the uterine wall, but the embryo absence of an embryo
does not develop  miscarriage
Missed Abortion Kematian janin < 20 Mg, tapi Diawali gejala abortus
tidak dikeluarkan selama  8 Mg. immines lalu menghilang
spontan, gejala kehamilan
menghilang, uterus mengecil,
tes kehamilan (-)
155. KANKER GINEKOLOGI
Kanker Serviks
 Neoplasm of the cervix
 Cells change from normal to
pre-cancer (dysplasia) and
then to cancer
 Incidence : 40-60 years old
Risk Factors :
Human papillomavirus
infection (HPV) – Primary
factor - 50% are caused by HPV
16 AND 18
Multiple sexual partner
Smoking
History of STD
Young age on first sexual
intercourse
Oral contraceptives
Multiple pregnancies
Low socioeconomic status
Family history
 Kanker Serviks Diagnosis
Signs and Symptoms • Cervical Cytology (Pap Test)
 Vaginal bleeding • Colposcopy
 Menstrual bleeding is longer • Cervical Biopsy
and heavier than usual
 Bleeding after menopause or
increased vaginal discharge
 Bleeding following intercourse
(post coital bleeding)
 Pain during intercourse
 Fluor albus
 Mass on the cervix, bleeds
easily

Gynecology Illustrated.; http://www.aafp.org

http://www.epgonline.org/images/cervarix/926_1.gif
Biopsi Pengambilan jarigan tubuh untuk pemeriksaan laboratorium.
Diagnosis pasti suatu keganasan.
Kolposkopi Pemeriksaan untuk melihat permukaan serviks dengan memasukkan
“teropong” bernama kolposkop je dalam vagina. Menggunakan
mikroskop sehingga dapat memperbesar 10-40 kali dari normal 
mengidentifikasi daerah permukaan serviks yang abnormal
DNA HPV Suatu pemeriksaan untuk memeriksa DNA dari Human
papillomavirus tertentu
Sistoskopi Pemeriksaan untuk melihat kelainan pada saluran kemih
156. PERDARAHAN POST PARTUM
Kehilangan darah > 500 mL setelah persalinan pervaginam
Inversio Uteri
 Uterus terputar balik
 2 jenis :
 Complete : bila fundus uteri terdapat
dalam vagina dengan selaput lendirnya
berada di bagian luar
 Incomplete : bila fundus hanya menekuk
ke dalam dan tidak keluar ostium uteri
 Bila uterus yang berputar balik keluar dari
vulva  inversio prolaps
 Sebab :
 Tonus otot rahim lemah
 Tekanan/tarikan pada fundus (tekanan
intrabadominal, tekanan dengan tangan,
tarikan pada tali pusat)
 Kanalis servikalis yang longgar
Inversio Uteri
Gejala : Terapi :
 Shock  Reposisi dalam anestesi
 Fundus uteri sama setelah shock teratasi. Bila
sekali tidak teraba plasenta belum lepas 
atau teraba lekukan plasenta jangan dilepaskan
pada fundus dulu sebelum uterus
 Kadang tampak
direposisi karena dapat
sebuah massa yang menimbulkan perdarahan
merah di luar vulva  banyak
fundus yang terbalik;  Reposisi dapat dilakukan
atau teraba massa secara manual atau operasi
dalam vagina
 Perdarahan
157. KONTRASEPSI DARURAT
Emergency Contraception
 Emergency contraception (EC), or emergency postcoital
contraception, are birth control measures that, if taken after
sexual intercourse, may prevent pregnancy.
 Forms of EC include:
 Emergency contraceptive pills (ECPs)—sometimes simply referred to as
emergency contraceptives (ECs) or the "morning-after pill"—are drugs
intended to disrupt ovulation or fertilization, which are steps necessary
for pregnancy (contraceptives).
 Intrauterine devices (IUDs)—usually used as a primary contraceptive
method, but sometimes used as emergency contraception.
EC-Pills
 There are 3 types of Emergency Contraceptive Pills
(ECP): combined ECPs containing both estrogen and progestin, prog
estin‐only ECPs, and ECPs containing an antiprogestin (either mifep
ristone or ulipristal acetate).
 The major mechanism is inhibition or delay of ovulation. Other
mechanisms include alteration of the endometrium, sperm
penetration, and tubal motility. Established pregnancies are not
harmed.
 Progestin‐only ECPs have now largely replaced the older combined
ECPs because they are more effective and cause fewer side effects.
 ECPs may be initiated sooner than the morning after—
immediately after unprotected intercourse—or later—
for at least 120 hours after unprotected intercourse.
 ECPs are highly effective and decrease the risk of pregnancy by 75
percent
 EC-Copper Bearing IUD
 Implantation occurs 6‐12 days following ovulation.
Therefore, copper IUDs can be inserted up to 5 days after ovulation to
prevent pregnancy.
 When the IUD was inserted up to 5 days after unprotected
intercourse, the failure rate was 1 percent. A secondary advantage is
that this method also puts in place an effective 5- to 10-year method
of contraception.
 Latest WHO guidelines allow IUDs to be inserted up to day 12 of the cy
cle with no restrictions and at any other time in the cycle if it is reason
ably certain that she is not pregnant
EC
 ECPs prevent pregnancy primarily by delaying or inhibiting
ovulation and inhibiting fertilization
 The primary mechanism of action of copper-releasing
intrauterine devices (IUDs) as emergency contraceptives is
to prevent fertilization because of copper toxicity to sperm
and ova
 Its very high effectiveness implies that emergency insertion
of a copper IUD must be able to prevent pregnancy after
fertilization
158. KONTRASEPSI HORMONAL
Mekanisme Kerja :
• ESTROGEN :
1. MENCEGAH OVULASI (MENEKAN FSH)
2. MENCEGAH IMPLANTASI (PENGARUH PADA ENDOMETRIUM)
• PROGESTERON
1. MENCEGAH OVULASI ( MENEKAN LH)
2. MENCEGAH SPERMA MASUK KE CERVIX (PERUBAHAN LENDIR
CERVIX)
3. MENCEGAH IMPLANTASI (ENDOMETRIUM)
• Pil KB berisi hormon (bisa kombinasi estrogen atau progesteron atau
progesteron saja).
• Pil kontrasepsi pada dasarnya memiliki tingkat efektivitas tinggi untuk
mencegah kehamilan (pil kombinasi memiliki kegagalan 1 dalam 1000).
• Jadi, jika terjadi kehamilan mungkin saja cara pemakaiannya salah.
 Pil KB ada yang berjumlah 21 tablet dan ada yang 28
tablet. 7 buah pil yang beda ukuran dan warna pada pil
28 tablet isinya adalah hanya tepung (plasebo) alias tidak
memiliki efek pengobatan.
 Pada saat memakan pil plasebo inilah haid diperkirakan
akan muncul atau terjadi. Tujuan disediakan pil tersebut
adalah supaya tidak repot dan tidak lupa, tinggal
menyambung dengan pil berikutnya tanpa perlu berpikir
dan mengingat.
 Sedangkan pil 21 tablet, setelah pil terakhir dimakan, ada
interval 7 hari libur/tidak makan pil sebelum memulai
blister pil berikutnya. Saat interval inilah diperkirakan
haid akan muncul, yang biasanya timbul 2-3 hari setelah
pil habis alias masa tidak subur.
Aturan Minum :
 Biasanya dimulai di hari ke 1 atau ke 5 haid.
 Minum pil KB sebaiknya diminum pada waktu yang sama
sehingga tidak kelupaan. Tidak harus jam yang sama selama tidak
lebih dari 12 jam.
 Jika lupa 1 hari (24 jam) maka masih dapat diminum 2 tablet
langsung pada saat ingat.
 Namun jika lupa lebih dari 1 hari bisa saja dilanjutkan namun
efektifitas berkurang sehingga perlu dikombinasikan dengan
kontrasepsi kondom saat berhubungan intim.
 Jika mengkonsumsi pil KB 21 tablet dan lupa melanjutkan pada
blister yang baru maka mens tidak akan terjadi. Hal ini karena
efek dari lanjutkan hormon estrogen dan progesteron pada pil KB
tersebut. Bila hentikan pil KB maka dalam beberapa hari mens
akan terjadi.
 Bila lupa minum 1 butir pil hormonal (berwarna
kuning) maka harus minum 2 butir pil hormonal
segera setelah Anda mengingatnya
 Apabila lupa meminum 2 butir atau lebih pil
hormonal (berwarna kuning), maka dalam 7 hari
gunakan kondom apabila melakukan hubungan
seksual atau hindari hubungan seksual selama 7 hari
 Apabila lupa meminum 1 butir pil pengingat
(berwarna putih) maka buang pil pengingat yang
terlupakan
 Bila lupa minum pil dalam dua hari, segera minum
dua pil sekaligus ketika ingat.
 159. INFEKSI DALAM KEHAMILAN-
Typhoid Fever
 An infectious feverish disease caused by the bacterium Salmonella typhi(Salmonella
enterica Serovar Typhi ) and less commonly by Salmonella paratyphi.
 Symptoms :
 No symptoms - if only a mild exposure; some people become "carriers" of typhoid.
 Poor appetite,
 Headaches,
 Generalized aches and pains; Lethargy,
 Diarrhea,
 Have a sustained fever as high as 103 to 104 degrees Fahrenheit (39 to 40 degrees
Celsius) in 5-7 days
 Chest congestion develops in many patients, and abdominal pain and discomfort
are common,
 Constipation, mild vomiting, slow heartbeat.
1
Using Antibiotics During Pregnancy
A few guidelines should be followed before prescribing an
antibiotic to a pregnant patient, include:
• Only use antibiotics if no other treatment option will suffice.
• Avoid prescribing antibiotics during the first trimester when
possible.
• Choose a safe medication (typically an older antibiotic tested
on pregnant women).
• Choose single prescriptions over polypharmacy when possible.
• Dose at the lowest possible amount proven effective.
• Advise patients not to use over the counter medications
during antibiotic treatment.
Some of the antibiotics that may be prescribed safely
during pregnancy include:
• Amoxicillin
• Ampicillin
• Clindamycin
• Erythromycin
• Penicillin
• Gentamicin
• Ampicillin-Sulbactam
• Cefoxitin
• Cefotetan
• Cefazolin
160. HIPERTENSI DALAM KEHAMILAN
Preeklampsia
Hipertensi Gestasional
Didapatkan desakan darah ≥ 140/90 mmHg untuk pertama kalinya pada
kehamilan, tidak disertai dengan proteinuria dan desakan darah kembali
normal < 12 minggu pasca persalinan
Preeklams
Kriteria minimum :Desakan darah ≥ 140/ 90 mmHg setelah umur kehamilan
20 minggu, disertei dengan proteinuria ≥ 300 mg/24 jam atau dipstick ≥ 1
Faktor Resiko yang meningkatkan Preeklampsia :Primigravida, umur terlalu
muda/tua, riwayat pernah preeklampsia, hipertensi kronis, penyakit ginjal,
obesitas, diabetes, antiphospholipid antibodies, kehamilan ganda.
Faktor yang dapat mengurangi : seks oral, merokok
Pencegahan : upaya untuk mencegah terjadinya preeklampsia pada wanita
hamil yang mempunyai resiko terjadinya preeklampsia. Dapat dengan medikal
dan non-medikal
Preeklampsia
Pencegahan Medikal :
Diuretik : tidak terbukti mencegah terjadinya preeklamsi bahkan
memperberat hipovolemia
Anti hipertensi tidak terbukti mencegah terjadinya preeklamsi
Kalsium : 1500 – 2000 mg/ hari, dapat dipakai sebagai suplemen pada risiko
tinggi terjadinya preeklamsi, meskipun belum terbukti bermanfaat untuk
mencegah preeklamsi.
 Zinc : 200 mg/hari
 Magnesium : 365 mg/hari
 Obat anti thrombotik :
 Aspirin dosis rendah : rata2 dibawah 100 mg/hari, tidak terbukti
mencegah preeklamsi.
 Dipyridamole

