KULIAH KE 2 IKA – Senin -12/6/2012

1. Pengenalan Tanda2 Perdarahan

Intracranial.
2. Resusitasi Cairan Anak
 HEAD INJURY AND INTRACRANIAL HYPERTENSION
(CEDERA KEPALA dan INTRACRANIAL HYPERTENSI)

Prof dr Hj Rafita Ramayati, SpA(K)

Prof. dr. H. Rusdidjas, SpA(K)
dr. Hj .Oke Rina Ramayani SpA
Medan

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 HEAD INJURY (CEDERA KEPALA)
• Pebyebab terbanyak morbidity and mortality in children
• Penyebab kematian terbanyak pd anak > 1 th ok trauma
• Cedera Kepala penyebab terbanyak kematian ok trauma
– Primary injury
• Kerusakan jaringan ok kekuatan mekanik pd saat awal
– Secondary ischemic injury
• Berhububgan dgn post injury hypotension, hypoxemia, dan
intracranial hypertension

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 ETIOLOGI
• 1).Motor vehicle accidents (kederaann bermotor)
– Responsible for most severe head injuries
• 2). Falls (terjatuh)
– Usually in children < 4 yrs and usually mild
• 3).Recreational activities (aktifitas Rekreasi)
– Half of these are bicycle accidents
• 4), Assault or nonaccidental trauma (bukan kecel’k’n)
– Most head injuries in kids < 1 yr are from falls

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 ANATOMY
• Uniquely susceptible to injury [unik rusak)
• Brain
– Inelastic and noncompressible
– Has no internal support
• Cranium
– Rigid and unyielding after sutures fused
– Bony buttresses at anterior poles and temporal
poles
• Membranous “slings”
– Falx cerebri compartmentalizes R and L
hemispheres
– Tentorium separates infra- and supratentorial
regions

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 MECHANISM OF BRAIN INJURY
• Brain is thrown against bony irregularities or
membranous slings or compressed against
these surfaces by…
– Contact injury
• Head strikes or is struck by an object
– Acceleration/deceleration injury
• Violent head motion causes compressive,
tensile, and shear strain in brain tissue

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 COUP - CONTRECOUP INJURY

LifeArt: Williams & Wilkins

08/24/2020 http://www.lifeart.com 7
 TYPES OF PRIMARY INJURIES

• Focal injuries • Diffuse injuries

– Skull fracture – Diffuse axonal injury
– Parenchymal contusion – Diffuse vascular injury
– Parenchymal laceration
– Vascular injury resulting
in hematoma (subdural,
extradural, or
parenchymal)

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 SKULL FRACTURES
• Most are uncomplicated
• Basilar skull fractures –frac Basis Cranii
– Battles sign, “raccoon eyes” –Hematoma kaca mata
– CSF rhinorrhea, CSF otorrhea possible
– Cranial nerve injury possible
• Depressed skull fractures represent more severe injury
– 1/3 are associated with dural laceration
– 1/3 are associated with cortical laceration
– May require surgical elevation
• Fracture crossing path of major vascular structure
increases risk for significant bleeding
– Middle meningeal artery
– Large dural sinus

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 CONTUSION
•Usually frontal or
temporal lobe
•Small cortical vessels
and neural tissue
damaged
•Damaged vessels may
thombose, leading to
ischemia

WebPath: University of Utah

http://www-medlib.med.utah.edu/WebPath/webpath.html
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 INTRACEREBRAL HEMORRHAGE

•Usually frontal or
temporal lobe
•Can be bilateral
(contracoup injury)
•Can act as mass
lesions and cause
intracranial
hypertension

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 EPIDURAL HEMATOMA
•Usually arterial in origin
•Between skull and dura,
limited by suture lines
•Often from tear in middle
meningeal artery
•Initial injury may seem minor,
followed by “lucid interval,”
then neurologic deterioration
•May expand rapidly and
require emergency
craniotomy
•Lihat mid line “terdorong”
“
WebPath: University of Utah
http://www-medlib.med.utah.edu/WebPath/webpath.html
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 SUBDURAL HEMATOMA
•Usually venous bleeding (bridging
veins)
•On surface of cortex, beneath
dura and outside arachnoid, not
limited by suture lines.
•Typically requires greater force to
produce than epidural hematoma
•Usually associated with severe
parenchymal injury

WebPath: University of Utah

http://www-medlib.med.utah.edu/WebPath/webpath.html
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 . ...... . ..

