Emergency Medicine Block

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

Tintinalli’s Emergency Medicine 8th ed

Tintinalli’s Emergency Medicine 8th ed
LI 1
HHS
 Hyperosmolar hyperglycemic state
(HHS)
• Hyperosmolar hyperglycemic
state (HHS)  characterized by
progressive hyperglycemia and
hyperosmolarity typically found
in a debilitated patient with
poorly controlled or undiagnosed
type 2 diabetes mellitus
• The syndrome does not
necessarily include ketosis or
coma
• Most cases of HHS occur in the
elderly with comorbid organ or
metabolic diseases, and about
70% of patients have been
previously diagnosed as diabetics
Clinical Features
• Complaints are often nonspecific 
weakness, anorexia, fatigue, dyspnea,
or chest or abdominal pain
• Many patients have previously
undiagnosed or poorly controlled type
2 diabetes precipitated by pneumonia
or urinary tract infection
• Underlying cardiovascular, respiratory,
renal, or neurologic disease is common.
• HHS is associated with a host of
conditions and drugs that may
predispose to hyperglycemia and
volume depletion
 Physical examination
• Generally, clinical signs of volume depletion  poor
skin turgor, dry mucous membranes, sunken eyes,
and hypotension will correlate with the degree of
hyperglycemia and hyperosmolality
• Normothermia or hypothermia (poor prognosis sign)
is common due to vasodilation
• > 15% patients  seizures
• The degree of lethargy and coma has a linear
relationship to serum osmolality.
• Patients with coma tend to be older and have higher
osmolality, more severe hyperglycemia, acidosis, and
greater volume contraction.
Diagnosis and Differential Diagnosis
http://bestpractice.bmj.com/best-practice/images/bp/en-gb/162-7-iline_default.gif
 Characteristics of DKA and HHS
Diabetic Ketoacidosis (DKA)
Absolute (or near-absolute) insulin
deficiency, resulting in
• Severe hyperglycemia
• Ketone body production
• Systemic acidosis
Develops over hours to 1-2 days
Most common in type 1 diabetes, but
increasingly seen in type 2 diabetes
Hyperglycemic Hyperosmolar State
(HHS)
Severe relative insulin deficiency,
resulting in
• Profound hyperglycemia and
hyperosmolality (from urinary free
water losses)
• No significant ketone production or
acidosis
Develops over days to weeks
Typically presents in type 2 or
previously unrecognized diabetes
Higher mortality rate
 Laboratory testing and Imaging
• A comprehensive metabolic
profile, calculated and
measured serum osmolality,
urine osmolality, lactic acid,
serum ketones, magnesium,
CBC with differential, and
blood and urine cultures 
should all be considered
• Cardiac markers, total creatine
phosphokinase, arterial or
venous blood gas, thyroid
function studies, procalcitonin,
and coagulation profiles 
might be needed
• Chest radiographs and
electrocardiograms 
recommended
• contraction alkalosis due to a
profound water deficit may
occur.
• An anion gap metabolic
acidosis is often attributable
to sepsis, poor tissue
perfusion, starvation ketosis,
or renal impairment.
 Laboratory testing and Imaging
• Sodium
– Hyperglycemia has a
dilutional effect on
measured serum sodium:
Serum Na+ decreases by
approximately 1.6 mEq/L
(1.6 mmol/L) for every 100
milligrams/dL (5.6 mmol/L)
increase in serum glucose
>100 milligrams/dL (5.6
mmol/L)
– For glucose levels >400
milligrams/dL (22.2
mmol/L), a correction factor
of 2.4 may be more
accurate.
• Osmolarity
– Serum osmolality correlates positively with severity
of disease as well as mental status changes and
coma.
– A calculated effective serum osmolality excludes
osmotically inactive urea, which is usually included
in laboratory measures of osmolality
– The normal serum osmolality  275 to 295
mOsm/kg.
– Values >300 mOsm/kg  significant hyperosmolality
– >320 mOsm are commonly associated with
alterations in cognitive function.
 Laboratory testing and Imaging
• Potassium
– Potassium losses range from 4 to 6 mEq/kg, although
deficits can be as high as 10 mEq/kg body weight
– Despite these total body deficits, initial serum laboratory
measurements may be normal or even high in the
presence of acidemia
• Other laboratory testing
– Hypomagnesemia (common)  Serum magnesium levels
should be monitored and replaced
– Prerenal azotemia (common) with plasma blood urea
nitrogen: creatinine ratios often exceeding 30:1
– Hypophosphatemia  uncommon (serum phosphate level
<1.0 mg/dL)
 Treatment
• Correction of hypovolemia, identifying and
treating precipitating causes, correcting
electrolyte abnormalities, gradual correction
of hyperglycemia and hyperosmolarity, and
frequent monitoring.
Treatment
 Disease Complications
• Despite cerebral edema representing >50% of
fatalities in children with diabetic
ketoacidosis, cerebral edema is an uncommon
complication in adults with HHS
• More common complications, such as
hypoglycemia, hypokalemia, and pulmonary
edema, are generally associated with
overzealous resuscitation and inadequate
monitoring
LI 1
AKI
 Introduction