• Obat2 : vitamin C, vitamin E, ßeta-carotene, CoQ10, N- Acetylcysteine,

• Asam lipoik.
 Preeklampsia
Pencegahan NonMedikal:
• Restriksi garam: tidak terbukti dapat mencegah
• Suplementasi diet yang mengandung: minyak ikan kaya
dengan asam lemak tidak jenuh (omega-3, PUFA); Antioksidan
(Vit.C, Vit.E, beta carotene, CoQ10, N-acetylcysteine, asam
lipoik); elemen logam berat (zinc, magnesium, kalsium)
• Tirah baring: tidak terbukti dapat mencegah

Catatan: pencegahan medikal merupakan evidence medicine

practice (yang sering dikerjakan), namun belum terbukti
memberikan manfaat secara EBM

Konsensus POGI, Hipertensi dalam Kehamilan

161. PERSALINAN
 1st Stage of Labor: dilatation and effacement
 The first stage of labor is referred to as the "dilating" stage.
 It is the period from the first true labor contractions to
complete dilatation of the cervix (10cm)
 The forces involved are uterine contractions.
 The first stage of labor is divided into three phases:
 (1) Latent (0-4cm)
 (2) Active (4-8cm)
 (3) Transition (8-10cm)
 2nd Stage: Birth of the Baby
 Begins when cervical dilatation is
complete and ends with birth of
the baby.
 Impending Signs:
 Bulging of the perineum.
 Dilatation of the anal orifice.
 Nausea, Irritability and
uncooperativeness.
 Complaints of severe discomfort.
 Dilatation and effacement –
complete - patient is instructed to
push with each contraction to bring
the presenting part down into the
pelvis
3rd Stage of Labor
 The period from birth of the baby through delivery of the
placenta.
 Dangerous time because of the possibility of hemorrhaging.
 Signs of the placental separation
 a. The uterus becomes globular in shape and firmer.
 b. The uterus rises in the abdomen.
 c. The umbilical cord descends three inches or more
further out of the vagina.
 d. Sudden gush of blood.
4th stage
 Period from the delivery of the placenta until the uterus
remains firm on its own.
 Uterus makes its initial readjustment to the non-pregnant
state.
 The primary goal is to prevent hemorrhage from the
uterine atony and the cervical or vaginal lacerations.
 Atony is the lack of normal muscle tone. Uterine atony is
failure of the uterus to contract.
162. KEHAMILAN EKTOPIK TERGANGGU
Kehamilan Ektopik : kehamilan yang terjadi di luar
kavum uteri, paling sering di tuba (90-95%) 
kehamilan ektopik terganggu bila telah terjadi ruptur
tuba dan memberikan gejala-gejala, antara lain :
• Nyeri perut
• Amenorrhea
• Perdarahan per vaginam (dapat juga tidak)
• Syok karena hipovolemia perdarahan (tergantung
beratnya perdarahan)
 KET
Diagnosis : Tatalaksana :
 Nyeri pada palpasi perut, oerut  Atasi Shock
tegang  Penghentian perdarahan
 Nyeri goyang portio segera  laparotomi
salpingektomi (memotong
 Urine b-hCG (+)
bagian tuba yang terganggu)
 Kuldosentesis (+) : darah pada
kavum douglas (warna merah
tua, tidak membeku setelah
diambil
 USG
 Diagnosis pasti : laparotomi

