Case write up-ICU

Name: MHA
Age:

11.4years old

Date of admission:

13/9/15

Date of ICU admission:

13/9/15

Premorbid:
large perimembranus VSD with pulmonary hypertension. Done closure at IJN on
6/7/2005 and was discharged from IJN on November 2009
Presented to emergency department due to alleged motor vehicle accident (motorbike versus car)
at 1500H was slided under the car and found unconscious. Brought to emergency department by
ambulance with loss of consciousness, nose and mouth bleed with GCS E1V2M4 and pupil
bilaterally 2mm reactive, vital signs were stable and hematoma at frontal area, abrasion wound at
chin at right forearm. Intubated at ED for airway protection, FAST scan no free fluid and proceed
with CT brain.
Surgical team review at resus. CT brain showed cerebral edema, contusion bleed at right
temporal and subdural hemorrhage at subtentorium cerebeli and left pariental bone. No midline
shift, no pneumocranium. CXR right lung contusion. Planned for cerebral protection, refer for
ICU care and case referred to neurosurgical HKL at 2155H. neurosurgical reply at 1100H for
conservative management, cerebral protection 24 hours and to repeat CT brain coming morning.
Impression : alleged MVA with ICB and right lung contusion
Upon GA review at resus
GCS E1VTM1 intubated and sedated, pupil bilaterally 2mm reactive
BP

:123/62

HR

:107

SpO2 :100%
lungs: fairly clear anteriorly
CXR: right lung contusion, no pneumothorax, no rib
Abdomen: soft, non tender
CBD: 80cc clear urine
FBC:14.7/18.3/451

facture

ABG post intubation: pH 7.382/ pCO2 32.8/pO2 401.1/ HCO3 19.6/BE -5.7
Plan to admit ICU
Transferred to ICU at 0145H:
GCS E1VTM5 ventilated, given IV midazolam 2mg d/t restless
Ventilated and sedated pupil bilaterally 2mm reactive
E1VTM1
Pupils 2mm/2mm bilaterally reactive
Blood pressure
Pulse rate

: 130/98} not supported

: 129

Respiratory rate
Oxygen saturation

: 12
: 100

lungs : crepitation at right base

suction: blood stain

ABG: pH: 7.380/ pCO2: 41.3/ pO2: 137.1/ HCO3: 23.3/ BE: -1.2/ SO2 99.0%
Lactate:3.79
On SIMV-PC FiO2 0.4 RR:12 IP:20 Psupp: 21 PEEP:8
GM: 5.6
Urine output: clear urine

Abdomen: soft

Temperature: 37.0C
TWBC:18.3
Not on antibiotics
HB: 14.7
PLT: 451
Impression:
Traumatic Brain Injury with Intracranial Bleed and right lung contusion
Initial management:
1. Keep NBM
2. IVD NS 80cc/hour
3. IV ranitidine 25mg TDS
4. Glucometer monitoring
5. For cerebral protection
6. Repeat CT brain coming morning
CT brain and cervical (14/9/15)x1:
BRAIN:
extradural bleed at left parietal region with depth of 0.6cm.

thin subdural bleed at left parieto occipital with depth of 0.2cm with extension to left tentorium
cereblelli with thickness of 0.5cm.
contusional bleed at right parietal 1.1cm x 1.0cm with minimal perilesional edema
subdural bleed at right temporal with thickness of 0.3cm.
subarachnoid bleed at left parietal, right frontal and right temporal area.
Hyperdensities in bilateral basal ganglia denser on the left side may represent bleed or early
calcification.
No significant midline shift. No hydrocephalus.
Basal cistern, the ventricles and cerebral sulci are preserved.
Fracture of left temporo-parietal bone.
Soft tissue swelling ot left vertex and left occipital.
Sphenoid haemosinus. Mastoid air cells are clear
CERVICAL:
Loss of cervical lordosis
Lateral atlantoaxial distance is symmetrical. Cervical alignment is intact.
Normal vertebral body height and disc height.
Prevertebral soft tissue is preserved.
No cervical spine fracture or joint dislocation.
Fracture of right scapula.
Bilateral lung contusion (R>L). no pneumothorax.
CT brain (15/9/15)x2:
The previously seen right frontal contusional hemorrahe is unchanged in size and appearance.
The left parieto-occipital subdural hemorrhage extending into left tentorium cerebella is
unchanged.
There are residual subarachnoid hemorrhages ssen in the right frontal and right temporal areas.
Subarachnoid hemorrhage in the left parietal lobe has resolved.
The hyperdensities in the basal ganglia are unchanged, suggestive of early calcification.
There is generalized cerebral edema with effaced basal cisterns.
There are well-defined hypodense areas in the right frontal and right temporal lobes which are
more apparent in this scan, likely representing early ischemic changes.
No new intra-cranial hemorrhages.
Ter rest of the findings remain unchanged.
PROGRESS
Started on iv ceftriaxone, cover for soft tissue injury and aspiration on D1 of icu and was
escalated to iv meropenem 800mg tds D5 in view of persistent temperature spike. Antibiotic was
off by AMS team on 22/9/15 in view of CRP 27, all the cultures NG(TBI with possible
thermoregulatory disturbance). Patient had continuous temperature spike prior to transfer out.
Feeding started on D1 nutrien junior 30cc/ 3 hourly, and was maximized 200cc/3hourly and IVD
off. Patient started to tolerate clear fluid orally prior to transfer out

