Emergency Medicine Block Seventh Problem: Group 15 Friday, November 3 2017
Emergency Medicine Block Seventh Problem: Group 15 Friday, November 3 2017
Emergency Medicine Block Seventh Problem: Group 15 Friday, November 3 2017
Seventh Problem
Group 15
Friday, November 3rd 2017
Learning Issues
1. Menjelaskan mengenai penurunan kesadaran
ekstrakranial :
– KAD
– HHS
– AKI
– Hipoglikemia
– Sepsis
– DSS
– Gangguan asam basa
– Bacteremia
2. Menjelaskan patofisiologi dari kasus
LI 1
KETOASIDOSIS DIABETIK
Tintinalli’s Emergency Medicine : A Comprehensive Study Guide. 8thed; 2016
DKA
DKA
Complications
• Physical findings in DKA are due to dehydration and metabolic acidosis.
Children appear dehydrated, are tachycardic, and may be hypotensive.
Respiratory compensation for acidosis is noted in the deep Kussmaul
respirations, which may be accompanied by paresthesias.
Acetoacetate is converted to acetone and is responsible for the classic
breath odor of nail polish. The level of consciousness may range from
alert to somnolent to comatose. In a child with DKA and a depressed
level of consciousness, consider the development of cerebral edema.
• An elevated glucose level in the presence of ketonemia/ketonuria and
acidosis almost always indicates DKA
http://www.niddk.nih.gov
Beggs IS, Yale J-F, Houlden RL, et al. Canadian Diabetes Association’s Clinical Practice Guidelines for Diabetes and Private Commercial Driving
DIAGNOSIS
• Hypoglycemia should always be considered early
(including the prehospital setting) as a potential
cause of altered mental status
• Patient using sulfonylurea
• Failure to determine hypoglycemia early CNS
dysfx & unnecessary th/ death! check using
bedside glucose testing
• Others Drug interactions, decreased
metabolism of the drug, and decreased drug
excretion are common precipitating causes
Beggs IS, Yale J-F, Houlden RL, et al. Canadian Diabetes Association’s Clinical Practice Guidelines for Diabetes and Private Commercial Driving
http://guidelines.diabetes.ca/browse/chapter14
Hypoglycemia
• The Somogyi phenomenon is a common problem associated with
iatrogenic hypoglycemia in the type 1 diabetic patient.
• The phenomenon is initiated by excessive insulin dosing, resulting
in an unrecognized hypoglycemic episode that usually occurs in the
early morning while the patient is sleeping.
• The counterregulatory hormone response produces rebound
hyperglycemia, evident when the patient awakens.
• Often, the patient and physician interpret this hyperglycemia as an
indication to increase the insulin dosage, which exacerbates the
problem.
• Instead, the insulin dosage should be lowered or the timing
changed.
• Initial managements DX & IV/PO carbs (glucose/dextrose)
– Altered mental status 50% dextrose in water IV bolus 50 mL (contains 25g glucose)
•
– Regain consciousness keep glucose th/ (PO long-acting carbohydrates / continuous IV
10% dextrose in water to maintain the serum glucose >100 milligrams/dL [5.55 mmol/L]))
Blood glucose check every 30 minutes for the first 2 hours looking for rebound
hypoglycemia
Th/
• (+) hyperglycemia ? lower the dose/ w/draw th/
Treatment
• Blood glucose <50mg/dL is • When feedings alone cannot
applicable after the initial 2–3 hr; maintain blood glucose
subsequently, blood glucose concentrations at levels >50 mg/dL,
levels begin to rise and achieve intravenous glucose at a rate that
values of 50 mg/dL or higher after supplies 4–8 mg/kg/min should be
12–24 hr started avoid hyperglycemia that
• In older infants and children, a evokes a prompt exuberant insulin
whole blood glucose release, which may result in
concentration of <50 mg/dL (10– rebound hypoglycemia
15% higher for serum or plasma) • Infants with transient neonatal
