Tuesday, November 29, 2011

Brain Injury (PART 2)

DIAGNOSTIC TEST :(1,4,6)




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.

Monday, November 28, 2011

Brain Injury (PART 1)

INTRODUCTION :


Injury in medicine ,any stress upon a part or the whole of an organism that disrupts its structure or function or both,to such a degree as to result in a pathologic process.
Brain injury may be of traumatic or non traumatic origin (2)


Traumatic brain injury may be due to the trauma associated with accident or personal violence.


Alternatively the trauma may accompanying a variety of operative procedure including retraction,shear forces,direct tissue destruction,hemorrhage,vessels disruption with subsequent infarction.(2)


Traumatic brain injury can be devided into primary and secondary injury(5).


Primary injury is the injury occuring during the traumatic event therefore can not be minimized.


Secondary injury on the otherhand occuring after traumatic event as a result of hypoxia,hypercarbia and ischaemia induced by hypotension,vasospasm or increased intracranial pressure (ICP).


The most common contributors to secondary injury are hypoxaemia and hypovolemia with hypotension.(5,6)


At the tissue level hypoxia can be defined as a reduction in O2 availability to a level insufficient for tissue demands. 


This hypoxia can be caused by either hypoxaemia (Low PaO2) or ishaemia(low cerebral blood flow)(CBF).


When the blood supply to the brain is decreased below a critical level,ischemic damage is occur.


Ischaemic can be global or focal,complete or incomplete. 


Incomplete ishaemia differs from complete ischaemia in that there is a continuing supply of glucose sustain anaerobic metabolism increasing the brain lactic acid level.


Mechanical injury,haemorrhage,edema and ischaemia are the most important causes of brain damage in patient with head injury, particularly edema and ishaemia that are concern to the anesthesiologist (5,6).


BASIC MECHANISM OF INJURY:(2,5,6)


The pathophysiology associated with this process may reflect simple patho physiological consequence of ischaemia arising from pressure effects to underlying and distant brain regions. Shift of vital structures and axonal disruption reduction of CBF,hydrocephalus and herniation.


Ischaemia may not just be due to local microcirculatory compression but also the consequence of vasoactive substance released from the hematoma.


The extravasated subarachnoid blood can cause vasospam both locally and distant sites with aggravation of ischemia.


Systemic physiolological insult may occur as a consequence of primary injury include (hypoxia,hypotension,hypercarbia,
hyperthermia,anaemia and electrolyte disturbances) can contribute worsening neural injury.


Hypoxia may be the result of airway obstruction,aspiration,
thoracic injury,primary hypoventilation, or pulmonary shunting.


Hypotension has been found to occur in 32-35% in emergen
cy department which may be due to systemic causes.


This cause a decrease in cerebral perfusion pressure(CPP) which may aggravated by a high ICP;disruption cerebral vascular autoregulation,vasospasm and change in cerebral blood flow pattern.


Cerebral perfusion pressure(CPP) is the driving force for substrate (O2 and glucose)delivery to the brain.


Hyperthermia may be due to infection,thrombophlebitis,
drug reaction,or defect in the thermoregulatory center.


This results in excessive excitotoxic neurotransmitter,
altered protein kinase activity and augmented pathophy
siological effects of ischaemia.


Hypercarbia causes vasodilation of cerebral blood vessels with increased ICP and exacerbation of any mass or edema effects and cerebral acidosis.


Imbalance between cerebral oxygen delivery and demand arise a consequence of systemic and local secondary insults may result in focal or global ischaemia. Ischaemia is defined as severe reduction of bloodflow such the energy production is compromised. The reduced energy production is due to the limited availability of both oxygen and glucose.


The reduced blood flow also leads to impairment of the removal of metabolites such as CO2 and lactic acid.


INITIAL ASSESSMENT (1,3,4,6)


A patient who initially presents unconscious with focal neurologic deficits or with deteriorating neurologic signs should be assumed to have on going brain injury.


Any evidence of trauma should raise the suspicion of associated occult injured involving the spinalcord,thorax or abdomen.


Data regarding physical trauma,pre existing cardiovascular
pulmonary,renal and hepatic disease as well evidence of drug abuse should be found.


The patient level conciousness is the single most important clinical sign in the assessment of the severity of head injury and this should be noted at the scene immediately following 
the accident.


Based on GCS,head trauma patient is classified into mild (13-15),mode rate(8-12) and severe head injury (0-7).


Other variables such as pupillary activity,brain stem function,vital signs,age,Ht and type of injury can be used as a basic for predicting outcome.


Two major factors associated with severe head injuries are hypoxia and hypovolemia with hypotension.


These complications are most often associated with a bad outcome, and should be initially addressed in field.


Patient with altered states of conciousness have difficulty maintaining and protecting their airway.


Respiratory obstruction is the primary cause of death in 15% of these pa-tients.Spontaneous hyperventilation and mild hypocarbia (PaCO2 30-35 torr) are frequently seen after brain injury.