Cerebral protection continued until D2 (16/9/15 @ 0205H) in view of worsening CT brain

findings, and off after neurosurgical reply. Neurosurgical plan to off cerebral protection and for
wake & wean.
Extubated on 17/9/15@ 0730H and put of FM 5L/min. on 18/9/15 @ 1245H noted pt not very
active and tachypnic, hence intubated and extubated on 22/9/15 @0800H put on HM 5L/min,
and was on room air (ABG showed good oxygenation, no acidosis) since 1500H and was
transferred out to peads surgical ward on 23/9/15 @ 0800H with GCS E4V4M6 .
DISCUSSION
Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain from an
external mechanical force, possibly leading to permanent or temporary impairment of cognitive,
physical, and psychosocial functions, with an associated diminished or altered state of
consciousness.
TBI can be classified as mild, moderate, or severe, typically based on the Glasgow Coma Scale
(GCS) and/or neurobehavioural deficits after the injury.TBI can manifest clinically from
concussion to coma and death.
Injuries are divided into primary injury and secondary injury. Primary injury is due to the
immediate mechanical force, whether blunt, penetrating, or blast, and may include skull fracture,
contusion, haematoma, subarachnoid or focal haemorrhage and axonal shear or laceration. While
secondary refers to the evolving pathophysiological consequences of the primary injury and
encompasses a multitude of complex neurobiological cascades altered or initiated at a cellular
level following the primary injury which evolves over the ensuing hours and day. Improved
outcome results when these secondary, delayed insults, resulting in reduced cerebral perfusion to
the injured brain and prevented or respond to treatment. This is reflected in the progressive and
significant reduction in severe TBI mortalitiy from 50% to 30% to 25% and lower over the last
30 years.
Anesthetics, analgesics and sedatives
Narcotics, such as morphine, fentanyl and remifentanil considered for first line therapy since
they provide analgesia, mild sedation and depression of airway reflexes which required in
intubated and mechanically ventilated patients. Adequate sedation provides analgesics,
anxiolysis, limit elevation of ICP related to agitation, discomfort, cough or pain, facilitates
nursing care and mechanical ventilation, decrease O2 consumption, CMRO2 and CO2 production,
improves patient comfort; prevents harmful movements. Ideal sedative in TBI would be rapide
onset and offset, easily titrated to effect and lack active metabolites. It would be anticonvulsant,
able to lower ICP and CMRO2 , preserve neurologic examination and lack deleterious
cardiovascular effects. For example propofol which permit sedation and periodic neurologic
evaluation, and benzodiazepines such as midazolam and lorazepam provide sedation, amnesia
and anticonvulsive effect. . Clinically should keep patient sedated at RAAS -3 to -5.
Hemodynamic support