Obstetri Patologi Buku Ajar FK Unpad

163. HIPERTENSI DALAM KEHAMILAN
William’s Obstetrics,22 ed.
164. PERSALINAN dengan ALAT BANTU
• Ekstraksi cunam/forceps adalah suatu tindakan bantuan persalinan di
mana janin dilahirkan dengan suatu tarikan cunam / forceps yang
dipasang pada kepalanya
• Forceps / cunam adalah alat bantu persalinan, terbuat dari logam,
terdiri dari sepasang (2 buah) sendok yaitu sendok cunam kiri dan
sendok cunam kanan.
Indikasi :
• Prinsip : keadaan yang memerlukan pertolongan persalinan kala dua
yang dipercepat, karena jika terlambat dapat membahayakan keadaan
ibu dan / atau janin.
Indikasi ibu : preeklampsia / eklampsia, ruptura uteri membakat, penyakit
jantung, asma, dan lain-lain.
Indikasi janin : gawat janin.
Ekstraksi Forseps
Kontraindikasi :
1. Bayi prematur (karena kompresi pada tulang kepala yang belum
matang / belum memiliki kemampuan moulage yang baik dapat
menyebabkan terjadi perdarahan periventrikular.
2. Disproporsi sefalopelvik.
Syarat :
1. Janin aterm.
2. Janin harus dapat lahir pervaginam (tidak ada disproporsi)
3. Pembukaan serviks sudah lengkap.
4. Kepala janin sudah engaged.
5. Selaput ketuban sudah pecah, atau jika belum, dipecahkan.
• Bila Ekstraksi Vakum  harus ada HIS dan tenaga mengejan ibu
No. 165 Kaidah Dasar Moral
 Kaidah dasar moral terdiri atas:
1. Autonomy: pasien dapat mengambil keputusan sendiri &
dijamin kerahasiaan medisnya  dasar informed
consent & kerahasiaan medis.
2. Nonmaleficence (Do No Harm): tidak dengan sengaja
melakukan tindakan yang malah merugikan/invasif tanpa
ada hasilnya  dasar agar tidak terjadi kelalaian medis.
3. Beneficence: mengambil langkah yang bermanfaat,
untuk mencegah atau menghilangkan sakit.
4. Justice: perlakuan yang sama untuk kasus yang sama.
Beneficence
 Beneficence is action that is done for the benefit of
others. Beneficent actions can be taken to help prevent or
remove harms or to simply improve the situation of
others.
 Prevent and remove harms
 Weigh and balance possible benefits against possible risks
of an action
 Balancing of beneficence and non-maleficence : Providing
informed consent, give patients the information
necessary to understand the scope and nature of the
potential risks and benefits in order to make a decision
No. 166 Euthanasia
“Dengan sengaja tidak melakukan sesuatu untuk
memperpanjang hidup seorang pasien atau sengaja
melakukan sesuatu untuk memperpendek hidup
atau mengakhiri hidup seorang pasien, dan ini
dilakukan untuk kepentingan pasien sendiri”

