Jesly Problem 2A KGD

PROBLEM 2A
JESLY CHARLIES
405100171
Group 10, Emergency Medicine Block
LO 1
Explain all about shocks
Harrison's principles of internal medicine, 18th
Shock
clinical syndrome that results from inadequate
tissue perfusion
Hypoperfusion / oxygen imbalance cellular dysfunction
inflammatory mediators & release of damage-
associated molecular patterns further compromise

perfusion
functional and structural changes within the microvasculature
leads to a vicious cycle

maldistribution of blood flow
further compromising cellular perfusion
MOF
Death
Nelsons pediatric, 19th edition
Pathogenesis & organ response

Micorcirculation
CO < vascular resistance > maintain systemic pressure
sustain adequate perfusion (brain & heart)

Vasodilators (prostacyclin, NO, adenosine) VS vasoconstrictors
(nor-/epinephrine, angiotensin II, vasopressin, endothelin-1,
tromboxane A2) maintain microcirculation
If there is imbalance SHOCK derangement of cellular
metabolism organ failure
If MAP < 60 mmHg organs falls & deteriorates
Cellular response
Transport of nutrients < mitochondrial dysfunction and
uncoupling of oxidative phosphorylation intracellular highenergy phosphate <
Hydrogen ion, lactate, other anaerobic metabolism product
(vasodilator metabolites) > further hypotension and

hypoperfusion
homeostasis of calcium via membrane channels is lost flooding of
calcium intracellularly + extracellular hypocalcemia
Normal cellular transmembrane potential < intracellular sodium
and water > cell swelling interferes further with microvascular
perfusion
selective apoptotic (programmed cell-death) loss of cells
organ & immune failure
Neuroendocrine response
Hypotension vasomotor center >
Adrenergic > norepinephrine > peripheral and splanchnic
vasoconstriction maintain central organ perfusion
Vagal < heart rate and cardiac output >
Severe pain / stresses

ACTH > cortisol > peripheral uptake of glucose and amino acids
<, lipolysis >, gluconeogenesis >
Glucagon > gluconeogenesis > blood glucose concentration >
Adrenergic discharge + perfusion of the juxtaglomerular
apparatus <
Renin release > angiotensin I angiotensin II aldosterone >
maintenance of intravascular volume
Vasopresin vasoconstriction + water reabsorption >
Cardiovascular response
Hypovolemia preload < SV <
Compensatory mechanism to maintain CO: HR >
Myocardial compliance < ventricular end-diastolic volume <
stroke volume < & filling pressure > brain natriuretic

peptide > sodium secretion > relieve the pressure on the
heart
Ventricular ejection < systemic vascular resistance >

Active venoconstriction (consequence of a-adrenergic activity)
maintenance of venous return & ventricular filling
Pulmonary response
relative increase in pulmonary vascular resistance (septic
shock), exceed systemic vascular resistance right heart

failure
Shock-induced tachypnea tidal volume < & minute
ventilation >
Relative hypoxia & tachypnea respiratory alkalosis
Pain functional residual capacity < atelectasis
Renal response
e/ early aggressive volume repletion serious complication of
shock and hypoperfusion

Hypoperfusion renal blood flow < + afferent arteriolar
resistance for diminished GFR > + aldosterone & vasopresin >
conserve salt & water (urine <)
Metabolic derangements
disruption of the normal cycles of carbohydrate, lipid, and
protein metabolism
Oxygen hepatic production of glucose > pyruvate & lactate >
clearance of exogenous triglycerides < + hepatic lipogenesis >
serum trygliceride concentration >
protein catabolism > negative nitrogen balance muscle wasting
Inflammatory response
Nelsons pediatric, 19 th edition
Signs & symptoms
Buku saku pelayanan kesehatan anak di rumah sakit,

WHO, 2009
DD
Pocket book of hospital care for children, 2nd edition,

WHO, 2013
Monitoring & treament
Nelsons pediatric 19 th edition
Nelsons pediatric 19th edition