• Acute kidney injury

is the deterioration
of renal function
over hours or days
resulting in the
accumulation of
toxic wastes and
the loss of internal
homeostasis
 Epidemiology
• Community-acquired renal failure is diagnosed in only 1% of hospital
admissions at the time of presentation and is usually secondary to
volume depletion; thus, the vast majority of cases presenting to the
ED have a reversible cause.
• Hospital-acquired renal failure is only apparent after admission.
• Hospital factors include advanced patient age, potential nephrotoxic
exposures in a hospital setting, sepsis and multiorgan system illness in
hospitalized patients
 Pathophysiology
• Renal insult is classified as :
– Prerenal (decreased perfusion of a normal kidney)
– Intrinsic (pathologic change within the kidney itself)
– Postobstructive (obstruction to urine outflow)
• The functions of the kidneys are glomerular filtration, tubular reabsorption, and secretion
• In prerenal failure, tubular and glomerular functions are still maintained  restoration of
circulating blood volume is usually sufficient to restore function.
• Postobstructive renal failure initially results in an increase in tubular pressure, which decreases the
driving force for filtration.
• This pressure gradient soon equalizes, and the maintenance of depressed GFR depends on
vasoconstrictors.
• Rapid relief of urinary obstruction in postrenal failure results in a prompt decrease of
vasoconstriction.
• Intrinsic renal failure occurs with diseases of the glomerulus, small vessels, interstitium, or tubule
and is associated with the release of renal vasoconstrictors.
• The most common cause of intrinsic renal failure is ischemic injury or ischemic tubular necrosis
(also historically called acute tubular necrosis), when renal perfusion is decreased so much that the
kidney parenchyma is affected.
• In intrinsic renal failure, clearance of tubular toxins and initiation of therapy for glomerular diseases
decrease vasoconstriction and help restore renal blood flow.
 AKI
Physical Examination
• Assess and correct volume
status.
• Evaluate mucous
membranes, jugular vein
distention, lung
auscultation, peripheral
edema, and tissue turgor to
identify dehydration.
Diagnosis
• Determine if kidney injury is
prerenal, postrenal, or intrinsic.
• ECG is often the fastest screening
test for hyperkalemia
• Chest radiography helps evaluate
for increased volume, effusions,
and pneumonia, all of which can
result from or precipitate renal
failure.
• Anuria is 100 mL urine per day
and can be present with prerenal,
postrenal, or intrinsic kidney
disease.
 Laboratory Evaluation
Creatinine and GFR BUN: Cr ratio
• Creatinine (Cr) is the mainstay for measuring
renal function  it is a breakdown product • The ratio of BUN to Cr can
of the skeletal muscle protein creatine, and
its level is thus linked to muscle mass. suggest hypovolemia
• In patients with no renal function (GFR = 0),
serum Cr level increases 1 to 3 milligrams/dL • If the patient has normal
a day.
• Normal kidney function is a GFR >90 concentrating ability, in the
mL/min/1.73 m2
• Stages of kidney disease are characterized by
setting of prerenal failure,
GFR:
– Stage 1  GFR 90 mL/min/1.73 m2
the serum ratio of BUN to
–
–
Stage 2  GFR 60 to 89 mL/min/1.73 m2
Stage 3  GFR 30 to 59 mL/ min/1.73 m2
Cr is typically >10.
– Stage 4  GFR 15 to 29 mL/min/1.73 m2
– Stage 5  GFR <15 mL/min/1.73 m2 (dialysis
or transplant needed).
 Prerenal Failure