• Konsep mati : Jika batang otak telah mati (brain stem

death) dapat diyakini bahwa manusia tersebut telah
mati baik secara fisik maupun sosial. Yang harus
diyakini adalah proses kematian tersebut bersifat
irreversible.
Jenis Euthanasia
 Dari cara dilaksanakan :
 Euthanasia pasif = menghentikan segala tindakan atau
pengobatan yang perlu untuk mempertahankan hidup
 Euthanasia aktif = intervensi aktif dengan tujuan untuk
mengakhiri hidup
 Aktif Langsung (Tindakan medik terarah dan diperhitungkan)
 Aktif Tidak Langsung (Tindakan medik ditujukan untuk
meringankan penderitaan namun ada risiko untuk
memperpendek atau mengakhiri hidup)
Jenis Euthanasia
 Ditinjau dari permintaan :
 Euthanasia voluntir (sukarela) = secara sadar diminta oleh
pasien secara berulang-ulang
 Euthanasia involuntir (tidak atas permintaan pasien) = pada
pasien yang tidak sadar, biasanya diminta oleh keluarga
Euthanasia dan Hukum
 Ketentuan pidana terkait euthanasia aktif dengan permintaan:
Pasal 344 KUHP:
 Barang siapa menghilangkan jiwa orang lain atas permintaan
orang itu sendiri, yang disebutnya dengan nyata & sungguh-
sungguh, dihukum penjara selama-lamanya dua belas tahun.
 Ketentuan pidana terkait euthanasia aktif/pasif tanpa
permintaan:
 Pasal 338, 340, 359 KUHP  dihukum penjara.
 Menurut KODEKI (pasal 9, bab II), dokter tidak diperbolehkan:
 Menggugurkan kandungan
 Mengakhiri hidup seseorang yang sakit meskipun menurut
pengetahuan tidak akan sembuh lagi.
No. 167 Patient Neglect
 Definisi :
"Abandoning or neglecting a patient or client under and in
need of immediate professional care, without making
reasonable arrangements for the continuation of such care,
or abandoning a professional employment by a group
practice, hospital, clinic or other health care facility, without
reasonable notice and under circumstances which seriously
impair the delivery of professional care to patients or
clients."
 Dalam hal pengalihan professional care :
 Wajib diberitahukan pada pasien
 Dokter pengganti harus kompeten dan bermutu
 Berlanjut menjadi hubungan dokter – pasien tersendiri
Sanksi Disiplin
 Dikatakan malpraktek medik jika:
 Dokter kurang menguasai ilmu pengetahuan yang sudah berlaku
umum.
 Memberikan pelayanan di bawah standar profesi (tidak lege
artis)
 Melakukan kelalaian yang berat atau pelayanan dengan tidak
hati-hati
 Melakukan tindakan medik yang bertentangan dengan hukum.
 Kelalaian tidak dianggap suatu pelanggaran hukum jika
kelalaian tidak membawa kerugian atau cedera dan orang
tersebut dapat menerimanya
 Sanksi terberat adalah sanksi pidana: KUHP pasal 304, pasal
306, pasal 350.
Sanksi Disiplin
 Pasal 53 UU No. 23/ Tahun 1992 : Tenaga kesehatan yang melakukan
kesalahan atau kelalaian dalam melaksanakan tugas profesinya,
dapat dikenakan tindakan disiplin.
 Dalam hal pertanggung jawaban atas pelayanan medis, yang mana
pihak pasien merasa dirugikan maka perlu untuk diketahui siapa
yang terkait di dalam tenaga medis tersebut.
 Pasal 1367 KUH Perdata : Seorang tidak saja bertanggungjawab
untuk kerugian yang disebabkan perbuatannya sendiri, tetapi juga
untuk kerugian yang disebabkan perbuatan orang-orang yang
menjadi tanggungannya atau disebabkan oleh barang-barang yang
berada di bawah pengawasannya.
 Jika kesalahan yang dilakukan oleh khusus dokter yang melakukan,
pihak rumah sakit yang bertanggung jawab secara umumnya dan
dokter sebagai pelaksana tindakan juga dapat dikenakan sanksi.
No. 168 Kepemilikan Rekam Medik
 RM dalam bentuk fisik adalah milik institusi kesehatan, tapi isi
rekam medis pada prinsipnya adalah milik pasien (Permenkes
tahun 1989 Pasal 9).
 Jika dokter merasa pasien perlu melihat isi RM, maka
sebaiknya didampingi dokter agar dapat dijelaskan hal-hal
yang sulit dipahami.
 Jika resume akhir telah dibuat, maka catatan inilah yang
disampaikan ke dokter lain yang akan merawat atau untuk
kepentingan lain oleh pasien.
 Berkas rekam medis hanya dapat diberikan atau dikeluarkan
dari rumah sakit (sarana kesehatan) atas perintah peradilan
(pro justitia).
Rekam Medis
 Rekam medis dapat diungkapkan dalam keadaan:
1. Memperoleh otorisasi tertulis dari pasien
2. Sesuai dengan ketentuan undang-undang
3. Untuk sarana kesehatan lain yang saat ini menangani
pasien
4. Untuk evaluasi perawatan medis
5. Untuk riset & pendidikan sesuai peraturan setempat.
No. 169 Fungsi Rekam Medik
 Sebagai alat komunikasi antara dokter dan tenaga
kesehatan lainnya
 Merupakan dasar untuk perencanaan
pengobatan/perawatan (Medis)
 Sebagai bukti tertulis atas segala pelayanan,
perkembangan penyakit dan pengobatan pasien
 Sebagai dasar analisis, studi, dan evaluasi terhadap mutu
pelayanan
Fungsi Rekam Medik (2)
 Melindungi kepentingan hukum bagi pasien, RS, dokter,
dan tenaga kesehatan lainnya
 Menyediakan data untuk keperluan penelitian dan
pendidikan
 Dasar dalam perhitungan biaya pelayanan medik
(Administrasi)
 Menjadi sumber ingatan yang harus didokumentasikan,
serta sebagai bahan pertanggungjawaban dan laporan
(Dokumentasi)
No. 170 Persetujuan Tindakan
Kedokteran
 Permenkes No. 589 tahun 1989 : Persetujuan Tindak medis
adalah persetujuan yang diberikan pasien atau keluarga atas
dasar penjelasan mengenai tindak medik yang akan dilakukan
terhadap pasien
 Permenkes No. 290 tahun 2008
 Persetujuan oleh keluarga/wali :
 Pada pasien dibawah 21 tahun
 Pasien dengan gangguan jiwa
 Pasien dalam keadaan tidak sadar/pingsan
 Atas dasar keraguan keluarga terhadap kesiapan mental
pasien, atau atas dasar alasan lainnya
No. 171 Perkiraan Waktu Kematian
(Tanatologi)
 Lebam mayat
 Mulai tampak 20-30 menit pascamati
 Lengkap & menetap setelah 8-12 jam, sebelumnya masih dapat
memucat pada penekanan dan berpindah
 Kaku mayat:
 Mulai tampak 2 jam pascamati, dimulai dari bagian luar
tubuh/otot-otot kecil (sentripetal)
 Lengkap setelah 12 jam & dipertahankan selama 12 jam, lalu
menghilang dalam urutan yang sama
 Pembusukan:
 Tampak kehijauan di perut kanan bawah 24 jam pasca mati
 Larva lalat dijumpai 36-48 jam pascamati
No. 172 Kaidah Dasar Moral
 Kaidah dasar moral terdiri atas:
1. Autonomy: pasien dapat mengambil keputusan sendiri &
dijamin kerahasiaan medisnya  dasar informed
consent & kerahasiaan medis.
2. Nonmaleficence (Do No Harm): tidak dengan sengaja
melakukan tindakan yang malah merugikan/invasif
tanpa ada hasilnya  dasar agar tidak terjadi kelalaian
medis.
3. Beneficence: mengambil langkah yang bermanfaat,
untuk mencegah atau menghilangkan sakit.
4. Justice: perlakuan yang sama untuk kasus yang sama.
N0. 173 Luka Akibat Kekerasan
 Kekerasan Benda Tumpul
Memar
 Perdarahan dalam jaringan bawah kulit akibat pecahnya
kapiler/vena;
 Dapat memberikan petunjuk tentang bentuk benda penyebab
Luka Lecet
 Cedera pada epidermis yang bersentuhan dengan benda yang
memiliki permukaan kasar atau runcing
Luka Robek
 Luka terbuka akibat trauma benda tumpul, menyebabkan kulit
teregang ke satu arah.
 Bentuk luka tidak beraturan, tepi tidak rata, jembatan jaringan
 Kekerasan Benda Setengah Tajam
 Cedera akibat benda tumpul yang memiliki tepi rata (mis.
meja, lempeng besi, gigi)
 Luka : seperti akibat benda tumpul tapi bentuknya
beraturan
 Jejas Gigit (bite-mark) : luka lecet tekan/hematom
berbentuk garis lengkung terputus-putus
 Kekerasan Benda Tajam
 Luka iris, luka tusuk, luka bacok
 Tepi dan dinding luka yang rata, berbentuk garis, tidak
terdapat jembatan jaringan, dasar luka bentuk garis atau
titik
Visum et Repertum untuk
Perlukaan
 Tujuan pemeriksaan forensik pada korban hidup : Untuk
mengetahui penyebab luka dan derajat parahnya luka
 Dalam pemberitaan disebutkan : Keadaan umum korban,
luka-luka dengan uraian letak, jenis, sifat, ukuran, serta
tindakan medik yang dilakukan, riwayat perjalanan
penyakit, dan keadaan akhir saat perawatan selesai.
 Dalam kesimpulan disebutkan : luka-luka atau cedera
yang ditemukan, jenis benda penyebab, serta derajat
perlukaan. Tidak dituliskan pendapat bagaimana
terjadinya luka dan oleh siapa.
Derajat Perlukaan
 Luka ringan :
 Tidak menimbulkan penyakit atau halangan untuk
menjalankan jabatan atau pekerjaan. (KUHP 352)
 Umumnya tanpa luka, atau dengan luka lecet atau memar
kecil di lokasi yang tidak berbahaya/tidak menurunkan
fungsi alat tubuh.
 Luka sedang : diantara luka ringan dan berat
 Luka berat (KUHP 90)
 Jatuh sakit atau mendapat luka yang tidak memberi
harapan akan sembuh sama sekali. Atau menimbulkan
bahaya maut
 Tidak mampu terus menerus untuk menjalankan tugas
jabatan atau pekerjaan
 Kehilangan salah satu panca indra
 Cacat berat
 Sakit lumpuh
 Terganggu daya pikir selama empat minggu lebih
 Gugur atau matinya kandungan seorang perempuan
174. Sebab, Cara, & Mekanisme
Kematian
 Sebab mati adalah penyakit atau cedera/luka yang
bertanggung jawab atas terjadinya kematian.
 Cara kematian adalah macam kejadian yang menimbulkan
penyebab kejadian:
 Wajar: semata-mata karena penyakit
 Tidak wajar: kematian dipercepat oleh adanya luka/cedera
(kecelakaan, bunuh diri, pembunuhan)
 Mekanisme kematian:
 Gangguan fisiologik dan atau biokimiawi yang ditimbulkan
oleh penyebab kematian sehingga seseorang tidak dapat
terus hidup.
Sebab, Cara, & Mekanisme
Kematian
 Contoh:
1. Penderita tb paru yang mengalami hemoptoe hebat &
meninggal.
 Penyebab kematian: tb paru. Mekanisme kematian: shock
akibat perdarahan paru-paru. Cara kematian wajar.
2. Autopsi lebam mayat merah gelap, paru & hati merah
gelap, ada massa putih di jantung 2x3 cm.
 Penyebab kematian: trombus putih di jantung. Mekanisme
kematian: asfiksia akibat sumbatan di jantung. Cara kematian:
wajar.
Sebab, Cara, & Mekanisme
Kematian
 Contoh:
3. Seseorang mengalami perdarahan subdural akibat
terjatuh dari sepeda motor yang mengalami slip. Selama
perawatan 4 hari tidak pernah sadar, mendapat
komplikasi pneumonia ortostatik & meninggal.
 Sebab kematian: trauma kapitis. Cara kematian: tidak wajar.
Mekanisme kematian: perdarahan subdural dengan penyulit
radang paru-paru.
Atherosklerosis
Atherosclerotic Plaque.
 Atheromatous plaques impinge on the lumen of the artery and grossly
appear white to yellow; superimposed thrombus over ulcerated plaques is
red-brown.
 Plaques vary from 0.3 to 1.5 cm in diameter but can coalesce to form larger
masses.
Infark Miokard
 Infark Miokard
 Early recognition of acute MI can be difficult, particularly when
death has occurred within a few hours after the onset of
symptoms.
 MIs less than 12 hours old are usually not apparent on gross
examination.
 If the patient died at least 2 to 3 hours after the infarct, however, it
is possible to highlight the area of necrosis by immersion of tissue
slices in a solution of triphenyltetrazolium chloride  infarct
appears as an unstained pale zone (see picture).
 By 12 to 24 hours an infarct can be identified grossly in transverse
slices as a reddish-blue area of discoloration caused by stagnated,
trapped blood.
 By 10 days to 2 weeks, it is rimmed by a hyperemic zone of highly
vascularized granulation tissue.
 Over the succeeding weeks, the injured region evolves to a fibrous
scar.