Hypotension defined as SBP <90mmHg of MAP < 65mmHg, is a frequent and detrimental
secondary systemic brain insult. The target of MAP 80mmHg is recommended to maintain CO
60 mmHg for treatment threshold of ICP > 20 mmHg.Aggressive fluid administration to
achieve adequate intravascular volume is the first step in resuscitating a patient with hypotension
in severe TBI followed by using vasopressors. CVP used to guide fluid management and
recommended to be maintained at 8-10mmHg. Reliable predictors of fluid responsiveness are
pulse pressure variation, systolic pressure variation, stroke volume variation and collapse
inferior vena cava. Isotonic cyrstalloids are the fluid choice. Norepinephrine titrated through
central venous line is recommended. Dopamine causes cerebral vasodilation and icrease ICP.
Phenylephrine, a pure alpha-agonist vasoactive agent is recommended in TBI patients with
tachycardia.
Hypertension defined as SBP > 160 mmHg or MAP >110 mmHG is aloes a secondary systemic
brain insult that can aggravate vasogenic brain edema and intracranial hypertension. It may be a
physiological response to a reduced cerebral perfusion.lowering an icreased B to maintain an
adequate CPP exacerbates cerebral ischemia.
Cerebral ischemia ia important secondary event affecting outcome. Cerebral perfusion pressure
(CPP= MAP-ICP) should be >60mmHg which will enhance perfusion to ischemic regions of
the brain. The CPP should be maintained at minimum of 60mmHg in the absence of cerebral
ischemia and at a minimum of 70mmHg in the presence of cerebral ischemia
Anemia is common in secondary systemic brain insult. Targeted hemoglobin 100 g/L of
hematocrit 0.3. Brain tissue reach in thromboplastin and cerebral damage which cause
coagulapathy and it should be treated with blood products.
Mechanical ventilation
Hypoxia defined as O2 saturation <90% or PaO2 < 60mmHg should be avoided in TBI patient.
Hyperventilation need to avoided in first 24hours in TBI patients as it can reduce cerebral
perfusion. Excessive and prolonged hyperventilation results in cerebral vasoconstriction and
ischemia. But a brief period (15-30min) if hyperventilation to a PaCO2 30-35 mmHg is
recommended to treat acute neurological deterioration reflecting increased ICP while monitor
cerebral oxygenation and avoid cerebral ischemia by measuring SjvO2 or PbtO2.
Ventilator setting should be adjusted to maintain pulse oximetry (SpO2) of > 95% and PaO2
>80mmHg and to achieve normoventilation with PaCO2 35-40mmHg.hence, protective
ventilaton with low tidal volume and moderate positive and end-expiratory pressure (PEEP)
recommended to prevent ventilator- associated lung injury and icreased ICP.
Prior suctioning through endotracheal tube, preoxygenation with a fraction of inspired oxygen
(FiO2)=1.0 and administration of additional sedation recommended to avoid desaturation and
sudden increase in ICP.
Hypothermia
Hypothermia is a condition of metabolic inhibition that reduces O2 and glucose consumption and
thus reduce the production of cytotoxic radicals, penumbral ischemia and brain swelling.
Evidence of hypothermia in TBI is controversial. Therapeutic hypothermia has yielded

promising results in animal models of TBI, but its usefulness in clinical practice is still debated.
In severe TBI, therapeutic hypothermia permits control of intracranial pressure elevation, but its
effects on outcome and mortality have not been conclusively demonstrated.
Fever should most likely be treated aggressively in the first days of TBI.
Hyperosmolar therapy
Mannitol is widely used in control of raised ICP following ICP. One effect may be an immediate
plasma expanding effect, which reduces the hematocrit, increase the deformability of
erythrocytes and thereby reduce blood viscosity, increase CBF and increase cerebral oxygen
delivery. These may explain why mannitol reduce ICP within few minutes of its administration.
The osmotic effect of mannitol is delayed for 15-30min while gradients are established between
plasma and cells. Its effects persist for a variable presiod of 90min to 6hours depending on
clinical conditions such as preexisting renal disease which can increased risk for renal failure.
Prophylactic mannitol administration is not recommended. Its use restricted to patients with sign
of transtentorial herniation of progressive neurological deterioration. Mannitol should not be
administered if serum osmolarity is > 320mOsm/kg H2O. The effective dose is 0.25-1 g/kg,
administered intravenously over a period of 15 to 20 minutes. Mannitol is contraindicated in
patients with TBI and renal failure because of the risk of pulmonary edema and heart failure.
Hyper tonic saline
Hypertonic saline have been suggested as alternative to mannitol The principal effect of ICP is
possibly due to osmotic mobilization of water across the intact blood brain barrier which reduce
cerebral water content. It also dehydrates endothelial cells and erythrocytes which increases the
diameter of the vessels and deformability of erythrocytes and leads to plasma. Prolonged
administration of a Hypertonic saline was associated with lowered ICP, controlled cerebral
edema, with no adverse effects of supraphysiologic hyperosmolarity such as renal failure,
pulmonary edema, or central pontine demyelination.