• The causes of prerenal

azotemia can be broken
down into volume loss,
hypotension, and
diseases of the large
and small renal arteries
• Prerenal failure is also a
common precursor to
ischemic and
nephrotoxic conditions,
leading to intrinsic renal
failure.
 Postobstructive
Renal Failure
• Postrenal or postobstructive kidney
injury accounts for 5% to 17% of all
community-acquired disease, and in
the elderly population, the rate is as
high as 22%
• Risk factors include both extremes of
age, male sex, malignancy,
nephrolithiasis, retroperitoneal
disease, GU surgery, and indwelling
urinary catheters.
• Permanent loss of renal function
develops over the course of 10 to 14
days in the setting of complete
obstruction.
• The risk of permanent renal failure
increases significantly if obstruction is
complicated by urinary tract infection.
 Intrinsic Renal Failure
• Intrinsic kidney injury is not common in patients with community-
acquired disease, but it is the most common cause in hospitalized
patients.
• Intrinsic renal failure can result from injury to the glomerulus, tubule,
interstitium, and vasculature. In community-acquired intrinsic renal
failure, drugs and infection are common precipitants, whereas in the
hospital, toxic and ischemic insults cause most cases
 Treatment
• In the critically ill patient, resuscitation is the first priority, and multiple
diagnostic and therapeutic processes advance simultaneously.
• Treat hypovolemia, and identify and treat sepsis, myocardial ischemia, and
occult GI or retroperitoneal hemorrhage.
• Crystalloid infusion is often sufficient to treat or improve many forms of
acute renal failure, but accurate determination of volume status is
essential to prevent volume overload, and often requires invasive
hemodynamic monitoring, particularly in the setting of cardiac
dysfunction.
• In general, for IV contrast studies in patients with GFR of 30 to 59
mL/min/1.73 m2, weigh benefits of the study against the risk of renal
function decline
• For patients with GFR <30 mL/min/1.73 m2, avoid IV contrast studies if
possible
• Make sure to avoid gadolinium for GFR <30 mL/ min/1.73 m2.
LI 1
HYPOGLYCEMIA
 Hypoglycemia
• Most commonly caused by
drugs used to treat diabetes
mellitus or by exposure to
other drug
• Other : critical organ failure,
sepsis and inanition, hormone
deficiencies, non-ß-cell
tumors, insulinoma, and prior
gastric surgery
• Hypoglycemia can cause
serious morbidity if severe and
prolonged, it can be fatal
Diagnosis
• The development of
autonomic or
neuroglycopenic symptoms
• A low plasma glucose level
(<4 mmol/L)
• Symptoms responding to
the administration of
carbohydrate
Harrison’s Principles of Internal Medicine
 Diabetes medication cause hypoglicemia
• chlorpropamide (Diabinese)
• glimepiride (Amaryl)
• glipizide (Glucotrol, Glucotrol XL)
• glyburide (DiaBeta, Glynase, Micronase)
• nateglinide (Starlix)
• repaglinide (Prandin)
• sitagliptin (Januvia)
• tolazamide
• tolbutamide
Certain combination pills can also cause hypoglycemia, including
• glipizide + metformin (Metaglip)
• glyburide + metformin (Glucovance)
• pioglitazone + glimepiride (Duetact)
• rosiglitazone + glimepiride (Avandaryl)
• sitagliptin + metformin (Janumet)

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/

Octreotide (somatostatin analog )

Failure to respond to parenteral glucose 
consideration of other causes of
hypoglycemia (sepsis, toxin, insulinoma,
hepatic failure, or adrenal insufficiency).
Other th/
Diazoxide
• I/  th/ of refractory
sulfonylurea-induced
hypoglycemia.
• It acts by directly i⊣ insulin
secretion from pancreatic β cells.
• Diazoxide  hypotension and so
should be administered as a slow
IV infusion (300 milligrams over
30 minutes every 4 hours).
• suppress insulin secretion.
• I/  treatment of sulfonylurea-induced hypoglycemia.
• Dose 
• Single 50-100-microgram SC injx after a single
hypoglycemic episode, to serial SC injections (50 to
100 micrograms every 6 to 8 hours)
• Constant IV infusion (125 micrograms/h) after a
second hypoglycemic episode.
• Octreotide is only recommended if :
• Initial glucose therapy has been initiated for
sulfonylureainduced hypoglycemia
• Irresponse to dextrose th/
• It is primarily used to reduce the risk of recurrent
hypoglycemia.
Glucagon 
• In adults, glucagon is administered at the dose of 1 milligram
as an SC or IM injection.
• Intranasal glucagon has also been used safely in some studies
for the treatment of hypoglycemia.
• Glucagon should be used cautiously in patients with
sulfonylurea-induced hypoglycemia.
 Hypoglycemia in Neonates & Children
• Blood glucose <50mg/dL is
applicable after the initial 2–3 hr;
subsequently, blood glucose
levels begin to rise and achieve
values of 50 mg/dL or higher after
12–24 hr
• In older infants and children, a
whole blood glucose
concentration of <50 mg/dL (10–
15% higher for serum or plasma)
represents hypoglycemia
• In neonates, maybe symptomatic
or asymptomatic
Treatment
• When feedings alone cannot
maintain blood glucose
concentrations at levels >50 mg/dL,
intravenous glucose at a rate that
supplies 4–8 mg/kg/min should be
started  avoid hyperglycemia that
evokes a prompt exuberant insulin
release, which may result in
rebound hypoglycemia
• Infants with transient neonatal
hypoglycemia can usually maintain
the blood glucose level
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)

