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Pemicu 2 KGD
Septiany Indahsari
405100244
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Neurogenic shock is shock caused by the sudden loss of the
sympathetic nervous system signals to the smooth muscle in
vessel walls.
This can result from severe central nervous system (brain andspinal cord) damage. With the sudden loss of background
sympathetic stimulation, the vessels suddenly relax resulting
in a sudden decrease in peripheral vascular resistance and
decreased blood pressure. Conditions in which Neurogenic shock can occur include spinal anesthesia,
emotional stress, drugs that inhibit the sympathetic nervous
system, spinal injury etc.
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Causes of neurogenic shock
Trauma to the spinal cord which may be apenetrating or blunt injury. Injury to the spinalcord in the neck causes extremely severe
symptoms while injury in the thoracic orlumbar spine causes less severe symptoms.
Regional anaesthesia if improperly given canlead to neurogenic shock.
Drugs that affect the autonomic nervoussystem
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NEUROGENIC
SHOCK
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Reduction in sympathetic vasomotor activitye.g. spinal cord injury results in loss ofsympathetic output
>> Loss of vascular tone>> REDUCED vascular resistance>> REDUCED Arterial pressure due to
vasodilation>> Decreased Perfusion (delivery of blood) ofvital organs
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Hemodynamic phenomenon-
Loss of vasomotor tone& Loss of sympathetic nervous
system tone > inpaired cellular metabolism
Mekanisme utama: vasodilatasi perifer disertai penimbunan darah
Occurs
Within 30 min cord injury level T 5 or above; last up to 6 weeks;
also due to effect some drugs that effect vasomotor center of
medulla as opioids, benzodiazepines
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*Critical features-
Hypotension(due to massive vasodilation)
Bradycardia- due to unopposed paraynmpathetic stimulation
Poikilothermia;*Unable to regulate temperature. The limbs arewarm while the rest of the body is cold, the patient may feel very cold
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Diagnosis of neurogenic shock
A thorough history must be taken, and road traffic accident,
adventure sports such as playing a contact sport should lead
the physician to suspect injury to the spinal cordand
consequently, neurogenic shock.
Investigations to diagnose neurogenic shock
All emergency blood, urine investigations should be carried
out immediately.
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Treatment of neurogenic shock
Firstly, the patients condition should be stabilised by paying
attention to the airway, breathing and circulation. The spine
should be immobilised to avoid further damage.
The blood pressure should be brought up by giving intravenous
fluids and drugs like dopamine and dobutamine. In severebradycardia, a drug called atropine can be given.
Intravenous steroids should be started if neurological signs are
seen.
A neurologist or an orthopaedic surgeon should assess theinjury, and if needed, surgery should be undertaken in a well-
equipped hospital with intensive care facilities available.
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Management (*Determine underlying cause)
Airway support
Fluids as needed- Typically 0.9 NS , rate depends upon need,to restore normal hemodynamics
Atropine for bradycardia (speeds up heart rate and CardiacOutput)
Vasopressors as phenylelphrine(Neo-synephrine) for BP
support
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Syok Hipovolemik
Terganggunya sistem sirkulasi akibat dari volume darah dalam
pembuluh darah yang berkurang
Bisa terjadi akibat perdarahan masif atau kehilangan plasma
darah Penurunan perfusi dan oksigenisasi jaringan
Respon terhadap hilangnya darah akut dipengaruhi oleh
faktor:
Usia
Keadaan kesehatan
Obat-obatan
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ETIOLOGI
Perdarahan
Hematoma subkapsular hati
Aneurisma aorta pecah
Perdarahan gastrointestinal Perlukaan berganda
Kehilangan plasma
Luka bakar luas
Pankreatitis Deskuamasi kulit
Sindrom dumping
Kehilangan cairan
ekstraseluler
Muntah
Dehidrasi Diare
Terapidiuretik yang sangat
agresif
Diabetes insipidus
Insufisiensi adrenal
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GEJALA KLINIS Pemeriksaan fisik:
Hipotensi
Takikardia
Penurunan status mental
Produksi urin sedikit
Tanda-tanda nyata trauma atau perdarahan Pasien dapat datang dengan:
Gawat napas
Penurunan bunyi napas
Perkusi redup
Distensi abdomen
Nyeri tekan difus
Peritonitis
Ekimosis pinggangpada cedera pelvis