represents hypoglycemia hypoglycemia can usually maintain
• In neonates, maybe symptomatic the blood glucose level
or asymptomatic spontaneously after 2–3 days of life
Clinical Manifestation
ACTIVATION OF AUTONOMIC
NERVOUS SYSTEM AND EPINEPHRINE CEREBRAL GLUCOPENIA
• Anxiety • Headache
• Prespiration • Mental confusion
• Palpitation (tachycardia)
• Visual disturbance (diplopia,
• Pallor
decrease acuicity)
• Tremulousness
• Weakness • Organic personality change
• Hunger • Inability to concentrate
• Nausea • Dysarthria
• Emesis • Staring
• Angina (with normal coronary
artery) • Parasthesia, amnesia, ataxia,
dizziness, seizures, coma,
LI 1
SEPSIS
Sepsis
• Sepsis sindr klinik karna reaksi yg berlebihan dari respon
imun tubuh yg distimulasi mikroba/bakteri baik dari dalam &
luar tubuh
• Systemic inflammatory response syndrome pasien yg
memiliki dua atau lebih kriteria:
– Suhu >38C atau <36C
– Denyut jantung >90 denyut/menit
– Respirasi >20/menit atau Pa CO2 <32 mmHg
– Hitung leukosit >12.000/mm3 atau >10% sel imatur
• Sepsis ialah SIRS ditambah tempat infeksi yg diketahui
(ditentukan dgn biakan positif trhdp organisme dari tempat
tersebut)
• Derajat sepsis
– SIRS ditandai dgn > 2 gejala
• Hipertermia/hipotermia (>38,3C/<35,6C)
• Takipneu
• Takikardi
• Leukositosis >12000/mm atau leukopenia <4000/mm
• Sel imatur >10%
– Sepsis: infeksi disertai SIRS
– Sepsis berat: disertai MODS, hipotensi, oliguri, anuri
– Sepsis dgn hipotensi (tek sistol <90 mmHg, pe↓ tek sistol >40 mmHg
– Syok septik: subset dari sepsis berat, didefinisikan sgb hipotensi yg diinduksi sepsis
& menetap walaupun tlah mndapat resusitasi cairan & disertai hipoperfusi jaringan
Ilmu Penyakit Dalam Jilid 1
• Having systemic
SIRS
inflammatory response
syndrome criteria does not
confirm the presence of
infection or sepsis because
these features are shared by
many other noninfectious
conditions such as trauma,
pancreatitis, and burns
• The systemic inflammatory
response syndrome
response is not a diagnosis
or a good indicator of
outcome; it is a crude means
of stratification of patients
with systemic inflammation.
• Most common sepsis trigger acute bacterial
pneumonia. (S. pneumoniae, S.aureus, gram –ve bacili,
Legionella pneumophila).
– Chest radiograph identify air space changes and pneumonia
• Acute pyelonephritis bc gram –ve enteric bacteria /
enterococci
• if abd tendernes / peritonitis probably perforated
viscous, appendicitis, diffuse colitis or intra-abd abscess
• Skin/ soft tissue infx e.c S. aureus / Streptococcus
pyogenes
– Shock + generalized erythematous macular rash TSS
SEPSIS BUNDLES
• The Institute for Healthcare
Improvement developed
recommendation for early,
initial treatment of the patient
with severe sepsis or septic
shock
• These recommendations are
based on the best current
available evidence from the
Surviving Sepsis Campaign’s
management guidelines.
ANTIMICROBIAL THERAPY
• Patients should receive antibiotic coverage, early and presumptively.
• Coverage should be directed at the source, if known, but broad-spectrum
antibiotics are generally advisable.
• Early administration of adequate antibiotics favors improved outcomes, whereas
delays in administration result in increased mortality for this patient population
LI 1
DENGUE SHOCK SYNDROME
Viral Hemorrhagic Fevers
Dengue Virus
• Viruses in the Flaviviridae family can also cause hemorrhagic
fevers.
• Dengue is the most common virus in this family to cause
human infection.
• It can be found all over the world, with most infections
occurring in Southeast Asia, the Western Pacific, and Central
and South America. It is one of the most important causes of
fever in the returned traveler.