Konsensus Pengendalian dan Pencegahan Diabetes Mellitus Tipe2 di Indonesia 2011 7

Tamponade Jantung
 Clotted and liquid blood in
the pericardial cavity
No. 175-176 Asfiksia Mekanik
 Asfiksia mekanik : Mati lemas yang terjadi bila udara
pernapasan terhalang oleh berbagai kekerasan (yang
bersifat mekanik)
 Meliputi : Pembekapan, penyumbatan, pencekikan,
penjeratan, gantung diri, serta penekanan pada dada
Tanda Kematian akibat Asfiksia
 Sianosis pada bibir, ujung-ujung jari dan kuku
 Lebam mayat yang gelap dan luas
 Perbendungan pada bola mata
 Busa halus pada lubang hidung, mulut, dan saluran
pernapasan, perbendungan pada alat-alat dalam
 Bintik perdarahan (Tardieu’s spot) pada mukosa usu halus,
epikardium, subpleura visceralis
 Perbendungan sistemik maupu pulmoner dan dilatasi
jantung kanan (lorgan lebih berat, gelap, pada pengirisan
banyak mengeluarkan darah)
Kasus Gantung (Hanging)
 Bila jerat kecil dan keras : Hambatan total arteri, muka tampak
pucat, tidak terdapat peteki
 Bila Jerat lebar dan lunak : Hambatan terjadi pada saluran
pernapasan dan pada aliran vena, sehingga tampak
perbendungan pada daerah sebelah atas ikatan
 Jejas Jerat :
 Retalif lebih tinggi pada leher, lebih meninggi di bagian simpul,
kulit mencekung ke dalam sesuai dengan bahan penjerat
 Pada tepi jejas, terdapat perdarahan (resapan darah), pada
jaringan bawah kulit dan otot terdapat memar jaringan (Tanda
Intravital)
 Distribusi lebam mayat mengarah ke bawah yaitu pada kaki,
tangan, dan genitalia eksterna.
 • Tanda kekerasan di sekitar bagian muka yang
Pembekapan menonjol, serta permukaan belakang bibir
• Pada orang dengan fisik lemah atau tidak berdaya

• Benda asing/sisa benda masih terdapat dalam

Penyumbatan rongga mulut/ ada tanda penekanan benda asing
pada rongga mulut

• Tanda-tanda kekerasan pada kulit daerah leher

Pencekikan (ditimbulkan ujung jari atau kuku)
• Tulang lidah patah unilateral

• Jerat horisontal/mendatar, menimbulkan luka lecet

Penjeratan tekan melingkari leher

• Tanda asfiksia yang jelas disertai tanda-tanda

Dada tertekan penekanan pada dada (luka memar atau luka lecet)
Tanda Intravital
 Reaksi tubuh yang masih hidup terhadap trauma
 Tanda Intravital :
 Perdarahan berupa ekimosis, peteki;
 Emboli lemak atau udara (pada patah tulang dan trauma
tumpul jaringan lemak)
 Kadar laktat darah (Cerminan reaksi adrenergik)
 Reaksi radang (Edema, Ekstravasasi cairan)
No. 177 dan 179
Menentukan
Design Penelitian
Observational Study
 Cohort
 Analisa faktor risiko, dengan mengikuti kelompok yang
tidak/belum menderita penyakit dengan faktor risiko dan
tidak dengan faktor risiko.
 Keuntungan : Dapat menentukan faktor risiko terjadinya
penyakit karena bersifat longitudinal observation
 Kelemahan : Mahal, memakan waktu yang lama, drop-out
rasio yang tinggi
 Case Control
 Menganalisa faktor risiko
dengan menentukan dua
kelompok yang memiliki
perbedaan outcome
(penyakit), kemudian
dihubungkan dengan causal
attribute- nya
 Keuntungan : Membutuhkan
sumber daya, dana yang
lebih sedikit, serta waktu
yang lebih singkat. Good for
rare cases, long latent
period, ethical related cases
 Kelemahan : provide less
evidence for causal inference
 Cross-Sectional
 Descriptive, comparative, etiology or risk study
 Prevalence study
 Easy, cheap and fast
 Temporal relationship is unclear
 Difficulty in recalling past events may also contribute bias.
 Tidak tepat bila digunakan untuk menganalisis hubungan
kausal paparan dan penyakit (Hanya ada/tidaknya
hubungan)
No.178 Odds ratio
The ratio of the odds of an event occurring in one group
to the odds of it occurring in another group (probability
that the event of interest occurs to the probability that
it does not)
The odds ratio treats the two variables being compared
(paired binary data) symmetrically, and can be estimated
using some types of non-random samples.
Example : OR = 5.44 means those with the disease are
5.44 times as likely to have had the exposure compared
to those without the disease
Case-Control Study Results
Cases Controls
Exposed a b
Unexposed c d
a+c b+d
Odds ratio = (a/b)/(c/d)
= ad/bc

Simplest form of results for a case-control study. The odds ratio, or

relative odds, is the key measure of association. Because of the sampling
used, the total number of exposed subjects is not a + b, and the risk in
exposed subjects is not a/(a + b)
Odds Ratio vs Relative Risk (RR)
 RR : the risk of an event (or of developing a disease)
relative to exposure. Relative risk is a ratio of
the probability of the event occurring in the exposed
group versus a non-exposed group
 Example : RR = 5.44 means Those with the exposure
are 5.44 times as likely to develop the disease
compared to those without the exposure
Comparing Odds Ratios and Relative Risks
Outcome

Exposure Cases Controls

Exposed 70 300 370

Not Exposed 30 700 730

100 1000 1100

OR = AD/BC = 5.44 RR= A/(A+B)

C/(C+D)
= 4.41
536
Soal 178
Outcome Ya Tidak TOTAL
(Katarak (Case) (Control)
Kongenital)
Exposure (Rubella)
Ya 160 80 240

Tidak 40 120 160

TOTAL 200 200 400

OR = AD/BC = (160x120)/(80x40)
No. 180 Types of bias
1. Sample (subject selection) biases
• Selection biases occur when the groups to be compared
are different. May result in the subjects in the sample
being unrepresentative of the population
2. Measurement (detection) biases
• which include issues related to how the outcome of
interest was measured
3. Intervention (performance) biases
• which involve how the treatment itself was carried out.
Selection Bias
 Volunteer or referral bias
 People who volunteer to participate in a study (or who are referred
to it) are often different than non-volunteers/non-referrals. This bias
usually, but not always, favors the treatment group, as volunteers
tend to be more motivated and concerned about their health.
 Non-response bias
 When those who do not respond to a survey differ in important
ways from those who respond or participate. This bias can work in
either direction.
 Self-selection bias
 Arises in any situation in which individuals select themselves into
a group
 Prevalence-incidence bias
 Happens when mild or asymptomatic cases as well as fatal short
disease episodes are missed when studies are performed late in
disease process
http://www.umdnj.edu/idsweb/shared/biases.htm
 Measurement Bias
 Instrument bias. Calibration errors lead to inaccurate measurements
being recorded
 Insensitive measure bias. When the measurement tool(s) used are
not sensitive enough to detect what might be important differences
in the variable of interest.
 Expectation bias. Occurs in the absence of masking or blinding,
when observers may measuring data toward the expected
outcome.
 Recall or memory bias. If outcomes being measured require that
subjects recall past events. Often a person recalls positive events
more than negative ones.
 Attention bias. Occurs because people who are part of a study are
usually aware of their involvement, and as a result of the attention
received may give more favorable responses or perform better than
people who are unaware of the study’s intent.
 Verification or work-up bias. Associated mainly with test validation
studies. In