yang menunjukkan cedera pada toraks
Cedera abdomen
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Terapi cairan
Peningkatan kapasitas vaskular (pe aliran balik vena)
Dehidrasi (krn asupan menurun, kehilangan cairan melalui pernapasan / keringat)Terjadi perdarahan dan kebocoran kapiler
Hipovolemik
G3 transport O2 &nutrisi ke jaringan
Hipotensi & syok
Pemberian cairan:
Kristaloid (Nacl 0.9% / RL)
Koloid (albumin)mempertahankan
tekanan onkotik plasma
Transfusi eritrositdipertahankan pada batas >8-10g/dL
Dimonitor
kecukupannya
Kristaloid pilihanpada terapi awal,
o.k:
Murah dan
mudah didapat
Tapi, perlu diberidgn volume besar
Penilaian kecukupan pemberian cairan melalui :
Pe tekanan darah, pe frekuensi jantung,
kecukupan isi nadi
Perabaan kulit & ekstremitas
Produksi urin
Membaiknya pe kesdaran
Tekanan vena sentral, tekanan arteripulmonalis
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shock hipovolemic
Inadequate supply of blood flow to tissues to
meet the demands of the tissues
Nutrient requirements are not fulfilled.
Toxic metabolites are not removed.
If untreated, inevitable progression from
inadequate perfusion to organ dysfunction
and ultimately to death.
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Main components of blood flow:
Cardiac output
Blood volume
Peripheral resistance of arteriolar and venous
system (systemic vascular resistance [SVR])
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Major categories of Hypovolemic shock:
Decreased blood volume
Suspect hemorrhage if acute onset
Severe dehydration if progressive onset and elevatedhematocrit, blood urea nitrogen, and creatinine
Decrease in cardiac output leads to compensatory
increase of the SVR in an attempt to normalize
perfusion pressure.
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Signs and Symptoms
Generalized shock:
Hypotension
Decreased peripheral pulses
Tachycardia Tachypnea
Decreased urine output
Diaphoresis Obtundation
Lethargy
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Hypovolemic shock:
Cold and clammy extremities
Pallor
Flattened neck veins
Decreased capillary refill
Narrowed pulse pressure
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Differential Diagnosis
Hypovolemic shock:
Abdominal trauma, blunt orpenetrating
Abortioncomplete, partial,or inevitable
Anemiachronic or acute
Aneurysmsabdominal,thoracic, dissecting
Aortogastric fistula
Arteriovenous malformations
Blunt trauma
Burns
Diabetes
Diarrhea
Diuretics
Ruptured ectopic pregnancy
Epistaxis
Fractures (especially longbones)
Hemoptysis
Gastrointestinal bleed
Mallory-Weiss tear
Penetrating trauma
Placenta previa Postpartum hemorrhage
Retroperitoneal bleed
Severe ascites
Splenic rupture
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Management
aggressive fluid resuscitation with lactated Ringer
solution or normal saline in all patients with signs
and symptoms of shock, regardless of underlying
cause
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Respond to rescucitation
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Septic shock
Sepsis-induced hypotension despite fluid
resuscitation
Systolic blood pressure (BP) 40 mm Hg from baseline
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Etiology
Gram-negative bacteria most common: Escherichia coli
Pseudomonas aeruginosa
Rickettsiae
Legionella species Gram-positive bacteria:
Enterococcus species
Staphylococcus aureus
Streptococcus pneumoniae Fungi (Candida species)
Viruses
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Etiology
Major causes of pediatric bacterial sepsis
Neisseria meningitis
Streptococcal pneumoniae
Haemophilus influenzae
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Signs and Symptoms
Fever
Tachycardia
Tachypnea
Hypothermia (poor prognosis)
Hypoxemia
Diaphoresis
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Physical Exam
Cardiovascular:
BP
Normal early in sepsis
Hypotension when septic shock occurs
Poor perfusion with septic shock:
Prolonged capillary refill
Cool and clammy extremities
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Gastrointestinal/Genitourinary
Abdominal pain
Nausea, vomiting
Diarrhea
Dysuria/Frequency
Reduced urine output
Abdominal tenderness: Diffuse
Localized to right upper quadrant (liver or gallbladder source)
Right lower quadrant (appendicitis with or without abscess)
Suprapubic area or lower quadrants (urinary tract or pelvic sourceor diverticulitis)
Flank pain: With pyelonephritis or retroperitoneal abscess
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Pulmonary
Shortness of breath
Tachypnea:
Present even when the lungs are not the source of
sepsis Productive cough
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Dermatologic
Any rash is important.