DIFFUSE BRAIN INJURY

• Diffuse axonal injury
– Usually from rapid acceleration/deceleration
– Shear forces disrupt small axonal pathways
• After disruption, axons degenerate, fragment, then
disappear
• The neurons then undergo Wallerian degeneration
– Spectrum from mild to severe
• Diffuse vascular injury
– Microvasculature more resistant to shear than axons
– Results in multiple small hemorrhages throughout
brain
– Usually seen in fatal head injuries

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 SECONDARY ISCHEMIC BRAIN INJURY

• Compounds the potential for adverse

neurologic outcome
• Caused by:
– Post injury hypotension
– Hypoxemia
– Intracranial hypertension which impairs cerebral
blood flow

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 INTRACRANIAL HYPERTENSION
• Vascular etiologies
– Vasogenic edema
• BBB impaired, protein rich
fluid leaks to ECF
– Hyperemia
• Occurs days 1 to 3 after
injury
– Obstructed venous
drainage
• Hydrostatic pressure
increased, protein poor
fluid leaks into ECF
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• Nonvascular etiologies
– Cytotoxic edema
• Ionic gradients impaired
and cells swell
– Obstruction to CSF outflow
– Hematoma
– Osmotic brain edema
• Decreased osmolality
from iatrogenic
hemodilution or SIADH
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 INTRACRANIAL HYPERTENSION
• Normal intracranial pressure:
– Adults: < 10 mm Hg
– Infants/children: somewhat lower,
depending on age
• Elevated ICP impairs cerebral perfusion
• Risk for herniation with ICP > 40 mm Hg
• Herniation can occur at lower ICP’s when
mass lesion is present

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 MANAGEMENT OF HEAD INJURY
• Goals of resuscitation and treatment is to
minimize secondary ischemic brain injury by
promoting and preserving cerebral perfusion
– Prevent or treat post injury hypotension
– Prevent or treat hypoxemia and reduce oxygen
demand of the brain
– Prevent or treat intracranial hypertension
– Avoid measures that decrease cerebral
perfusion

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 RESUSCITATION
• A, B,C’s
• Major early risk is hypotension
– Adequate fluid resuscitation to restore normal BP
does NOT worsen neurologic outcome
– Avoid hypotonic fluids
• Emergent airway control for
– GCS 8 or less
– GSC 10 or less with abnormal head CT
– Rapid neurologic deterioration
– If needed for other injuries

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 INTUBATION OF PATIENT WITH HEAD INJURY
• Preserve cerebral oxygenation
• Maintain cerebral perfusion
– Adequate analgesia and anxiolysis
– Avoid meds that increase ICP
– Avoid meds that cause hypotension
– Avoid Trendelenburg position
• Avoid aggravating C spine injury
– C-spine injuries in as many as 10% of head
injury patients
– In-line axial stabilization by an assistant
recommended

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DRUGS FOR RAPID SEQUENCE INTUBATION
• Analgesia/sedation
– Fentanyl, etomidate
• little effect on BP
– Thiopental
• decreases ICP but can
drop BP
• Anxiolysis
– Midazolam
• little effect on BP
• Lidocaine IV
• blunts sympathetic
response to intubation
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• Neuromuscular blockade
– Succinyl choline
• short acting
• muscle fasciculations can
increase ICP
• use with defasciculating
dose of nondepolarizing
– Non depolarizing
• vecuronium
• longer acting and no
increase in ICP
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 RULE OUT & PREVENT NEUROSURGICAL
EMERGENCIES
• Head CT as soon as possible
– Initial CT may be normal in severe head injury
– Repeat CT in 12 to 24 hours
• Moderate hyperventilation advisable during
transport and initial evaluation
• If signs of impending herniation develop
(lateralizing signs, pupil asymmetry)
– Hyperventilate
– Give mannitol

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 MONITORING OF INTRACRANIAL PRESSURE
• Ventriculostomy catheter
– Catheter tip in frontal horn of lateral ventricle
– Can drain CSF
– Can be recalibrated as necessary
• Transducer tipped catheter
– Intraparenchymal or subdural
– Cannot drain CSF
– Cannot be recalibrated
– Exhibits drift in values measured over time

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 MONITORING OF INTRACRANIAL PRESSURE

• Indications
– GCS < 8 after resuscitation
– Abnormal head CT
– Rapid neurologic deterioration
• ICP monitoring is continued for as long as
treatment of intracranial hypertension is
required

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 CEREBRAL PERFUSION PRESSURE
• Can be determined from ICP and mean arterial
pressure:
CPP = MAP - ICP
• Calculated CPP does not reflect perfusion of
entire brain
– CPP further decreased in areas of injury
– Factors that cause cerebral vasoconstriction without
lowering MAP result in a falsely low calculated CPP

