Pemicu 2 KGD Septiany

8/10/2019 Pemicu 2 KGD Septiany

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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

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