Ilmu Penyakit Dalam Jilid 1

 Sepsis
• Sepsi berat  sepsis yg berkaitan dgn disfungsi organ, kelainan hipoperfusi/hipotensi.
Kelainan hipoperfusi meliputi
– Asidosis laktat
– Oliguria
– Perubahan akut pd status mental

• 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
– I: fever + constitutional ssx
(non-specific); the only
hemorrhagic manif: torniquet
test (+)
– II: additional manifestation
from I; (+) spontaneous
bleeding (skin and or other
hemorrhage)
– III: Circulatory failure w/ rapid
& weak pulse, pulse pressure
<< 20 mmHg or hypertension
+ irritability & cold
extremities
– IV: Shock w/ undetectable
pulse & BP
DENGUE SHOCK SYNDROME
• All criterias of DHF +
evidence of circulatory
failure:
– Rapid & weak pulses
– <20 mmHg narrow pulse
pressure
Or: hypotension, cold & clammy
extremities, irritable
Patients with dengue can
rapidly progress into DSS,
which, if not treated correctly,
can lead to severe
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
of bacteria in the bloodstream.
• When bacteremia occurs in a
young child and produces
relatively few signs or symptoms,
other than fever, the patient is
considered to have the syndrome
of occult bacteremia.
• Because these syndromes
represent a continuum, whereby
some children with occult
bacteremia proceed to develop
the manifestations of sepsis, a
separation into distinct diagnostic
categories is not always possible.
• Bacterial bloodstream infections
may occur in isolation (primary) or
in association with focal disease
(secondary).
• In areas without widespread use
of multivalent conjugate
pneumococcal vaccine
Streptococcus pneumoniae causes
70% to 90% of primary occult
bacteremias.
• Other bacteria now represent an
increasing proportion of
bactermias including Salmonella,
Neisseria meningitidis, group A
streptococcus, group B
streptococcus, Staphylococcus
aureus, and, rarely in the
developed countries at present,
Haemophilus influenzae or other
pathogens.
 Bacteremia
• Occult bacteremia occurs with
predictable regularity among
febrile children younger than 2 to
3 years. (peak 6-12 mo)
• A continuum of disease exists,
starting with colonization of the
host and then progressing to occult
bacteremia if bacteria have the
opportunity to gain access to the
bloodstream.
• Occult bacteremia may have one
of four outcomes:
– (i) spontaneous resolution,
– (ii) sepsis,
– (iii) focal infection,
– (iv) sepsis and focal infection.
• Clearly, pathogens such as N.
meningitidis and H. influenzae
have a greater tendency than S.
pneumoniae to produce sepsis or
invasive disease.
• A concurrent viral infection may
increase the likelihood of
bacteremia in a colonized child by
disrupting mucosal barriers to
invasion.
• Pathogen-specific bactericidal
antibodies in the serum have been
shown to protect carriers against
the development of sustained
bacteremia for several bacterial
pathogens; however, some persons
without such antibodies do not
progress beyond colonization.
 Clinical Features
• The complaints are usually
those of malaise or an upper
respiratory infection (URI).
• Fever, without evidence of a
source, may be the only
physical finding, or the patient
may have a minor focus of
infection, such as otitis media
(OM).
• The white blood cell (WBC)
count is usually elevated in
children with S. pneumoniae
bacteremia.
– risk of bacteremia was greater
among the more highly febrile
patients with leukocytosis
• A shift to the left in the
differential count and signs of
toxicity on the peripheral smear
are seen more often in
bacteremic children than in those
with viral infections, but neither
serves to reliably distinguish the
two groups.
• Although the erythrocyte
sedimentation rate (ESR), the C-
reactive protein (CRP), and other
acute phase reactants (e.g.,
procalcitonin) are usually
elevated in patients with
bacteremia, these tests provide
minimal, if any, additional
information
 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

Lipolisis : pecah lemak

History : DM + DD : hypoglycemia DKA
untuk energy cell
insulin therapy

Infection right Penggunaan Penurunan

glukosa untuk sel HHS kesadaran
calf
menurun
Dehidrasi &
Predisposisi DKA/HHS Osmotic
Peningkatan hemoconcentration
Peningkatan stress hormone diuresis
glucogenesis

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