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 CEREBRAL PERFUSION PRESSURE
• Goal of therapy
CPP > 60 mm Hg if ICP < 22 mm Hg
or
CPP > 70 mm Hg if ICP > 22 mm Hg

– Lowering ICP while maintaining MAP will

increase CPP
– Increasing MAP will increase CPP

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 FACTORS AFFECTING INTRACRANIAL PRESSURE
• Increases ICP • Decreases ICP
– hypercarbia – hyperoxia
– hypoxia (pO2 < 50) – hypothermia
– seizures or shivering – barbiturates
– hyperthermia – hypocapnia
– arousal • via cerebral
• pain, anxiety vasoconstriction
– venous congestion • lowers CPP and is
• fluid overload undesirable
• intrathoracic pressure

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 EFFECT OF pCO2 and pO2 ON CBF AND CPP
• Hypoxia increases CBF by
vasodilation
• Hypercapnia increases CBF
• Hyperventilation and resulting
hypocapnia decrease CBF
– Hyperventilation is
useful to prevent
impending herniation
but will worsen
secondary ischemic
injury

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 MANAGEMENT OF INCREASED ICP
• Head position
– Head elevated 30 degrees and midline
• Sedation and pain control
– Analgesic + anxiolytic
• Fentanyl, morphine, or propofol plus a benzodiazepine
• Continuous infusions or scheduled doses to maintain
sedation
– Watch for and treat hypotension
• Seizure prophylaxis
– Phenytoin or phosphenytoin

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 MANAGEMENT OF INCREASED ICP
• Neuromuscular blockade
– Facilitates mechanical ventilation and control of pCO2
– Prevents shivering
– Use if movement increases ICP
• Temperature control
– A rise in temp of 1o C increases cerebral metabolic
rate by 10%, increasing ICP by several mm Hg
– Maintain temp < 37.5 o C
• Scheduled acetaminophen, body exposure, cooling blanket

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 MANAGEMENT OF INCREASED ICP
• Osmotherapy with mannitol
– Decreases extracellular fluid in brain
– Intermittent doses for ICP spikes or scheduled if elevated ICP
is persistent
– Adverse effects:
• Hypernatremia, hypokalemia
• Hyperosmolality
• Hemodilution and drop in hematocrit
• Hypotension
– Follow serum osmolality and Na
• Hold mannitol if serum osm > 320 mOsm/l

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 MANAGEMENT OF INCREASED ICP
• Drainage of CSF
– Possible if ventricular catheter is in place
– CSF drainage pressure usually set at 20
cm H2O
– CSF drains when ICP exceeds drainage
pressure
– Ventricular catheters cannot be placed if
cerebral edema has obliterated or
significantly compressed ventricles

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 MANAGEMENT OF INCREASED ICP
• Second tier therapies for intracranial hypertension
refractory to sedation, muscle relaxation,
osmotherapy, and moderate hypothermia:
– barbiturate “coma”
– induced hypertension
– decompressive craniotomy
– hypothermia

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 MANAGEMENT OF INCREASED ICP
• Barbiturate “coma”
– ICP control is the principal endpoint
– EEG burst suppression is a useful guide to optimal
barbiturate dosage
• Pentobarbital 10mg/kg followed by infusion at 1
mg/kg/hr, titrated to effect
• May give additional boluses during infusion for
acute spikes in ICP
• Moderate doses cause sluggishly reactive pupils
while large doses may cause mid position to 5 mm
nonreacting pupils
• Watch for hypotension

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 MANAGEMENT OF INCREASED ICP
• Induced hypertension
– Inotropes to increase MAP, even beyond normal for age,
to achieve an optimal CPP
• Dopamine
• Norepineprine
– Rise in ICP in tandem with a rise in MAP implies total loss
of autoregulation and is a poor prognostic sign
• Decompressive craniotomy
– Large portion of cranium removed to allow room for brain
to swell and minimize ischemia
– Dura must be opened as well

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MANAGEMENT OF INCREASED ICP
• Hypothermia
– Core body temp of 32o to 33o C
– Reduced cerebral metabolic activity, reducing ICP
– Also has cytoprotective effects
– Adverse effects
• Arrythmias
• Coagulopathies
• Hypokalemia
• Increased risk of infection