Central hypoventilation and apnoe are only present with injuries involving the respiratory centers nevertheless in patient in comatose hypoventilation commonly occurs due to upper airway obstruction related to relaxation of the
base of the tongue. Therefore controle airway by endotra
cheal intubation is necessary.But management of airway should begin at the scene with step A for impact coma that is backward tilt of the head and jaw thrust.


And step B for impact apnoe that is mouth to mouth(in tris
mus mouth to nose) ventilation when health professional arrive attempt intubation. Almost 20% of persons killed in vehicular accidents had isolated upper cervical spine injury,usually occur at the C1-2 or C5-6 vertebrae. 


All suspect cervical spine injuries should be carefully immobilzed,preventing extension, rotation or flexion of the head until a thorough physical and radiologic examination has occured.


Signs of basilar skull fracture are important  to the anesthesiologist. Look for hemotympanum,otorrhoea,
echymosis over the mastoid area (Battle's sign) and echymosis around the eyes without extension beyond the orbit(raccoon eyes).Nasal intubation in these patients is relatively contra indicated because of the significantly increased likelihood of seedling the CSF with bacteria which cause of infection,and because of the risk of inadvertenly placing the tip of endotracheal tube into the cranium.


Possible cause of hypoxaemia include neural induced ventilation/perfusion mismatching,microatelectasis,
increase pulmonary capillary permeability,and unobserved aspiration thus supplemental oxygen is essential in all patients during the initial hours after acute head injury.


Continuous monitoring of oxygen saturation levels by pulse oxymetri is recomended until the patient is clinically stable.


Injuries involving the lower brainstem or spinalcord may result in the loss of autonomic control of blood pressure
however,one should never assume hypotension is secondary a CNS lesion.


As a general rule hypotension is always related to concomittant systemic injury and haemorrhage, pre existing hypovolemia or drug intoxication.


A scalp laceration alone may bleed enough to produce hypovolemia especially in children.


Fear of aggravating cerebral edema should never limit appropriate intravascular volume expansion. Because cerebral hypoperfusion only worsen the initial injury
Vasopressor medications should only be administered transiently during resuscitation to maintain a systolic blood pressure level greater than 90 mmHg (adults).


The optimal choice of fluids for shock resuscitation in brain injury is controversial both isotonic crystalloid or colloid solution are used.


Hypertension occurs commonly after cerebral injury.


In patients with chronic hypertension the limits of autoregulation are shifted upwards improving tolerance for acute elevation in mean arterial pressure (MAP) and
impairing tolerance of lower arterial pressure.


Therefore hypertension and the concomittant increase in CPP may institute an appropriate compensatory response to improve blood flow in ischaemic area of the brain but in the otherhand lowering the blood pressure to normal levels may precipitate a secondary ischaemic insult.


Treatment should be attempted only if the systolic pressure greater than 200 mmHg or MAP greater than 125 to 135 mmHg, Even in that cases an initial lowering of MAP by only 25% is recomended.


Agressive control of blood pressure is allowed with hypertensive encephalophaty and intracranial bleeding.


Cardiac dysrythmia may be related to an elevation of circulating catechol amine and compromise of the CNS centers that modulate sympathetic and parasympathetic outflow.


Ventricular and atrial ectopic as well as supraventricular and ventricular tachycardia all occur with increased frequency especially in patients with intracranial haemor
rhage when arrythmia develop contributing metabolic abnormalities such as hypokalemia,hypocalcaemia and hypomagnesemia should be treated promptly.


Because adrenergic excess contribution to cardiac disturbance beta blocker is the most appropriate therapy for non ventricular tachyarrythmia.


Metabolics abnormalities such as hypogglycaemia,hyponat
remia,hypercalcemia uremia may also cause coma.


Decreasing of conciousness accompanied by fever and leukocytosis suggest meningitis and cerebrospinal fluid(CSF) examination is mandatory.


But if the CT scan reveals evidence of a mass effect or massive cerebral edema a lumbar puncture must be postponed because can precipitate a herniation syndrome.
Early therapy for bacterial meningitis before performing imaging study with appropriate antibiotics may be life
saving.


Seizure activity after an acute brain injury increase cerebral oxygen consumption and may increase the ICP if intracranial compliance is reduced, It should be promptly treated with diazepam 0,3-05 mg/kg or lorazepam 0,05-0,1 mg/kg intravenously. Subsequently intravenous loading dose of phenytoin(18-20 mg/kg in non glucose solution,infused no faster than 50mg/min) should be given.If phenytoin is ineffective,intravenous phenobarbital at a rate of 100 mg/min in 5 t0 10 mg/kg boluses to a maximum dose of 20mg/kg usually terminates all seizure activity.


Avoid the use of neuromuscular blocking agents in patients at risk for seizure since seizure activity would be undetec
ted. If neuromuscular blocking agents must be administered
bedside electroencephlography(EEG) monitoring is recom
mended. Rectal diazepam may be administered to children with ongoing seizure who have no intravenous access(dose 0,5 mg/kg).


Midazolam,diazepam or lorazepam can be used in the initial treatment of seizures in children at a dose of 0,1mg/kg iv,with maximum dose of 2 mg.


