Critical care to head injured patient
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Transcript of Critical care to head injured patient
ผศ.ดร.กรองได อุณหสูต
คณะพยาบาลศาสตร ์มหาวิทยาลัยมหิดล
Critical care to
Head-Injured Patient
Brain tissue injury
Inflammatory & cerebral edema
Brain tissue
hypoxia CBF ICP vasodilation
Cell death
Necrotic
tissue
edema
Vasodilation ICP from
Blood volume
Further
ICP
Herniation &
compress
brain stem
Accumulate
CO2
Death
CBF
24-48 hours after injury,
CBF to base line
The brain is already swollen
Cause exacerbate neuronal injury
ผศ.ดร.กรองได อุณหสตู
Severe TBI (GCS = 3-8)
obtain CT brain
secondary insult; hypotension, hypoxia
1survey &
resuscitation
Assess GCS, pupil,
motor response
Monitor : V/S, N/S, GCS
Re-assess
Airway & breathing
Assisting in ET intubation
Monitoring blood gas
Monitoring O2 sat
Circulation
Volume replacement
Assisting in FAST, DPL
IV fluid
Monitor : V/S, LOC
Neurological
examination
2survey &
management
Assess GCS, pupil
reaction, lateralization,
Assess herniation
Repeated CT scan
Assisting in diagnostic
test, surgical treatment
Record & repot
ผศ.ดร.กรองได อุณหสตู
Initial brain resuscitation
ABCs
secure airway
guarantee gas exchange
stabilize circulation
ICP management protocols
Prevent hypoxia, hypotension
ผศ.ดร.กรองได อุณหสตู
Nursing management
• cranial blood or CSF volume
• Osmotic diuretics
• Systemic diuretics
• Monitor electrolytes, urine output
• Medication: dexamethasone, histamine
• Posture position
ผศ.ดร.กรองได อุณหสตู
CPP = MAP - ICP
CPP = 70 - 100 mmHg
MAP = 50 - 150 mmHg
ICP = 5 - 20 mmHg
ผศ.ดร.กรองได อุณหสตู
The postoperative patients in the
first 24 hours CBF 50%
Head-injured patient after surgery:
CPP should be kept 70 mmHg
MAP should be kept 80-90 mmHg
(Moppett, 2007)
Classic signs of ICP
“Cushing’s triad”
• SBP
• Widening PP
• Bradycardia with a full bounding pulse
• Rapid or irregular respiration
ผศ.ดร.กรองได อุณหสตู
Late signs of ICP
• Restlessness, then apparent calm
• Deeping stupor and LOC
• Headache and intensity
• Projectile vomiting
• Unequal size of pupils, abnormal reaction
• Widening PP, slow bound pulse
Score for comatose patient
Glasgow Coma Score
(GCS) : 15 points
• Eye response
• Motor response
• Verbal response
Full Outline of
UnResponsiveness
(FOUR) : 16 points
• Eye response
• Motor response
• Brain stem reflexes
• Respiration
ผศ.ดร.กรองได อุณหสตู
FOUR Scale Glasgow coma scale
Eye response
4 Eyelids open/opened, tracking, or blink to command
3 Eyelids open but with no tracking
2 Eyelids are closed but open to loud voices
1 Eyelids are closed but open to pain
0 Eyelids remain closed with pain
Eye opening
4 Spontaneous eye opening
3 Eye opening to speech
2 Eye opening to pain
1 No reaction to pain
Motor response
4 Thumb –up, fist, or peace sign
3 Localized pain
2 Flexion response to pain
1 Extension response to pain
0 No response to pain or generalized myodonous status
Best motor response
6 Obeying commands
5 Localization to pain
4 Normal flexion to pain
3 Abnormal flexion to pain
2 Extension to pain
1 No response to pain
Brainstem Reflex
4 Pupil and corneal reflexes present
3 One pupil wide and fixed
2 Pupil or corneal reflexes absent
1 Pupil and corneal reflexes absent
0 Absent pupil, corneal, and cough reflex
Best verbal response
5 Oriented
4 Confused conversation
3 Inappropriate words
2 Incomprehensible sounds
1 No response
Respiration
4 Not intubated, regular breathing pattern
3 Not intubated, cheyne-strokes breathing pattern
2 Not intubated, irregular breathing
1 Breathes above ventilator rate
0 Breathes at ventilator rate or apnea
Severity of injuries
Mild
head injury
• GCS = 13-15
• associated with
loss of
consciousness
or amnesia for
less
• than 1 hour
Moderate
head injury
• GCS = 9-12
• associated with
a loss of
consciousness
for up to a day
Severe
head injury
• GCS less than
or equal to 8
• associated with
loss of
consciousness
for more than
24 hours
ผศ.ดร.กรองได อุณหสตู