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MANAGEMENT OF OTHER SYSTEMS
• Respiratory
– Maintain normocapnia
• Hyperventilation only appropriate during early diagnosis and
management or if herniation is impending
– Maintain oxygenation
• pO2 > 100 is optimal
– PEEP to maintain alveolar recruitment
• ARDS, neurogenic pulmonary edema frequent complications
• Hypoxemia has more deleterious effects on brain than modest
venous congestion caused by PEEP
• PEEP of 5 to 10 cm H2O not shown to have detrimental effect
on neurologic outcome

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MANAGEMENT OF OTHER SYSTEMS
• Cardiovascular
– Maintain normal blood pressure
• Hypotension significantly reduces CPP
• Inotropes if necessary to maintain normal BP
– Induced hypertension if necessary

• Gastrointestinal
– Stress gastritis prophylaxis with H2 blocker
– Jejunal feeds to maintain healthy intestinal mucosa and prevent
bacterial translocation from gut

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MANAGEMENT OF OTHER SYSTEMS
• Fluids, Electrolytes, Nutrition
– Goal is NORMOVOLEMIA
• Total fluid intake should be @ 100% maintenance
• Bolus as necessary to achieve normal CVP
– Avoid hypotonic fluids
• Lactated Ringer’s and 0.9% saline w/ 20 mEq KCl/l
are good choices for maintenance fluids
– Follow electrolytes closely
• Avoid hyponatremia
• Mannitol can cause electrolyte abnormalities
• Watch for SIADH, diabetes insipidus, cerebral salt
wasting

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MANAGEMENT OF OTHER SYSTEMS
• Fluids, electrolytes, nutrition
– Provide calories to meet metabolic demands of patient
• Increased metabolic demands during acute phase of injury
• Heavily sedated, relaxed, cooled patient has decreased
metabolic demands
• Enteral feedings via nasojejunal catheter preferable to TPN if
gut deemed to be healthy
– Avoid hyperglycemia
• Associated with poor neurologic outcome
• Watch serum glucose closely if dextrose containing fluids used

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MANAGEMENT OF OTHER SYSTEMS
• Renal
– Place foley for strict I’s and O’s
• Hematologic
– Coagulopathy common with head injuries
• Brain derived thromboplastin activator substances
released
– Follow PT/PTT or DIC screens
– Blood component replacement if evidence of active
bleeding or if surgical intervention anticipated
– Maintain normal hematocrit to optimize oxygen delivery

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 MANAGEMENT OF OTHER SYSTEMS
• Endocrine
– DIABETES INSIPIDUS
• Complete or partial failure of ADH secretion from shearing
of pituitary stalk
• Polyuria, hypernatremia, urine osm < plasma osm
• Treatment:
Run maintenance fluids @ 100%
Replace urine output cc for cc with dextrose-containing
fluids
Continuous vasopressin infusion or DDAVP (subQ or
intranasal) q 12 to 24 hrs

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 MANAGEMENT OF OTHER SYSTEMS
• Endocrine
– CEREBRAL SALT-WASTING
• ANP-like substance released from brain, inducing natriuresis
and diuresis

– SIADH
• Elevated level of ADH inappropriate for prevailing osmotic or
volume stimuli
• Hyponatremia, hypo-osmolality, urine osm > plasma osm,
high urine Na
• Treatment is water restriction

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 SUMMARY
• Identify and treat primary brain injury
– Rule out neurosurgical emergency
• Minimize secondary ischemic brain injury by
promoting cerebral perfusion
– Maintain normovolemia and adequate BP
– Maintain normal electrolytes and euglycemia
– Maintain normocapnia and adequate oxygenation
– Avoid factors that increase ICP
– Treat intracranial hypertension

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 TKS

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 Subpokok Bahasan
2. RESUSITASI CAIRAN
PADA ANAK
[vital DEHIDRASI]
Rafita Ramayati, Oke Rina Ramayani
Rusdidjas. Medan

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 PERLU DIKETAHUI
Peny. DIARE penyebab Dehidrasi
Indonesia Juara 3 diare di Dunia
(Juara 1 Guatemala, 2. Banglades)
 Penyebab Dehidrasi
Kekurangan cairan tubuh

• Diare / Muntah Mecet (Terbanyak)

• Kurang Input cairan (Makan / Minum)
• Pernafan yang cepat / dalam
• Panas tinggi
• Luka bakar
• dll

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 TANDA KLINIS
(Klasifikasi DEHIDRASI: WHO/DepKes 1992)

• Dulu : Ringan
• : Sedang
• : Berat
• Sekarang : Tanpa Dehidrasi (No Dehydr.)
• : Ringan/Sedang (Some Dehydr.)
• : Berat (Severe Dehydr.)