WHO, 2009

WHO, 2009

WHO, 2009

WHO, 2013

WHO, 2013

WHO, 2013
NEUROGENIC SHOCK
Neurogenic shock
Definition
Kondisi medis yang ditandai dengan ketidakcukupan aliran
darah ke tubuh yang disebabkan karena gangguan sistem
saraf yang mengendalikan konstriksi dari pembuluh
pembuluh darah.
Etiology
Interruption of sympathetic vasomotor input after
a high cervical spinal cord injury
inadvertent cephalad migration of spinal anesthesia
devastating head injury
arteriolar dilation + venodilation pooling in the
venous system venous return and cardiac output <
Signs and symptomps

Kulit hangat dan kering
Kecemasan
Kehilangan kesadaran
Menderita hipotensi
Menunjukkan gejala gejala hipotermia
Sesak nafas
Treatment
Excessive volumes of fluid + norepinephrine or a pure
-adrenergic agent (phenylephrine) if hemorrhage has been
ruled out
Complication
Perkembangan kegagalan organ
Kematian dini
HYPOADRENAL SHOCK
Hypoadrenal shock
Etiology
illness or major surgery
consequence of the chronic administration of high doses of
exogenous glucocorticoids
trauma and sepsis
secondary to idiopathicatrophy
etomidate for intubation, tuberculosis, metastatic disease,
bilateral hemorrhage, and amyloidosis
Characteristics
loss of homeostasis with reductions in systemic vascular
resistance, hypovolemia, and reduced cardiac output
Diagnostic
means of an ACTH stimulation test but is inconsistent
Treatment
persistently hemodynamically unstable patient
dexamethasone sodium phosphate, 4 mg intravenously
absolute or relative adrenal insufficiency is established as
shown by nonresponse to corticotropin stimulation (cortisol

<= 9uL/dL
hydrocortisone, 100 mg every 68 h, and tapered as the
patient achieves hemodynamic stability

volume resuscitation + pressor support
TRAUMATIC SHOCK
Traumatic shock
Etiology
Hemorrhage
even when hemorrhage has been controlled, loss of plasma
volume into the interstitium of injured tissues can be still

happening
e/ injury-induced inflammatory responses that which contribute to the
secondary microcirculatory injury, induced by DAMPs released from
injured tissue
Treatment
"ABCs" of resuscitation
Control of ongoing hemorrhage immediately
Early stabilization of fractures, debridement of devitalized or
contaminated tissues, and evacuation of hematomata
Supplementation of depleted endogenous antioxidants
HYPOVOLEMIC SHOCK
Hypovolemic shock
Etiology
loss of red blood cell mass and plasma from hemorrhage
loss of plasma volume alone due to extravascular fluid
sequestration or GI, urinary, and insensible losses
Diagnosis
signs of hemodynamic instability + obvious source of
volume loss
Difficult diagnosis if the source of blood loss is occult
GI tract, or when plasma volume alone is depleted
Sign & symptoms

Severe classic signs of shock
blood pressure declines and becomes unstable even in the
supine position
mental obtundation is an ominous clinical sign
Treatment
Volume resuscitation isotonic saline / Ringer's lactate
23 L of salt solution over 2030 min
severe traumatic brain injury (TBI) small volumes of
hypertonic saline
Continuing acute blood loss + Hb <= 10 g/dL blood
transf
Administration of fresh-frozen plasma (FFP) and platelets,
packed red blood cells (PRBCs)
Extreme emergencies type-specific or O-negative
packed red cells
norepinephrine, vasopressin, or dopamine may be required
ONLY IF blood volume has been restored
Supplemental oxygen + intubation
CARDIOGENIC SHOCK
Cardiogenic shock &

pulmonary edema
life-threatening conditions that should be
treated as medical emergencies