Fluids and electrolytes

The goal is to establish and maintain euvolemia to moderate hypovolemia (CVP= 8- 10mmg) .
isotonic crystalloids should be used for fluid management, and normal saline is recommended
solution. Aggressive fluid resuscitation using NS can cause hyperchloremic metabolic acidosis.
Hypotonic solusion such as Dextrose 5% should be avoided. Glucose contain solution should be
avoided first 24 -48 hours unless patient develop hypoglycemia because it can cause anaerobic
cerebral metabolism of glucose which produce acidosis and free water, subsequently worsen
brain edema.
In severe TBI patient with increased ICP of brain edema sodim level Na+ 150-155 mEq/L is
acceptable. Injury to hypothalamic-pituitary system is a major contributing factor in sereum
electrolytes disturbance. Common cause for hypernatremia (Na+> 150 mmol/L) in TBi patient
are central or neurogenic diabetes insipidus, osmotic dieresis(mannitol) and use of HSS.

Correction of severe hypernatremia(Na+>160 mmol/L) should b gradual as abrupt change in

serum osmolarity and serum sodium fall can worsen cerebral edema. Hyponatremia is
detrimental and major secondary systemic brain insult in patient with sever TBI, as it leads o
exacerbation of brain edema and increase in ICP. It is usually secondary to cerebral salt wasting
syndrome or to the syndrome of inappropriate anti-diuretic hormone secretion (SIADH).
Nutrition
Head injured patients have high nutritional requirements and feeding should be instituted early
(within 24 h). Enteral feeding is preferred as it tends to be associated with a lower incidence of
hyperglycemia and because of its protective effect against gastric ulceration. Impaired gastric
emptying is a common finding in head injury, and can be treated with prokinetic agents. In those
who cannot be fed enterally, parenteral nutrition should be considered together with some form
of prophylaxis against gastric ulceration (H2 antagonists or sucralfate) and rigorous blood sugar
control.
Stress ulcer prophylaxis
Prophylaxis includes early enteral feeding, and pharmacological prophylaxis such as H2blockers, proton pump inhibitors and sucralfate should be used in TBI.
Glycemic control
Stress hyperglycemia is common secondary systemic brain insult. Although hyperglycemia is
detrimental, maintaining low blood glucose level can cause hypoglycemia which caninduce and
aggravate underlying brain injury. Therefore, clinical practice is to keep normoglycemic level,
6-10mmol/l
Antiseizure prophylaxis
Studies do not support the use of the prophylactic anticonvulsants evaluated thus far for the
prevention of late posttraumatic seizures. Routine seizure prophylaxis later than 1 week
following TBI is, therefore not recommended. If late PTS occurs (after 7 days), patient should be
managed in accordance with standard approaches to patients with new onset seizures. Phenytoin
has been shown to reduce the incidence of early PTS (<7 days) in patients who are at risk for
seizures. The risk factors include GCS <10, cortical contusion, depressed skull fracture, subdural
hematoma, epidural hematoma, intracerebral hematoma, penetrating TBI and seizures within
24hours of injury.. Valproate may also have a comparable effect to pheytoin on reducing early
PTS but may also associated with higher mortality. Phenytoin a loading dos of 15-20 mg/kg
admisnistered intravenously over 30min followed by 100mg iv every 8 hous, titrated to plasma
level for 7 days is recommended.
Deep vein thrombosis prophylaxis

The risk of developing DVT and pulmonary embolism in severe TBI is 20%. Mechanical
thromboprophylaxis including graduated compression stockings and sequential compression
devices are recommended until patients are ambulatory. In absence of contraindication low
molecular weight heparin or low dose of unfractioned heparin should be initiated as early 48-72
hours in combination of mechanical prophylaxis. The use of pharmacological prophylaxis
associated with increased risk for expansion of intracranial hemorrhage.
Reference
1. Assessment of traumatic brain injury, acute- British Medical Journal
2. Traumatic brain injury Medscape
3. Guidelines for the management of severe traumatic brain injury, 3rd edition- Brain Trauma
Foundation
4. Critical care management of severe traumatic brain injury in adults- Scandinavian journal
of trauma, resuscitation and emergency medicine
5. Cerebral protection: a review of current techniques- Med & health Rev 2009
6. Cerebral protection- British Journal Of Anaesthesia
7. Cerebral protection-current concepts- Indian Journal of Neurotrauma