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 TANDA KLINIS DEHIDRASI .....
• Kead.Umum Baik/ *Geiisah/ *Lemas/
Sadar Rewel Lesu/ tak
Sadar
• Mata Normal Kering Sangat K
• Bibir Normal Kering Sangat K
• Lidah Basah Kering Sangat K
• Rasa Haus Biasa *Haus *Tak bisa/
Tidak ha Ingin Mi> Tak mau mi
• Turgor kulit Cepat *Lambat *Sangat L
• Dikatakan Tanpa D D. R/S D. Berat
=1* + td L =1* + td L
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 PENGOBATAN DEHIDRASI
• TANPA D [Rencana Pengobatan A]
• MINUM CUKUP: CRT(Cairan Rumah Tangga):
kuah soup, saur bening air kelapa, Lar GG, Oralit,
Pharolit, Pedialyt, Minum sepuasnya
• Kl masih ASI diteruskan, Kalau PASI diencerkan ½
kali
• Kl sudah makan, beri makanan lembik, tidak
merangsang, porsi kecil ulang2.
• Kalau masih sakit kembali kesarana kes.
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 RENACANA PENGOBATAN
SETELAH REHIDRASI
A B C
TANPA D. D-R/S D-B
A B C

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 Rencana Pengobotan A
• Aman bila diberikan dlm jumlah besar
• Mudah menyiapkannya
• Dapat diterima anak
• Efektif
• Mis. CRT (kuah soup, kuah sayur bening air tajin, air
kelapa, larutan gula- garam. Atau sedian yg sudah ada :
Oralit, Renalit, Pharolit, Pedialit
HARUS DILAKUKAN KIE + PUJIAN
(Koordinasi, Informasi dan Edukasi)

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 RENCANA PENGOBATAN B
• A. Bila BB tidak diketahui : RUMUS 300.
(Harus dihabiskan dalam 4 jam)
• Umur < 1Thn 1-5 Thn > 5 Thn Dewasa
• Jml 300 ml 600 ml 1200 ml 2400

• Kalau BB diketahui = BB Kg x 75 ml
(Habis diberikan dlm 4 jam)

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RENCANA PENGOBATAN B utk Dehidrasi R/S.

• A. Bila BB tidak diketahui : RUMUS 300.

(Harus dihabiskan dalam 4 jam)
• Umur < 1Thn 1-5 Thn > 5 Thn Dewasa
• Jml 300 ml 600 ml 1200 ml 2400

• Kalau BB diketahui = BB Kg x 75 ml
(Habis diberikan dlm 4 jam)

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 RENCANA PENGOBATAN C
• HARUS SEGERA DIBERIKAN SECARA IV
(Emergency)
• Umur Pemberian I Kemudian

30 ml/Kg 70 ml/Kg
< 12 bln ( 1 Jam ) ( 5 Jam )

> 12 bln ( ½ Jam ) ( 2½ Jam)

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 Conto anak <12 bln D-Berat
dgn BB 10 Kg
Pemberian 1 10 x 30 ml = 300 ml (1 jam)
Kemudian 10 x 70 ml = 700 ml (5 jam)
1000 ml
Anak rehidrasi ( 1 + 5 = 6 jam) dan cairan
yang habis = 1000 ml. BB anak naik menjadi
10 Kg + 1 Kg = 11 Kg
( 1000 ml cairan = 1 Kg)
(Anak dimonitor tiap 1 jam Sampai Rehidrasi
TANDA BINTANGNYA TIDAK ADA LAGI.

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 Kententuan :
• 1 ml = 20 tetes makro
• = 60 tetes mikro
• 1000 ml = ± 1 Kg
• Kecepatan tetesan ivfd:
? tetes makro / min
? tetes mikro / min

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• Contoh soal
• Bila seorang anak usia 11 bulan BB 10 Kg dengan
dehid.berat datang ke RS. Diobati sesuai
• WHO/DapKes.
• Berapa BBnya sesudah 7 jam IVFD?
• Berapa kecepatan cairan pada jam pertama?
• Berapa kecepatan cairan pada jam ke 6’ ?

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Gunakan grid waktu!
10 Kg
Ren A -B I---------!-----’-----’-----’-----’-----’-----’------’------’----I

1 jam 5 jam 4 jam

30 70 75 ml/Kg
300 700 11 x 75 = 825
jml cairan 1+5 jam = 1000 ml = 1 Kg
BB sesudah Ren C = 10 + 1 = 11 Kg

BB sesudah 7 jam = 11 + ¼ x 825 = 11 + 0. 20625 =

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TKS

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