Etiology
severe left ventricular (LV) dysfunction pulmonary
congestion and/or systemic hypoperfusion
Cardiogenic shock
systemic hypoperfusion due to severe depression
of the cardiac index [<2.2 (L/min)/m2]

sustained systolic arterial hypotension (<90
mmHg)
elevated filling pressure [pulmonary capillary
wedge pressure (PCWP) > 18 mmHg]
Most common etiologies
acute myocardial infarction
cardiomyopathy or myocarditis
cardiac tamponade
Other etiologies
Post cardiac arrest
Refractory sustained
tacchyarrhythmias
Pulmonary embolus
Severe valvular heart
disease
Critical aortic / mitral
stenosis
Acute severe aortic /
mitral regurgitation
RV failure
Refractory sustained
bradyarrhythmias
Toxic metabolic
Beta blocker/CCB
overdose
Severe acidosis &
hypoxemia
Incidence
leading cause of death of patients hospitalized with MI
LV failure accounts for ~80% of the cases of CS complicating
acute MI
fell from 20% in the 1960s but has plateaued at ~8% for
>20 years
typically associated with ST elevation MI (STEMI)
Pathophysiology
Large infarctions and
shock SIRS
Inflammatory cytokines,
inducible nitric oxide

synthase shock
Pump failure
Poor tissue perfusion
lactic acidosis
Pulmonary edema
hypoxemia
vicious cycle of
worsening MI &
hypotension
Risk factors
acute MI
older age
female sex
prior MI
diabetes
anterior MI location
reinfarction soon after
MI
Timing
1/4 of MI patients
develop CS rapidly
(within 6 hour of MI
onset)
3/4 later on the 1st
day
Subsequent onset of
CS
reinfarction,
marked infarct
expansion,
a mechanical
complication
Clinical findings
Continuing chest pain &
dyspnea
Pale, apprehensive,
diaphoretic
Altered consciousness
weak and rapid pulse
90110 beats/min
Systolic BP <90 mmHg
+ narrow pulse pressure

(<30 mmHg)
quiet precordium +
weak apical pulse
Tachypnea, Cheyne
Stokes respirations
jugular venous distention
S1 is usually soft, and an
S3 gallop may be audible
Acute, severe MR and
VSR systolic murmurs
LV failure causing CS
rales
Oliguria
urine output < 30 mL/h
ECG
Laboratory findings
WBC count > with left
shift
BUN & creatinin >>
Hepatic transaminase
>>
Lactic acid >
Arterial blood gases
hypoxemia and
metabolic acidosis
creatine
phosphokinase,
troponin I & T >
acute MI with LV
failure
Q waves and/or >2-mm
ST elevation in multiple
leads
LBBB
1,5 of infarct
anterior
severe left main
stenosis global
ischemia
severe (e.g., >3 mm)
ST depressions in
multiple leads
Chest X ray
pulmonary vascular
congestion
pulmonary edema
CS results from a first
MI hearts size is
normal
Echocardiogram
left-to-right shunt in
patients with VSR

Pulmonary embolism
Proximal aortic
dissection with aortic
regurgitation or
tamponade
Pulmonary artery catheterization
Prognosis
wide range of expected death rates
age, severity of hemodynamic abnormalities, severity of the
clinical manifestations of hypoperfusion, and the performance

of early revascularization
Independent risk factors
advanced age; depressed cardiac index, ejection fraction, and
BP; more extensive coronary artery disease; and renal

insufficiency
Pulmonary edema
Etiology
Cardiogenic & non
cardiogenic
Pathophysiology (cardiogenic)
Cardiac abnormality pulmonary venous & hydrostatic
pressure > fluids exit the capillary interstitial &
alveolar edema pleural effusion breathing discomfort
Clinical findings
rapid onset of dyspnea at rest, tachypnea, tachycardia,
and severe hypoxemia
Rales and wheezing
due to airway compression from peribronchial cuffing
Hypertension
due to release of endogenous catecholamines
Other examinations
Echocardiography
systolic and diastolic ventricular dysfunction and valvular lesions
Electrocardiography
ST elevation and evolving Q waves is usually diagnostic of acute
MI
Brain natriuretic peptide levels > heart failure as the
etiology
X ray
peribronchial thickening, prominent vascular markings in the
upper lung zones, and Kerley B lines

patchy alveolar filling (in perihilar distribution) diffuse alveolar
infiltrates
Swan-Ganz catheter
high pressure PCWP
Treatment
Oksigen therapy
Positive pressure ventilation
Diuretics
Furosemide <=0.5 mg/kg
Nitrates
Sublingual nitroglycerin (0.4 mg x 3 every 5 min) IV
nitroglycerin, commencing at 510 ug/min

