In emergencies the CT scan remain the best brain imaging study available, the initial procedure of choice in evaluating intracranial mass lesion and has great
help to differentiate surgical form lesion from non surgical lesion.
A noncontrast CT scan differentiates hemorrhagic from non hemorrhagic lesion identifies the severity of cerebral edema,the presence of mass effect,and the potential for herniation synfdrome.In addition after traumatic injury the CT scan characterizes the extent of the primary injury..identifies the need for emergent-surgical intervention (i.e.delineates mass lesion with midline shift) and predict the likelihood of subsequent increased ICP.
An imaging study (magnetic resonance imaging)(MRI) or CT scan should be performed in all patients with new onset seizures.
MRI appears to be more sensitive than the CT scan in the diagnosis of contusion and residual parenchymal shearing type injury.
EEG is a necessary adjunct for the diagnosis of some seizure disorders. Lumbal puncture is an essensial diagnostic tool in patients with suspected subarachnoid hemorrhage who have a normal CT scan and should be performed promptly in all patients suspected to have CNS infection who do not display focal neurologic findings or papiledema on physical examination.
A coagulation study (prothrombin time, partial thromboplastintime and plate let count) is needed in the presence of cerebral thrombosis,hemorrhage,
trauma or anticoagulant therapy.
Require neurosurgical consultation for any patients who with :
1.high risk for developing an expanding intracranial mass lesion.
2.open or depressed skull fracture.
3.acute ventricular obstruction
4.fourth ventricular/cerebellar bleeding or subarachnoid hemorrhage.
5.CSF leakage
6.Non traumatic disease process (spontaneous intracerebral hematoma,large brain tumors and brain abscesses) if clinical finding or an imaging study indicates significant mass effect.
Remember that cerebellar hemorrhage is always a surgical emergency need immediate consultation.
TREATMENT (1,4):
General treatment goals in the brain injured patient :
-Control airway if necessary
-Oxygenation /supplemental oxygen
-Establish hemodynamic stability control
-Establish normo volemia.
-Control seizure
-Correct anemia
-Control hyperthermia
-Control pain
-Correct metabolic abnormalities
-Avoid agitation,excessive stimulation,shivering.
Hyperthermia,seizure,pain,shivering,agitation may increase brain metabolism and oxygen consumption.
Elevated temperature develops frquently after brain injury. Arise of 1 degree Celcius above normal increases the cerebral oxygen consumption by 10% to 15% and may increase brain damage. Therefore should be immediately controlled with antipyretics and cooling blankeet if necessary.
Any focal or generalized seizure activity requires promptly treatment.
Since an increased incidence of new onset seizures follow acute injury, prophylactic anticonvulsant therapy is recomended in traumatic head injury, subarachnoid hemorrhage, brain tumor and brain abscess.
Phenytoin 300-400 mg/day in adults after an appropriate loading dose is the agent of choice im most instances.
In patients after subarachnoid hemorrhage from a ruptured cerebral aneurysma,vasospasm and secondary ischemic infarction are the major cause of secondary morbidity.In the patients who develops vasospasm, the cerebro spesific calcium channel blocking agent(nimopdipine) 60 mg orally every 4 hrs for 21 days initiated upon hospital admission may improve neuroloogic income but no definitive therapy to prevent vasospasm is available.
Latrogenic hypotension is more dangerous than mild or moderate hypertension therefore antihypertensive agents should be administered for systolic blood pressure level > 200mmHg. But control of hypertension is mandatory in hypertensive encephalopathy and may necessary with very high blood pressure after intracranial hemorrhage.
Since excess catecholamine release is partially responsible for acute increase of blood pressure after brain injury agents that block alpha or beta receptors provide a logical choice where labetalol 20-40 mg continuous iv infusion has
been shown to control blood pressure. Angiotensin converting enzyme inhibitor(e.g. analaprilat 1,25-5 mg iv every 6-8 hrs are also effective without affecting cerebral hemodinamic.
One of intracranial problem that requires immediate treatment is increased ICP. Disease entities that are frequently complicated by an elevated ICP include significant brain traumatic injury,large hemispheric stroke and severe subarachnoid hemorrhage. ICP may increase within minutes to hours after primary injury especially head trauma. In the setting of hematom and contusions a normal ICP may progressive increase over 24 to 72 hrs as edema
develops. General nonspesific measures to control ICP include appropriate sedation and analgesia but unfortunately may negate the value of serial neurologic exams in following patients with CNS injury,this is especially problematic in the absence of ICP monitoring.
Neuromuscullar blocking agent may also be helpful if excessive muscle activity persist although the aggressive use of sedative and analgesics but in patients with seizure is not recomended unless contineous EEG monitoring is in place. Fluid management includes conventionally administered isotonic crystalloid solution to maintain normovolemia and normal serum electrolyte, volume restriction has not been shown to benefit the brain injured
patient and may compromise cerebral perfusion.
Furesemide and acetazolamide may decrease the production of CSF by 50%.
These agents are beneficial in patients with obstructive hydrocephalus but probably have only minor value in acute brain injury.
Removal of as little as 1to2ml of CSF may decrease elevated ICP but the increase risk of infection make this methode a less than ideal altrenative.