• It is transmitted via the mosquito vector, Aedes aegypti and
Aedes albopictus, and humans are the natural host.
Diagnosis
• Anamnesis:
– Sudden high fever (biphasic type) + hemorrhagic tendencies (skin, gum,
epistaxis, hemathemesis, melena, hematuria), headache, muscle & joint pain,
rash, retroorbital pain, nausea & vomiting, prolonged menstruation cycle)
• Physical Exam:
– Fever
– Ssx of viral infx: conjunctival injection, myalgia, arthralgia
– W/out hemorrhage: petechiae, purpura, ecchymosis
– Hepatomegali
– Signs of plasma extravasation: pleural effusion, ascites, edema
• Diagnostic studies:
– Routine blood: leucopenia, thrombositopenia, hemoconcentration
• Ht & thrombocyte should be evaluated every 12/24 hrs
– Serology: IgG-IgM Antidengue (+), viral protein NS-1 Dengue
– CXR: blunt costophrenic angle
– USG abdomen: double layer on wall of vesica fellea/gall bladder, or ascites
• Diagnostic Criteria (DHF)
– Probable: acute fever + 2 or > ssx as following:
• Headache
• Retroorbital pain
• Myalgia
• Arthralgia
• Rash
• Hemorrhagic/bleeding manifestation
• Leucopenia and
• (+) serology or evidence of DHF during the same time or in the same
location
– Confirmed: (w/ lab criteria)
• Isolated dengue virus from serum or autopsy sample
• >> 4x titer of IgG Ab or IgM from plasma sample
• (+) Ag virus dengua on sample (tissue, plasma, CSF) w/
immunohistochemical, immunofluorescens or ELISA
• Dtx sequence viral genome on sample w/ PCR
– Reportable: every cases (probable or confirmed) should be reported
• Dx criteria of DHF WHO 1997
– Fever or acute fever history b/w 2-7 days, usually biphasic
– (+) at least one of bleeding/hemorrhagic manifestation as
follow:
• (+) torniquet test
• Petechiae, ecchymosis, or purpura
• Mucosal bleeding (>> epistaxis or gum bleeding) or other sites
• Hemathemesis or melena
– Thrombositopenia (<100.000/ml)
– At least 1 plasma leakage signs as follow:
• Ht >> 20% from standard based on age & gender
• << Ht >20% after fluid replacement, compared to Ht value before
• (+) plasma leakage: pleural effusion, ascites, hypoproteinemia or
hyponatremia
• Severity of DHF DENGUE SHOCK SYNDROME
– I: fever + constitutional ssx • All criterias of DHF +
(non-specific); the only evidence of circulatory
hemorrhagic manif: torniquet
test (+) failure:
– II: additional manifestation – Rapid & weak pulses
from I; (+) spontaneous – <20 mmHg narrow pulse
bleeding (skin and or other pressure
hemorrhage) Or: hypotension, cold & clammy
– III: Circulatory failure w/ rapid extremities, irritable
& weak pulse, pulse pressure Patients with dengue can
<< 20 mmHg or hypertension
rapidly progress into DSS,
+ irritability & cold
extremities which, if not treated correctly,
– IV: Shock w/ undetectable can lead to severe
pulse & BP complications and death.
WHO Library Cataloguing-in-Publication Data Handbook for clinical management of dengue. 2012
LI 1
ACID BASE DISORDER
http://www.elsevier.es/ficheros/publicaciones/22562087/0000004300000003/v3_201512070814/S22562
08715000383/v3_201512070814/en/main.assets/gr1.jpeg
KOREKSI KALIUM
• Per oral
– 40 – 60 mEq → ↑ 1 – 1,5 mEq/L
– 135 – 160 mEq → ↑ 2,5 – 3,5 mEq/L
• IV → larutan KCl
– 20 mEq KCl dilarutkan dalam 100 cc NaCl isotonik
– Melalui vena perifer → 60 mEq KCl (maksimal) dilarutkan
dalam 1000 cc NaCl isotonik
– Kecepatan 10 – 20 mEq/jam
– Aritmia yang berbahaya / kelumpuhan otot pernapasan →
40 – 100 mEq/jam
Setiati S, Alwi I, Sudoyo AW, Simadibrata M, Setiyohadi B, Syam AF, editors. Buku ajar ilmu penyakit dalam. Edisi 6.