Morphine
2- to 4-mg IV boluses
ACE-I
A low dose of a short-acting agent may be initiated and
followed by increasing oral doses
Other Preload-Reducing Agents

IV recombinant brain natriuretic peptide (nesiritide) potent
vasodilator + diuretic (refractory patients & not recommended

in ischemia or MI)
Physical Methods
Patients without hypotension should be maintained in the
sitting position with the legs dangling along the side of the bed
Inotropic and Inodilator Drugs
dopamine and dobutamine
bipyridine phosphodiesterase-3 inhibitors (inodilators)
milrinone (50 g/kg followed by 0.250.75 ug/kg per min) stimulate
myocardial contractility + peripheral and pulmonary vasodilation
Digitalis Glycosides
rarely used at present
Intraaortic Counterpulsation
IABP
Treatment of Tachyarrhythmias and Atrial-Ventricular
Resynchronization
a primary tachyarrhythmia may require cardioversion
patients with reduced LV function and without atrial contraction
/ with lack of synchronized atrioventricular contraction

atrioventricular sequential pacemaker
Stimulation of Alveolar Fluid Clearance
IV Beta-adrenergic agonist treatment decreases extravascular
lung water
Comprehensive cardiogenic
shock
Etiology
Extrinsic compression
tension pneumothorax,
herniation of abdominal viscera through a diaphragmatic
hernia,
excessive positive-pressure ventilation to support pulmonary
function,
cardiac tamponade
heart and surrounding structures are less compliant
inadequate diastolic filling and stroke volume
Diagnosis
clinical findings, the chest radiograph, and an
echocardiogram
Cardiac tamponade
Signs & symptoms
Hypotension
neck vein distention
muffled heart sounds
pulsus paradoxus
an inspiratory reduction in systolic pressure >10 mmHg
Diagnosis
echocardiography
Treatment
immediate pericardiocentesis or open subxiphoid pericardial
window
Tension pneumothorax
Signs & symptoms
ipsilateral decreased breath sounds
tracheal deviation away from the affected thorax
jugular venous distention
Radiographic findings
intrathoracic volume >
depression of the diaphragm of the affected hemithorax
shifting of the mediastinum to the contralateral side
Treatment
Chest decompresion
Large bore needle inserted into the pleural space through the
second anterior intercostal space
SEPSIS & SEPTIC

SHOCK
Sepsis & septic shock

SIRS
2/more of
fever (oral temperature >38C) or hypothermia (<36C)
tachypnea (>24 breaths/min)
tachycardia (heart rate >90 beats/min)
leukocytosis (>12,000/L), leucopenia (<4,000/L), or >10% bands
Sepsis
SIRS that has a proven or suspected microbial etiology
Septic shock
Sepsis with hypotension (arterial blood pressure <90 mmHg
systolic, or 40 mmHg less than patient's normal blood
pressure) for at least 1 h despite adequate fluid resuscitation
Etiology
Pathophysiology
Clinical manifestations
Hyperventilation
Disorientation, confusion, and other manifestations of
encephalopathy
in the elderly and in individuals with preexisting neurologic
impairment
Cellulitis, pustules, bullae, or hemorrhagic lesions
develop when hematogenous bacteria or fungi seed the skin or
underlying soft tissue/the effect of bacterial toxins

Hypotension and DIC predispose to acrocyanosis and
ischemic necrosis of peripheral tissues

nausea, vomiting, diarrhea, and ileus acute
gastroenteritis
Clinical manifestations in children

Primary
fever, shaking chills, hyperventilation, tachycardia, hypothermia
cutaneous lesions
petechiae, ecchymoses, ecthyma gangrenosum, diffuse erythema
changes in mental status
confusion, agitation, anxiety, excitation, lethargy, obtundation, or coma
Secondary
hypotension, cyanosis
symmetric peripheral gangrene (purpura fulminans)
oliguria or anuria
jaundice (direct hyperbilirubinemia)
Signs of heart failure
evidence of focal infection such as meningitis, pneumonia,
arthritis, cellulitis, or pyelonephritis
Laboratory findings
Blood lactate levels > early
accumulation of lactate metabolic acidosis (with increased
anion gap)
increased glycolysis
impaired clearance of the resulting lactate and pyruvate by the
liver and kidneys
blood glucose concentration >
Patients with DM
Hypoglicemia
impaired gluconeogenesis
excessive insulin release on occasion
Cytokine acute phase response
inhibits the synthesis of transthyretin
C-reactive protein, fibrinogen, and complement components >
leukocytosis with a left shift, thrombocytopenia,
hyperbilirubinemia, and proteinuria

thrombocytopenia worsens
prolongation of the thrombin time, decreased fibrinogen, and
the presence of d-dimers suggesting DIC

levels of aminotransferases >, azotemia and
hyperbilirubinemia become more prominent