http://www.umdnj.edu/idsweb/shared/biases.htm
 Intervention Bias
 Contamination bias. When members of the 'control' group inadvertently
receive the treatment or are exposed to the intervention
 Co-intervention bias. When some subjects are receiving other
(unaccounted for) interventions at the same time as the study treatment.
 Timing bias(es). If an intervention is provided over a long period of time,
maturation alone could be the cause for improvement. If treatment is very
short in duration, there may not have been sufficient time for a noticeable
effect in the outcomes of interest.
 Compliance bias. When differences in subject adherence to the planned
treatment regimen or intervention affect the study outcomes.
 Withdrawal bias. When subjects who leave the study (drop-outs) differ
significantly from those that remain.
 Proficiency bias. When the interventions or treatments are not applied
equally to subjects. This may be due to skill or training differences among
personnel and/or differences in resources

http://www.umdnj.edu/idsweb/shared/biases.htm
No. 181 Confounding Bias
 Mixing of effects that occurs when a factor (confounder)
associated with the exposure of interest is also associated
with development of the disease or outcome of interest
independently of exposure.
 To be confounding, and extraneous variable must have
the following characteristics:
 It must be associated with the exposure under study in the
population studied
 It must not be an intermediate step in the casual path
between the exposure and the disease
 Con-founding can be minimized by:
(1) restriction of the confounder from the study;
(2) matching the confounding variable between groups
(3) by including it in the statistical analysis (including them
as covariates in multivariate analyses such as regression
analysis)

The best available defense against the possibility of spurious results due to
confounding is often to dispense with efforts at stratification and instead
conduct a randomized study of a sufficiently large sample taken as a whole,
such that all potential confounding variables (known and unknown) will be
distributed by chance across all study groups and hence will be uncorrelated
with the binary variable for inclusion/exclusion in any group
No. 182 Fungsi Dasar Keluarga
 Lima fungsi dasar keluarga menurut Friedman (1998)
 Fungsi Afektif (fungsi internal), berguna untuk pemenuhan kebutuhan
psikososial. Komponen :
 Saling mengasuh, cinta kasih, kehangatan, saling menerima, saling
mendukung antar anggota keluarga
 Saling menghargai dan mengakui keberadaan dan hak setiap
anggota keluarga serta selalu mempertahankan iklim yang positif
 Fungsi Sosialisasi
 proses perkembangan dan perubahan yang dilalui individu
menghasilkan interaksi sosial dan belajar berperan dalam lingkungan
sosial
 Fungsi Reproduksi
 Fungsi Ekonomi
 Fungsi Perawatan Kesehatan
No. 183 Referrals
 Interval Referral : the patient is referred for complete care
for a limited period
 Collateral Referral : the referring MD retains overall
responsibility but refers patient for care of some spesific
problem
 Cross Referral : the patient is referred to another MD,
once accepted, the referring MD has no more
responsibility in patient care (Transfer of service)
 Split Referral : the responsibility is divided between 2 or
more MD
No. 184 Sampling Method
 Sampling methods are classified as either probability
(random) or nonprobability (nonrandom).
Probability Samples
 Each member of the population has a known non-
zero probability of being selected.

Multistage Sampling Complex form of cluster sampling. Instead of using all the
elements contained in the selected clusters, the researcher
randomly selects elements from each cluster. The technique is
used frequently when a complete list of all members of the
population does not exist and is inappropriate.
When population is small,
homogeneous & readily
available. All subsets of the
frame are given an equal
probability.

The frame organized into

separate "strata." Each
stratum is then sampled as an
independent sub-population,
out of which individual
elements can be randomly
selected
In this technique, the total
population is divided into
these groups (or clusters) and
a simple random sample of
the groups is selected (two
stage)
Ex. Area
sampling or geographical
cluster sampling
Nonprobability Sampling
 Members are selected from the population in some
nonrandom manner.
No. 185 Hazard
 Hazard is a situation that poses a level of threat
to life, health, property, or environment
 Type of Occupational Health Hazard
 Physical (Falls, Noise, Confined Spaces, Electricity)
 Chemical
 Biological (Pathogens)
 Mechanical
 Psychosocial (Work-related stress, violence, bullying,
exposure to unhealthy elements (Tobacco), sexual
harassment), long-term exhaustion and diminished interest
(burn-out))
 Modes of Disease Transmission
 Direct Transmission : Direct transmission of pathogens occurs through person-to
person contact
 Indirect Transmission : microorganisms first are transmitted to an object or surface,
and then are transferred to another person who touches those objects or surfaces
 Airborne Transmission : spread of disease through droplets of moisture that
contain bacteria or viruses
 Parenteral Transmission/ Blood-Borne Transmission : Parenteral means through
the skin, as with cuts or punctures. Certain pathogens, are carried in the blood and
body fluids of infected individuals and can be transmitted to others
 Food and Water Transmission : Many diseases are transmitted by contaminated
food that has not been cooked or refrigerated properly and by water that has been
contaminated with human or animal fecal material
 Fecal-Oral Transmission : If proper sanitation procedures, such as handwashing
after use of the toilet, are not followed, these pathogens may be transmitted
directly by touching another person, or they may be transmitted indirectly through
contact with contaminated surfaces or food.
 Vector-Borne tranmission : Pathogens carried by vector

Disease Transmission and Infection Prevention. CDC

No. 186. Uji Hipotesis

* : Uji Parametrik; Tanda panah ke bawah : Uji alternatif jika parametrik tidak
terpenuhi
 Variabel Kategorik vs Numerik
 Kategorik : Memiliki kategori variabel. Nominal (kategori
sederajat, cth laki-laki-perempuan)/Ordinal (kategori
bertingkat, cth baik-sedang-buruk)
 Numerik : Dalam angka numerik, rasio (memiliki nilai nol
alami, cth tinggi badan)/interval (tidak memiliki nilai nol
alami, cth suhu)
 Hipotesis Komparatif vs Korelatif
 Komparatif : perbedaan/hubungan (cth. Apakah
terdapat/hubungan antara kadar gula darah dengan jenis
pengobatam?)
 Korelasi : Cth. Berapa besar korelasi antara kadar trigliserida
dan kadar gula darah?
 Skala Pengukuran
 Komparatif : Dianggap skala kategorikal bila kedua variabel
kategorik. Skala numerik jika salah satu variabel numerik
 Korelatif : Dianggap skala kategorikal bila salah satu variabel
kategorik. Skala numerik jika kedua variabel numerik
 Berpasangan vs Tidak Berpasangan
 Berpasangan : Dua atau lebih kelompok data berasal dari
subyek yang sama atau yang berbeda tapi telah dilakukan
matching
 Tidak berpasangan : Data berasal dari kelompok subyek
yang berbeda, tanpa matching
 Uji Parametrik vs Non-parametrik
 Syarat uji parametrik : Skala numerik, sebaran data normal,
untuk >2 kelompok data tidak berpasangan kesamaan
varians merupakan syarat mutlak (Uji varians, p>0.05)
 Tabel B (Baris) x K (Kolom)
 Antara variabel independen (Baris) dan variabel dependen
(Kolom)
 Prinsip P (Pengulangan) x K (Kategori)
 Cth. Pengulangan pengukuran nilai pengetahuan sebelum
dan sesudah penyuluhan
No. 187 One- and Two-tailed tests
 The two-tailed test (two-sided) is a statistical test used
in inference, in which a given statistical hypothesis,
H0 (the null hypothesis), will be rejected when the value
of the test statistic is either sufficiently small or
sufficiently large
 one-tailed test (one sided), in which only one of the
rejection regions "sufficiently small" or "sufficiently large"
is preselected according to the alternative
hypothesis being selected, and the hypothesis is rejected
only if the test statistic satisfies that criterion

Statistics Notes: One and two sided tests of significance BMJ 1994;309:248
Two Tailed Test