Localized erythema with lymphangitis (streptococcal orstaphylococcal cellulitis)
Rash involving palms of hands and soles of feet (rickettsialinfection)
Petechiae scattered on the torso and extremities(meningococcemia)
Ecthyma gangrenosum (pseudomonas septicemia)
Round, indurated, painless lesion with surrounding
erythema and central necrotic black eschar Decubitus ulcers
Indwelling catheter: Surrounding skin erythematous with or without purulent drainage
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CNS
Change in mental status
Confusion
Delirium
Coma
Neck stiffness (meningitis)
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Lab
Serum lactate:
CBC with differential:
Electrolytes, bloodurea nitrogen,creatinine, glucose:
Ca, Mg, Ph
International
normalizedratio/prothrombintime/partialthromboplastin time
Type and screen
C-reactive protein
Cortisol level
Liver function testsArterial blood gas:
Blood cultures:
Urine analysis and
culture
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Imaging
Chest radiograph:
Soft tissue plain films
CT scan of the abdomen and pelvis
Abdominal ultrasound:
Pelvic ultrasound:
Transesophageal echo:
MRI:
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Diagnostic Procedures/Surgery
Lumbar puncture:
Indicated when meningeal signs are present or
altered mental status without a source of infection
Central venous access:
Central venous pressure (CVP) and ongoing
measurement of central venous oximetry cathetermay be helpful in guiding resuscitation.
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Differential Diagnosis
Pancreatitis Trauma
Toxic shock syndrome
Anaphylaxis Adrenal insufficiency
Drug or toxin reactions
Heavy metal poisoning
Hepatic insufficiency Neurogenic shock
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Treatment
Pre Hospital
Aggressive fluid resuscitation for hypotension
Initial Stabilization
ABCs
Supplemental oxygen to maintain PaO2>60 mm Hg
Intubation and mechanical ventilation if shock or
hypoxia are present
Administer 0.9% NS IV
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ED Treatment
Early goal-directed therapy: 500 cc boluses of 0.9% saline up to 12 liters
empirically
Place central line
Continue 500 cc saline boluses until CVP >8 cm H2O If the mean arterial pressure 8,
then initiate pressors: Dopamine or norepinephrine to raise blood pressure
Norepinephrine is preferred if tachycardia or dysrhythmiasare present.
Phenyl epinephrine for cases where shock is refractory toother pressors
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If the ScvO230, then add dobutamine.
Administer antibiotics early based on the most likelyorganisms or site of infection.
If no source identified after initial assessment: Normal immune function:
Second- or third-generation cephalosporin and gentamicin
Nafcillin and gentamicin
Add vancomycin if there is a history of methicillin resistantstaphylococcus aureous or the patient resides in a nursing facility or
there is a history of recent hospitalizations. Immunocompromised host:
Piperacillin and gentamicin
Ceftazidime and either nafcillin or vancomycin and gentamicin
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If source identified, or highly suspected, treatthe most likely organisms:
Pulmonary source:
Second- or third-generation cephalosporin andgentamicin, and possibly erythromycin
Intra-abdominal source:
Ampicillin and metronidazole and gentamicin
Cefoxitin and gentamicin Urinary tract source:
Ampicillin or piperacillin and gentamicin