Hyperventilation respiratory alkalosis
Other examinations
Chest radiograph
normal or may show evidence of underlying pneumonia,
volume overload, or the diffuse infiltrates of ARDS

ECG
Tachycardia & nonspecific STT-wave abnormalities
Major complications
Cardiopulmonary
Ventilation-perfusion mismatching fall in arterial PO2 early
generalized maldistribution of blood flow and blood volume
and from hypovolemia Sepsis-induced hypotension

Depression of myocardial function
Adrenal insufficiency
hypotension that is refractory to fluid replacement and requires
pressor therapy
Renal complications
Oliguria, azotemia, proteinuria, and nonspecific urinary casts
Coagulopathy
Thrombocytopenia & DIC
Neurologic complications
Treatment
Antimicrobial agents
Removal of the source of infections

lungs, abdomen, and urinary tract
Indwelling IV or arterial catheters should be removed
Hemodynamic, Respiratory, and Metabolic Support

IV fluids 12 L of normal saline over 12 h
central venous pressure should be maintained at 812 cmH 2O
avoid pulmonary edema

urine output (kept at >0.5 mL/kg per hour) with fluid
administration
mean arterial blood pressure of >65 mmHg (systolic pressure >90
mmHg)
Ventilator therapy
If hypoxemia, hypercapnia, neurologic deterioration, or respiratory
muscle failure
Erythrocyte transfusion if blood hemoglobin level <= 7 g/dL
General support
nutritional supplementation
reduce the impact of protein hypercatabolism
Prophylactic heparinization to prevent deep venous thrombosis

If not have active bleeding or coagulopathy
tight control of the blood glucose concentration in recovery
from critical illness

insulin only if it is needed to maintain the blood glucose
concentration below 150 mg/dL
must be monitored frequently (every 12 h) for hypoglycemia
Prognosis
2035% of patients with severe sepsis and 4060% of
patients with septic shock die within 30 days
Others die within the ensuing 6 months
result from poorly controlled infection, immunosuppression,
complications of intensive care, failure of multiple organs, or

the patient's underlying disease
Prevention
Most are complications of nosocomial infections
reducing the number of invasive procedures undertaken
limiting the use (and duration of use) of indwelling vascular
and bladder catheters

reducing the incidence and duration of profound neutropenia
(<500 neutrophils/ul)
treating localized nosocomial infections
ANAPHYLAXIS SHOCK
Anaphylaxis shock
life-threatening response of a sensitized human
appears within minutes after systemic exposure to

specific antigen
intense bronchospasm, vascular collapse, & shock
Cutaneous manifestations
pruritus and urticaria with or without angioedema
GI manifestations
nausea, vomiting, crampy abdominal pain, and diarrhea
Etiology
antibiotics
penicillins, cephalosporins, amphotericin B, nitrofurantoin,
quinolones
pollen extracts
ragweed, grass, trees
nonpollen allergen extracts
dust mites, dander of cats, dogs, horses, and laboratory
animals
Food
peanuts, milk, eggs, seafood, nuts, grains, beans, gelatin in
capsules
occupation-related products (latex rubber products)
Pathophysiology & manifestations

differ in the time of appearance of symptoms and signs
hallmark of the anaphylactic reaction is the onset of some
manifestation within seconds to minutes after introduction

