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 facture

Abdomen: soft, non tender

CBD: 80cc clear urine

FBC:14.7/18.3/451

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 restlessVentilated and sedated pupil bilaterally 2mm reactiveE1VTM1 Pupils 2mm/2mm bilaterally reactive

Blood pressure : 130/98} not supportedPulse rate : 129

Respiratory rate : 12 lungs : crepitation at right base Oxygen saturation : 100 suction: blood stain

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

GM: 5.6 Abdomen: softUrine output: clear urine

Temperature: 37.0CTWBC:18.3Not on antibiotics

HB: 14.7PLT: 451

Impression:Traumatic Brain Injury with Intracranial Bleed and right lung contusion

Initial management:1. Keep NBM2. IVD NS 80cc/hour3. IV ranitidine 25mg TDS4. Glucometer monitoring5. For cerebral protection6. 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 edemasubdural 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 clearCERVICAL:Loss of cervical lordosisLateral 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.

PROGRESSStarted 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 .

DISCUSSIONTraumatic 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 sedativesNarcotics, 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 ischemiaAnemia 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 ventilationHypoxia 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. HypothermiaHypothermia 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 therapyMannitol 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 salineHypertonic 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 electrolytesThe 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).

NutritionHead 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 prophylaxisProphylaxis includes early enteral feeding, and pharmacological prophylaxis such as H2-blockers, proton pump inhibitors and sucralfate should be used in TBI.

Glycemic controlStress 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 prophylaxisStudies 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.

Reference1. Assessment of traumatic brain injury, acute- British Medical Journal2. Traumatic brain injury – Medscape3. Guidelines for the management of severe traumatic brain injury, 3rd edition- Brain

Trauma Foundation4. Critical care management of severe traumatic brain injury in adults- Scandinavian journal

of trauma, resuscitation and emergency medicine5. Cerebral protection: a review of current techniques- Med & health Rev 20096. Cerebral protection- British Journal Of Anaesthesia7. Cerebral protection-current concepts- Indian Journal of Neurotrauma