 Ex. Compare the mean of a sample to a given value x using a t-test. Our
null hypothesis is that the mean is equal to x. A two-tailed test will test
both if the mean is significantly greater than x and if the mean significantly
less than x. The mean is considered significantly different from x if the test
statistic is in the top 2.5% or bottom 2.5% of its probability distribution,
resulting in a p-value less than 0.05
One Tailed Test
 If you consider the consequences of missing an effect in
the untested direction and conclude that they are
negligible and in no way irresponsible or unethical, then
you can proceed with a one-tailed test
 Right tailed : Positive Outcome
 Left tailed : Negative Outcome
 Soal : Kemungkinan untuk menurunnya jumlah perokok
setelah adanya iklan/kegiatan disponsori rokok, dianggap
tidak dapat terjadi atau dapat diabaikan (negligible).
No. 188 Case Fatality Rate (CFR)
 Definisi : Persentase jumlah orang meninggal akibat
penyakit tertentu terhadap populasi yang didiagnosa
penyakit tersebut dalam kurun waktu course of disease
(UCLA School of Public Health).
Jumlah Kematian akibat Penyakit x 100%
Jumlah Populasi Penderita Penyakit
 Diaplikasikan pada outbreak penyakit
CFR vs Mortality Rate
 Mortality Rate : Jumlah kematian akibat
penyakit/penyebab tertentu terhadap jumlah populasi
umum dan pada kurun waktu yang ditentukan
 CFR merupakan risiko, bukan angka insidensi
189. Deafness
Rinne Weber Schwabach Diagnosis
Positive No lateralization The same as Normal
examiner
Negative Lateralize to deafer ear prolonged Conductive
deafness
Positive Lateralize to better hearing ear shortened Sensorineural
deafness
190. Vertigo
Dizziness

Vertigo
Vertigo vestibular Presyncope Dysequilibrium
nonvestibular

Rasa akan Tungkai tidak

Ilusi berputar Ilusi melayang
pingsan stabil

Sistem visual,
proprioseptif Sistem serebelar,
Sistem vestibular Kardiovaskular
spinal
psikogenik

Spinning Light headed Fainting Falling

190. Vertigo
190. Vertigo
190. Vertigo
Peripheral Vertigo Central Vertigo
Involving Inner ear, vestibular nerve Brainstem, cerebellum,
cerebrum
Onset Sudden Gradual
Nausea, vomitting Severe Varied
Hearing symptom Often Seldom
Neurologic symptom - Often
Compensation/resolution Fast Slow
Spontaneous nystagmus Horizontal, rotatoir Vertical
Positional nystagmus Latency (+), fatigue (+) Latency (-), no fatigue (-)
Calory nystagmus Paresis Normal
190. Vertigo
 Symptomatic treatment:
 Antivertigo (vestibular suppressant)
 Ca channel blocker: flunarizin
 Histaminic: betahistine mesilat
 Antihistamin: difenhidramine, sinarisin
 Antiemetic:
 prochlorperazine, metoclopramide
 Psycoaffective:
 Clonazepam, diazepam for anxiety & panic attack
191. Allergic Rhinitis
 192. Otitis Media
Chronic suppurative otitis media
 a persistent or intermittent (> 2 months)
infected discharge through a nonintact
tympanic membrane.

 Essentials of diagnosis:
 Chronic or recurrent otorrhea or both.
 Hearing loss.
 Tympanic membrane perforation.

 Two main mechanisms by which a chronic

perforation leads to persistent infections:
 Bacteria can contaminate the middle ear
cleft directly.
 The intact tympanic membrane normally
results in a middle ear "gas cushion," which
helps to prevent the reflux of
nasopharyngeal secretions.
1) Lecture notes on diseases of the ear, nose, & throat. 2) Buku Ajar THT-KL FKUI; 2007.
192. Otitis Media
Chronic suppurative otitis media
Classification:

 Benign/mucosal type:
 Not involving bone.
 Perforation type: central.
 Th: ear wash with H2O2 3% for 3-5 Large central perforation
days, ear drops AB & steroid,
systemic AB

 Malignant/bony type:
 Involving bone or cholesteatoma.
 Perforation type: marginal or attic.
 Th: mastoidectomy.
Cholesteatoma at attic
1) Diagnostic handbook of otorhinolaryngology. 2) Buku Ajar THT-KL FKUI; 2007.
type perforation
193. Pharyngitis
 Modified Centor score and
management options using
clinical decision rule.
 Other factors should be
considered (e.g., a score of
1, but recent family
contact with documented
streptococcal infection).

 GABHS = group A beta-

hemolytic streptococcus;
 RADT = rapid antigen
detection testing.

 Adapted with permission from McIsaac

WJ, White D, Tannenbaum D, Low DE. A
clinical score to reduce unnecessary
antibiotic use in patients with sore throat.
CMAJ. 1998;158(1):79.
193. Bacterial Pharyngitis
194. Epistaxis
 Anterior epistaxis:
 Bleeding arises from kisselbach plexus or a. ethmoidalis
anterior
 it may be precipitated by infection or minor trauma & easy
to stop.
 Direct digital pressure for 10-15’ on the lower nose
compresses the vessel on the septum & will arrest the
bleeding.
 If bleeding source is seen  cauterise with AgNO3.
 If it’s still bleeding  apply anterior tampon for 2 x 24
hours.

Buku Ajar THT-KL FKUI; 2007.

194. Epistaxis
 Posterior epistaxis
 Bleeding arises from a. ethmoidalis posterior or a.
Sphenopalatina and often difficult to stop
 affect patient with hypertension or arteriosclerosis.
 Therapy: apply bellocq/posterior tampon for 2-3 days.

Buku Ajar THT-KL FKUI; 2007.

195. Vertigo
195. Vertigo
 Vertigo of peripheral origin
Condition Details
BPPV Brief, position-provoked vertigo episodes caused by
abnormal presence of particles in semisircular canal
Meniere’s disease An excess of endolymph, causing distension of
endolymphatic system (vertigo, tinnitus, sensorineural
deafness)
Vestibular neuronitis Vestibular nerve inflammation, most likely due to virus
Acute labyrinthitis Labyrinth inflammation caused by viral or bacterial
infection
Labyinthine infarct Compromises blood flow to labyrinthine
Labyrinthine concussion Damage after head trauma
Perylimph fistula Labyrinth membrane damage resultin in perylimph
leakage into middle ear
195. Vertigo
 Vertigo of central origin
Condition Details
Migraine Vertigo may precede migraines or occur
concurrently
Vascular disease Ischemia or hemorrhage in vertebrobasilar
syndrome can affect brainstem or cerebellum
function
Multiple sclerosis Demyelination disrupts nerve impulses which can
result in vertigo
Vestibular epilepsy Vertigo resulting from focel epileptic discharges in
the temporal or parietal association cortex
Cerebellopontine tumours Benign tumours in the interal auditory meatus
196. Rhinosinusitis
Diagnosis Clinical Findings
Allergic rhinitis History of atopy. Symptoms: sneezing, itching, watery
rhinorrhea, and congestion.
Signs: mucous membrane shows edema, wet, pale or livid,
with profuse secrete. Allergic shiner, allergic salute, allergic
crease, facies adenoid, geographic tongue.
Vasomotor rhinitis Symptoms: nasal congestion influenced by position, rhinorrea,
sneezing. Trigger: smoke/cigarrete, spicy food, cold, change in
temperature, fatigue, stress.
Signs: mucosal edema, dark red hypertrophic konka.
Acute rhinitis Warm, dry, & itchy followed by sneezing, congestion, & serous
(rhinovirus) secrete along with fever & headache.
Rhinoscopy: reddened & swollen mucous membrane.
Th: analgetic, antipiretic, decongestan.
Rhinosinusitis •Two or more symptoms, included nasal obstruction or nasal
discharge as one of them and: facial pain/pressure or
hyposmia/anosmia. cheek pain: maxillary sinusitis. Retroorbital
pain: ethmoidal sinusitis. Forehead or headache: frontalis
sinusitis.
Buku Ajar THT-KL FKUI; 2007.
196. Rhinosinusitis
 Pemeriksaan penunjang rhinosinusitis:
 Foto polos: posisi waters, PA, lateral. Tapi hanya menilai
sinus-sinus besar (maksila & frontal). Kelainan yang tampak:
perselubungan, air fluid level, penebalan mukosa.
 CT scan: mampu menilai anatomi hidung & sinus, adanya
penyakit dalam hidung & sinus, serta perluasannya  gold
standard. Karena mahal, hanya dikerjakan utk penunjang
sinusitis kronik yang tidak membaik atau pra-operasi untuk
panduan operator.