Laryngeal edema
"lump" in the throat, hoarseness, or stridor
feeling of tightness in the chest and/or audible wheezing
(bronchial obstruction)
Secretions >, peribronchial congestion, submucosal edema,
and eosinophilic infiltration, and the acute emphysema (severe
cases)
diffuse erythema and a feeling of warmth
Urticarial eruption + pruritus
Diagnosis
onset of symptoms and signs within minutes after the
responsible material is encountered
immunoassays using purified antigens
presence of specific IgE in the serum of patients with
anaphylactic reactions
intracutaneous skin testing
elicit a local wheal and flare in response to the putative
antigen
mast cell activation in a systemic reaction tryptase
levels in serum >
Treatment
0.3 to 0.5 mL of 1:1000 (1 mg/mL) epinephrine SC or IM
repeated doses as required at 5- to 20-min intervals for a
severe reaction
if intractable hypotension occurs
2.5 mL epinephrine, diluted 1:10,000, at 5- to 10-min intervals
IV infusion + normal saline + vasopressor agents (dopamine)

If hypoxia develops
Oxygen alone via a nasal catheter or with nebulized albuterol
+ endotracheal intubation or a tracheostomy

Ancillary agents
antihistamine diphenhydramine, 50-100 mg IM or IV
aminophylline, 0.25-0.5 g IV
References
Longo D, Fauci AS, Kasper D, Hauser S, Jameson JL,
Loscalzo J, editors. Harrisons Principles of Internal

Medicine. 18th edition. New York: The McGraw-Hills;
2012
Kliegman RM, Behrman RE, Jenson HB, Stanton BF.
Nelsons textbook of pediatric, 19th edition.
Philadelphia: WB Saunders Company; 2011
Buku saku pelayanan kesehatan anak di rumah
sakit, WHO, 2009
Pocket book of hospital care for children, 2nd
edition, WHO, 2013

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PROBLEM 2A

Harrison's principles of internal medicine, 18th

associated molecular patterns further compromise

leads to a vicious cycle

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Nelsons pediatric, 19th edition

Harrison's principles of internal medicine, 18th

Pathogenesis & organ response

sustain adequate perfusion (brain & heart)

If MAP < 60 mmHg organs falls & deteriorates

Harrison's principles of internal medicine, 18th

uncoupling of oxidative phosphorylation intracellular highenergy phosphate <

Hydrogen ion, lactate, other anaerobic metabolism product

(vasodilator metabolites) > further hypotension and

organ & immune failure

Harrison's principles of internal medicine, 18th

Severe pain / stresses

Harrison's principles of internal medicine, 18th

Myocardial compliance < ventricular end-diastolic volume <

stroke volume < & filling pressure > brain natriuretic

Ventricular ejection < systemic vascular resistance >

maintenance of venous return & ventricular filling

Harrison's principles of internal medicine, 18th

shock), exceed systemic vascular resistance right heart

shock and hypoperfusion

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Nelsons pediatric, 19 th edition

Nelsons pediatric, 19 th edition

Signs & symptoms

Buku saku pelayanan kesehatan anak di rumah sakit,

Pocket book of hospital care for children, 2nd edition,

Harrison's principles of internal medicine, 18th

Monitoring & treament

Harrison's principles of internal medicine, 18th

Nelsons pediatric 19 th edition

Nelsons pediatric 19th edition

Nelsons pediatric 19th edition

Nelsons pediatric 19th edition

Buku saku pelayanan kesehatan anak di rumah sakit,

Buku saku pelayanan kesehatan anak di rumah sakit,

Buku saku pelayanan kesehatan anak di rumah sakit,

Pocket book of hospital care for children, 2nd edition,

Pocket book of hospital care for children, 2nd edition,

Pocket book of hospital care for children, 2nd edition,

Harrison's principles of internal medicine, 18th

arteriolar dilation + venodilation pooling in the

venous system venous return and cardiac output <

Signs and symptomps

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

absolute or relative adrenal insufficiency is established as

shown by nonresponse to corticotropin stimulation (cortisol

patient achieves hemodynamic stability

Harrison's principles of internal medicine, 18th

volume into the interstitium of injured tissues can be still

Harrison's principles of internal medicine, 18th

Harrison's principles of internal medicine, 18th

Sign & symptoms

Harrison's principles of internal medicine, 18th

Supplemental oxygen + intubation

Harrison's principles of internal medicine, 18th

Cardiogenic shock &