Therapeutic hyperventilation (PaCO2 25-30 torr) has been a mainstay of therapy for the control of ICP but hypocarbia may decrease CBF induce secondary ischemia injury therefore hyperventilation has no rutine role as general
prolonged treatment for brain injured patient but acute hyperventilation for brief interval usually lowers the ICP in 5 to 10 mins, is indicated for the emergent control of ICP pending the implementation other therapeutic measures.
Osmotic agents appears have ability to lower ICP maybe the osmotic reduction of intracranial volume and by decreasing blood viscosity.
Mannitol (0,25-1,0g/kg)is effective within 20 to 30 mins after iv infusion and a concomitant dose of furesemide (0,5-1,0mg/kg) may improve efficacy. Since osmotic agents diffuse across a disrupted blood brain barrier into brain
tissue chronic or persistent use of these agents can precipitate worsening cerebral edema therefore continuous infusion are not recomended and the time interval between intermittent boluses should be guided by ICP monitoring.
Administration barbiturate often lower ICP if the above measures have failed by decreasing CBF and Cerebral oxygen consumption.
The ideal body position for brain injured patients is controversial espesially with cerebral edema and elevated ICP, but traditional teaching suggest that midline, neutral position and a head elevation of 30 degree promotes cerebral venous drainage, decreases cerebral edema, and improves ICP.
But this premise has failed to be verified based on results of clinical investigation so on some cases ICP is minimized in the supine position.
Significant deviation to the lateral sides may obstruct jugular venous drainage and increase ICP.
Steroid just recomended to treat peritumor edema in patients with primary or metastatic CNS malignancies not for traumatic brain injury,stroke or global ischemia and hemorrhage.
Dexamethason 4-10 mg or 0,25mglkg every 6-12 hrs is effective.
The methylprednisolone (30mg/kg iv over one hour followed by 5,4mg/kg hr for 24 hrs was shown in one study to improve functional motor scores at 6 months after spinalcord injury.
But preliminary studies indicate a reduction of hearing loss with steroid administration and no improvement in other neurologic complication.
Anticoagulant treatment is confined to patients with thromboembolic cerebral vascular disease (embolic non hemorrhagic,evolving stroke,posterior circulation thrombosis).
Continuous heparin treatment targetting a partial thromboplastin time 1,5 - 2 times control is attempted in acute anticoagulation.
The presence of blood on CT scan is absolute contra indication.
Hypertension and recent(within the last 5-7 days) head trauma or a neurosurgical procedure is also relative contra indication.
Thrombolic stroke involving the posterior circulation may benefit from heparin treatment in acute periode.
Progressing or evolving stroke of the anterior circulation may also benefit from short term anticoagulation.
There is no role for anticoagulant treatment in complete stroke.
SUMMARY :
-Brain injuries may be traumatic or non traumatic,and secondary injury usually results from ischemia and/or structural disruption of brain tissue.
-Hypoxaemia and hypovolemia with hypotension are the most common cause secondary ishemia.
-Optimizing systemic and CBF,normalizing ICP is the first step in critical care support in brain injury.
-Hypotension shoud be considered related to ascociated injuries and never assume as secondary to CNS injury.
-Cerebral hypoperfusion will aggravate the primary injury therefore never limit appropriate intravascular volume expansion because fear of increasing cerebral edema.
Mild or moderate hypertension may increase CPP to improve blood flow in ischemia area, hence lowering blood pressure to normal levels may induce ischemic insult.
-Cerebellar hemorrhage is always a surgical emergency need immediate surgical consultation and any patient who is at significant for developing an expanding intracranial mass lesion that neurosurgical consultation is mandatory.
Nimodipine, the cerebro spesific calcium blocking agent may improve outcome in patients with cerebral vasospasm and must be initiated upon hospital admission.
Acute hyperventilation for brief intervals usually lowers ICP in 5-10 mins and is indicated for the emergent control pf ICP but iatrogenic hyperventilation should be terminated.
A CT scan should be attempted before beginning anticoagulant therapy to eliminate the possibility of a hemorrhagic lesion.
REFERENCES :
1.The Society of Critical Medicine:Neurologic Support ;Course Syllabus,Fundamental Critical care Medicine,2nd edit,USA,1997,pp.83-96.
2.Doyle W.P et all : Mechanism of Injury and Cerebral Protection;Matta F.Basil,Menon K.David;Textbook of Neuroanesthesia and Critical Care,Greenwich Medical Ltd,London,2000,pp 37-39.
3.Gopinath P.Shankar,Robertson S.Claudia : Management of Severe Head Injury;Cottrell E.James,Smith S.David;Anesthesia and Neurosurgery,4th edit. Mosby A Harcourt Health Science, St. Louis,Missouri,2000,pp 664-72
4.Safar Peter : Resuscitation of the Ischemic Brain,Albine S.Maurice: Textbook of Neuroanesthesia with neurosurgical and Neuroscience Perspectives,The McGraw Hill Companies,Newyork,St Louis,San Franscisco,1997,pp.57-81.
5.Durieux E Marcel : Anesthesia for Head trauma;Stone J.D,Sperry JR: The Neuroanesthesia Handbook Mosby Year Book Inc,1996,pp387-95.
6.Cooper Mergen&Stone J.D: Anesthesia for Head Trauma;Sperry J.R, Stirt D.J: Manual of Neuroanesthesia,,B.C.Decker Inc,Totonto,Philadelphia,
1989,pp.229-37.
0 comments:
Post a Comment