Jakarta: Pusat Penerbitan Ilmu Penyakit Dalam FKUI; 2014.
LI 1
BACTEREMIA
Bacterimia
• Bacteremia refers to the presence • In areas without widespread use
of bacteria in the bloodstream. of multivalent conjugate
• When bacteremia occurs in a pneumococcal vaccine
young child and produces Streptococcus pneumoniae causes
relatively few signs or symptoms,
other than fever, the patient is 70% to 90% of primary occult
considered to have the syndrome bacteremias.
of occult bacteremia. • Other bacteria now represent an
• Because these syndromes increasing proportion of
represent a continuum, whereby bactermias including Salmonella,
some children with occult
bacteremia proceed to develop Neisseria meningitidis, group A
the manifestations of sepsis, a streptococcus, group B
separation into distinct diagnostic streptococcus, Staphylococcus
categories is not always possible. aureus, and, rarely in the
• Bacterial bloodstream infections developed countries at present,
may occur in isolation (primary) or Haemophilus influenzae or other
in association with focal disease pathogens.
(secondary).
Bacteremia
• Occult bacteremia occurs with • Clearly, pathogens such as N.
predictable regularity among meningitidis and H. influenzae
febrile children younger than 2 to have a greater tendency than S.
3 years. (peak 6-12 mo) pneumoniae to produce sepsis or
• A continuum of disease exists, invasive disease.
starting with colonization of the • A concurrent viral infection may
host and then progressing to occult increase the likelihood of
bacteremia if bacteria have the bacteremia in a colonized child by
opportunity to gain access to the disrupting mucosal barriers to
bloodstream. invasion.
• Occult bacteremia may have one • Pathogen-specific bactericidal
of four outcomes: antibodies in the serum have been
– (i) spontaneous resolution, shown to protect carriers against
– (ii) sepsis, the development of sustained
bacteremia for several bacterial
– (iii) focal infection, pathogens; however, some persons
– (iv) sepsis and focal infection. without such antibodies do not
progress beyond colonization.
Clinical Features
• The complaints are usually • A shift to the left in the
those of malaise or an upper differential count and signs of
respiratory infection (URI). toxicity on the peripheral smear
are seen more often in
• Fever, without evidence of a bacteremic children than in those
source, may be the only with viral infections, but neither
physical finding, or the patient serves to reliably distinguish the
may have a minor focus of two groups.
infection, such as otitis media • Although the erythrocyte
(OM). sedimentation rate (ESR), the C-
• The white blood cell (WBC) reactive protein (CRP), and other
count is usually elevated in acute phase reactants (e.g.,
children with S. pneumoniae procalcitonin) are usually
elevated in patients with
bacteremia. bacteremia, these tests provide
– risk of bacteremia was greater minimal, if any, additional
among the more highly febrile information
patients with leukocytosis
Management
• A discussion on the management of
bacteremia must address three issues:
– (i) evaluation for bacteremia in the febrile child
with a seemingly trivial febrile illness,
– (ii) treatment of the child with suspected
bacteremia but no signs of sepsis or focal
disease, and
– (iii) therapy of proven bacteremia.
LI 2
PATHOPHYSIOLOGY FROM CASE
Patient 1
Women 55 yo Ketoasidosis
Lab
Oliguri
AKI Creatinine, ureum
• Glucose 475 mg/L meningkat
• Leuko : neutrofil
meningkat
• Asidosis metabolik Electrolyte
imbalance
Patient 2
Boy 3 yo PF : Peningkatan vascular
• Multiple petechiae permeability
Fever, fatigue, • Sign of DHF + shock
nausea, vomiting, (cold extremities, BP
loss appetite menurun, RR Plasma
meningkat) DSS leakage
Hypoglycemi Hypovolemi
Platelet turun, Ht Hypovolemia
meningkat
Shock
Coagulopathy
DIC Severe
bleeding