FOUR scale 15-16 FOUR scale 8-14 FOUR scale 0-7
1 point Four score
mortality reduce 36%
poor function outcome reduce 29%
poor neurological outcome reduce 33%
Sadaka, et al., 2012
Nursing management
• Adequate oxygenation, perfusion, CPP
• Osmotherapy
• Prepare for surgical intervention
• Pharmacologic agent ; ICP, cerebral edema
• Close monitoring
ผศ.ดร.กรองได อุณหสตู
Severe TBI (GCS = 3-8)
obtain CT brain
secondary insult; hypotension, hypoxia
1survey &
resuscitation
Assess GCS, pupil,
motor response
Monitor : V/S, N/S, GCS
Re-assess
Airway & breathing
Assisting in ET intubation
Monitoring blood gas
Monitoring O2 sat
Circulation
Volume deplacement
Assisting in FAST, DPL
IV fluid
Monitor : V/S, LOC
Neurological
examination
2survey &
management
Assess GCS, pupil
reaction, lateralization,
Assess herniation
Repeated CT scan
Assisting in diagnostic
test, surgical tratment
Record & repot
ผศ.ดร.กรองได อุณหสตู
Medication therapy
Intravenous fluids
Maintain volume
Prevent hypovolemia
Should not use hypotonic fluids
Monitor serum Na+ level
ผศ.ดร.กรองได อุณหสตู
Medication therapy
Hyperventilation
PaCO2
Normocarbia
keep PaCO2 at 35 mmHg
For acute neurologic deterioration;
keep PaCO2 at 25-35 mmHg
ผศ.ดร.กรองได อุณหสตู
Medication therapy
Mannitol
elevate intracranial pressure
Usually use 20% IV, 1 g/kg
acute neurologic deterioration;
bolus mannitol 1 g/kg rapidly > 5 min,
then CT brain
ผศ.ดร.กรองได อุณหสตู
Medication therapy
Furosamide
Conjunction use with mannitol
Usually use 0.3-0.5 mg/kg IV
Steroids
Control ICP
Improve severe brain injury
Medication therapy
Barbitulates
ICP
Not indicated in the acute
resuscitative phase
Anticonvulsants
100 mg/8 hours,
1 gm.IV rate < 50mg/min
ผศ.ดร.กรองได อุณหสตู
SIRS
First hit: Tissue injury
Inadequate resuscitate
Host response:
- Local pro-inflammatory
- Local anti-inflammatory
Uncontrolled
inflammatory response
Shock
Tissue ischemia
/hypoxia
Endothelial
dysfunction
Injury
Primed inflammatory
system
Activation of complement,
coagulation, inflammatory cascades
Tissue
hypoperfusion
Renal dysfunction Hematologic dysfunction
MODS
Urden, et al., 2010; Deitch, Vincent & Windsor, 2002
Organ indicator none minimal mild moderate severe
Respiratory PaO2/FiO2
ratio
> 300 226-300 151-225 76-150 ≤ 75
Renal Serum
creatinine
(umol/L)
≤ 100 101-200 201-350 351-500 > 500
Hepatic Serum
birirubin
(umol/L)
≤ 20 21-60 61-120 121-240 > 240
Cardiovascular CVP/MAP < 10.0 10.1-
15.0
15.1-20.0 20.1-30.0 > 30.0
Hematologic Platelet
count
(mm3)
>
120,000
81,000-
120,000
51,000-
80,000
21,000-
50,000
≤ 20,000
Neurologic GCS 15 13-14 10-12 7-9 ≤ 6
Multiple Organ Dysfunction Score
Marshall,J.C.(2003) ACS Surgery : Principle and Practice
Dysfunction 0 1 2 3
Pulmonary PaO2/FiO2 >208 208-165 165-83 <83
Renal
Creatinine (umol/l)
>159 160-210 211-420 >420
Hepatic
Total Birilubin (umol/l)
<34 34-68 69-137 >137
Cardiac
Inotropes
No inotropes Only one
inotrope at a
small dose
Any inotrope at
moderate dose
or >1 agent,
all at small
dose
Any inotrope at
large dose
or >2 agents,
at moderate
dose
Denver Postinjury
Multiple organ Failure Score (Moore)
• ISS >15, survived longer 48 hr, 16 years of age
Principle emergency care
of critical patient
Adequate oxygenation
Adequate perfusion
Adequate cerebral perfusion
ผศ.ดร.กรองได อุณหสตู
(A-a)DO2 = PAO2 - PaO2
Oxygen in alveoli = PAO2
Arterial oxygen pressure = PaO2
Alveolar arterial gradient; (A-a)DO2
(A-a) DO2 > 20 mmHg = O2 deficiency (Hennessey & Japp, 2007)
Alveolar arterial gradient; (A-a)DO2
(A-a)DO2 = PAO2 - PaO2
= (713 x FiO2) - PaCO2 /0.85
www.globalrph.com/aagrad.cgi
ผศ.ดร.กรองได อุณหสตู
Blood glucose
aerobic metabolism ของกลโูคสให้
พลังงาน 38 ATP แต่ถ้า anaerobic
metabolism จะใหพ้ลังงานเพยีง 2 ATP
ท าให ้Na+ เคลือ่นเขา้สู่เซลล์ และ K+
เคลื่อนออกนอกเซลล ์เกิดการบวมน า
ของเซลล ์และ Ca++ เคลือ่นเขา้สูเ่ซลล์
ท าใหเ้ซลล์สูญเสยีหนา้ที่
ผศ.ดร.กรองได อุณหสตู
Hyperglycemia caused
intracellular osmotic pressure
Glucose > 200 mg/dl
O2 deficiency
Cerebral ischemia, anaerobic metabolism