Buku Ajar THT-KL FKUI; 2007.

196. Rhinosinusitis
 Terapi rhinosinusitis
 Tujuan:
 Mempercepat penyembuhan
 Mencegah komplikasi
 Mencegah perubahan menjadi kronik
 Prinsip:
 Membuka sumbatan di kompleks osteomeatal (KOM)  drainasi &
ventilasi pulih
 Farmakologi:
 AB amoksisilin 10-14 hari
 Dekongestan
 Lain-lain: analgetik, mukolitik, steroid oral/topikal, NaCl
 Operasi
 untuk sinusitis kronik yang tidak membaik, sinusitis disertai kista atau
kelainan ireversibel, polip ekstensif, komplikasi (kelainan orbita,
intrakranial, osteomielitis, kelainan paru), sinusitis jamur.

Buku Ajar THT-KL FKUI; 2007.

 197. Sore Throats
Peritonsillar abscess
Inadequately treated tonsillitis  spread of infection  pus formation between
the tonsil bed & tonsillar capsule

Symptoms & Signs

Quite severe pain with referred otalgia
Odynophagia & dysphagia  drooling
Irritation of pterygoid musculature by pus & inflammation  trismus
unilateral swelling of the palate & anterior pillar  displace the tonsil downward &
medially  uvula toward the opposite side

Therapy
Needle aspiration: if pus (-)  cellulitis  antibiotic. If pus (+)  abscess .
If pus is found on needle aspirate, pus is drained as much as possible.
197. Sore Throat
Peritonsillar abscess

Parapharyngeal abscess

Retropharyngeal abscess
Menner, a pocket guide to the ear. Thieme; 2003.
Buku Ajar THT-KL FKUI; 2007.
 197. Sore Throats
Diagnosis Clinical Features

Tonsillar neoplasm Tonsillar asymmetry associated with rapid enlargement,

constitutional symptoms, atypical tonsillar appearance,
ipsilateral cervical lymphadenopathy, and a history of
previous malignant growths
Acute tonsillitis Sore throat & dysphagia, earache, headache & malaise.
Fever, enlarged, hyperaemic tonsil, inflamed pharynx.

Parapharyngeal abscess Can be caused by spread of infection from peritonsilllar,

retropharyngeal, or submandibular space.
Trismus, induration or swelling around angulus
mandibularis, high fever, swelling of pharyngeal lateral
wall.
Submandibular abscess Infection is originated from teeth, mouth floor,
pharynx, salivary gland, submandibular lymph node.
Fever, neck pain, swelling below the mandible or
tongue.
1) Menner, a pocket guide to the ear. Thieme; 2003. 2) Buku Ajar THT-KL FKUI; 2007. 3) Cummings otolaryngology. 4th ed. Mosby; 2005.
198. Nasal Congestion
 Polyp is a white-greyish soft tissue containing fluid within
nasal cavity, which is caused by mucosal inflammation.
 Nasal polyps do not occur in children except in the
presence of cystic fibrosis.
 Symptoms & signs:
 nasal obstruction, nasal discharge, hyposmia, sneezing, pain,
frontal headache.
 Rhinoscopy: pale mass at meatus medius, smooth & moist,
pedunculated and move on probing.
 Therapy:
 Corticosteroid (eosinophilic polyp has good response compared
with neutrophilic polyp)
 polipectomy if no improvement.
198. Nasal Congestion
199. Otitis Media

Buku Ajar THT-KL FKUI; 2007.

199. Otitis Media
Acute Otitis Media
 The bacteria responsible:
Streptococcus pneumoniae 35%,
Haemophilus influenzae 25%,
Moraxella catarrhalis 15%.
 The sequence of events in acute otitis media:
1. Tubal occlusion: retracted tympanic membrane or dull.
2. Hyperemic/presuppuration: redness & edema.
3. Suppuration: painful, fever, exudate in middle ear, bulging
tympanic membrane.
4. Perforation: rupture of tympanic membrane, fever subsides.
5. Resolution: if there is no perforation  tympanic membrane
return to normal. Perforated membrane  secrete diminish.
1) Lecture notes on diseases of the ear, nose, and throat. 2) Buku Ajar THT-KL FKUI; 2007.
199. Otitis Media
Otitis Media with Effusion
 Serous otitis media
 Obstructed eustachian tube  negative
pressure  transudation of serous fluid.
  hearing loss, depending on the remaining air
in middle ear.
 if some air is still present, position changes of
the head  a sensation of moisture with
bubbling sounds.
 Tinnitus, if present: a low-frequency humming
or roaring sound. Pulsatile tinnitus, hearing his
own small arteries pulsate.
 In the absence of infection or rapid pressure
change  no pain.
 Th: nasal drop vasoconstrictor, antihistamin. If
symptoms persist after 1-2 weeks 
myringotomy.
199. Otitis Media
Otitis Media with Effusion
 Chronic serous otitis media/glue ear/mucous OM
 If a serous effusion continues for weeks  the
mucous glands of the middle ear & eustachian tube
tend to proliferate & secrete more actively  the
fluid can progressively thicken “glue” (gelatinous
mucus).
 Findings:
 As fluid increases & thickens, with loss of any air
content, the drum may look darker, thick, or dull.
 The serous and mucous ear effusions are usually
sterile & do not cause the diffuse thick redness .
 Audiometry will document conductive hearing
loss.
 Th: myringotomy & inserting ventilation pipe
(Grommet)

1) Diagnostic handbook of otorhinolaryngology. 2) Buku Ajar THT-KL FKUI; 2007. 3) Menner, a pocket guide to ear. 2003.
199. Otitis Media
Chronic serous otitis media

1) Diagnostic handbook of otorhinolaryngology. 2) Buku Ajar THT-KL FKUI; 2007.

200. Otitis Media
Chronic suppurative otitis media
 a persistent or intermittent (> 2 months)
infected discharge through a nonintact
tympanic membrane.

 Essentials of diagnosis:
 Chronic or recurrent otorrhea or both.
 Hearing loss.
 Tympanic membrane perforation.

 Two main mechanisms by which a chronic

perforation leads to persistent infections:
 Bacteria can contaminate the middle ear
cleft directly.
 The intact tympanic membrane normally
results in a middle ear "gas cushion," which
helps to prevent the reflux of
nasopharyngeal secretions.
1) Lecture notes on diseases of the ear, nose, & throat. 2) Buku Ajar THT-KL FKUI; 2007.
 200. Otitis Media
Chronic suppurative otitis media
Classification:
 Benign/mucosal type:
 Not involving bone.
 Perforation type: central.
 Th: ear wash with H2O2 3% for 3-
Large central perforation
5 days, ear drops AB & steroid,
systemic AB

 Malignant/bony type:
 Involving bone or cholesteatoma.
 Perforation type: marginal or
attic.
 Th: mastoidectomy.
Cholesteatoma at attic
1) Diagnostic handbook of otorhinolaryngology. 2) Buku Ajar THT-KL FKUI; 2007.
type perforation
200. Otitis Media
 Diagnosis OMSK:
 Gejala klinik + otoskopi
 Derajat gangguan pendengaran (penala, audiometri nada
murni)
 Pemeriksaan penunjang lain:
 Roentgen mastoid

 Kultur & uji resistensi kuman dari sekret telinga

Buku Ajar THT-KL FKUI; 2007.