Phenytoin dosing in children :


      Age            Loading dose (mg/kg)          Maintenance dose(mg/kg)
=================================================
       <= 3 yrs                16                                        10


        4 - 6 yrs              16                                        8,8


        7 - 9 yrs              14                                        7,6


       10-16 yrs             12                                        6,6
==================================================




GENERAL NEUROLOGIC EXAMINATION :


The preliminary neurologic examination includes vital signs and a funduscopic examination should establish :
                -level of conciousness
                -intergrity of brainstem function
                -presence of purposeful or reflex motor activity.
Cushing's triad(bradycardia,bradypnoe and hypertension) suggest a markedly increased ICP with impending herniation.


Irregular breathing suggest a subcortical lesion.
Fever implies systemic or CNS infection. Funduscopic examination may reveal evidence of hemorrhage,extensive
exudates or papil edema.


Coma or complete unresponsiveness is generally caused by either bilateral hemispheric lesions,or barin stem involving the reticular activating system. Most coma are toxic or metabolic etiology.


Eye examination :


Pupillary size and responsiveness give important informafion
about the function of upper portion of the midbrain.


Preservation of light reflex differentiates metabolic from structural lesion. Small,symmetrical,reactive pupils are seen with bilateral deep cortical lesion and toxic metabolic encephalopathies.


Pontine lesions and narcotic overdose produce pint point pupil with preserved light reflex with midbrain lesions,the pupil are midposition and fixed.


When the third nerve is compressed as in uncal herniation the pupil in the ipsilateral side is dilated and non reactive.
Wide,fixed,non reactive pupils are not uncommon after severe global hypoxia injury.These pupillary changes may be reversible although persistence for >24 hrs implies a poor prognostic.


Eye movement reveal significant information regarding the intergrity of the lower midbrain,pons and medulla.
Spontaneous or roving eye movements indicate normal function. Spontaneous conjugate deviation of the eyes is associated with an ipsilateral frontal hemispheric or contra lateral brainstem lesion.


Conjugate eye movement in the opposite direction of the head movement af-ter moving the head from side to side slowly then briskly indicates normal brainstem function.(Doll's eye or occulocephalic reflex).


After cold caloric test there is no conjugate eye movement toward the side of the ear irrigated with cold solution implies brainstem structural damage.


Unfortunately these reflex eye movements may be abnormal with severe drug intoxication (e.g.phenytoin,
barbiturat and antidepressant) and are therefore not definitive for structural brainstem injury.


Motor movement :


Spontaneous,purposeful movements or movements induced by mild stimulation imply intact corticospinal tracts and minimal injury.


Abduction -avoidance movements with noxious stimulation also indicate relatively mild injury.


Decerebrate posturing(extension and internal rotation of the arms and legs) or decorticate posturing(flexion of the arms with extension of the legs) either spontaneously or with noxious stimulation indicates severe damage to the cerebral hemispheres or midbrain.


In a comatose patient absence of motor response to a noxious stimulation suggest drug overdose or devastating structural injury.


to be continued

Saturday, November 19, 2011

Aspiration Pneumonitis (PART 2)

MANAGEMENT :


The first periority is to clear the upper airway and prevent asphyxia.


Whenever an aspiration is observed endotracheal suctioning should be attempt promptly even if difficult intubation precipitated the aspiration.


Bronchopulmonary lavage is not recomended for acidic aspirates because damage to the lungs occurs within 12 to 18 seconds(3).


In addition more extensive pulmonary damage may occur due to the spread of acidic aspirates to lower regions of the lung.


An immediate danger of particulate aspirates is mechanics obstruction.


Bronchoscopy to remove particulate materials should be performed in this situation. Bronchoscopy is indicated for any patients who shows clinical or rongentnologic signs of large airway obstruction.


Lobar and segmental collapse or atelectasis are the usual findings.


Large food particles may also cause a ball valve obstruction.


Expiratory film or fluoroscopy can confirm this diagnosis.
In these cases bronchoscopy with straight scope is the most effective means of removing aspirated material.a(5,6).


Postural drainage and respiratory therapy with bronchodilators may be useful.


It had been hoped that corticosteroid might interrupt the pulmonary inflamatory response to acid aspiration and ameliorate the subsequent clinical course. Unfortunately after decades of investigation no beneficial effect has been shown (3,5).


There is controversy about the value of systemic steroids in reducing bronchial odema and the alveolar exudate.


Although corticosteroid may attenuate inflamatory pneumonitis the immuno suprresant effect glucocorticoid may exacerbate any seondary bacterial pneumonia or sepsis (3,5).


Secondary bacterial invasion may be an additional threat to recovery and samples of bronchial aspirates should be cultured by bacteriologist.


The use of prophylactic antibiotics cannot be shown to improve the course of the disease or reduce mortality.(5)


The most important measure after pulmonary aspiration is maintainance of pulmonary gas exchange.


Often mechanical ventilation is instituted immediately after any major pulmonary aspiration.Although the prophylactic beneficities of positive pressure ventilation and positive end expiratory pressure on the development
of subsequent lung injury have been debated, such measures are often required merely to provide adequate oxygenation.


PREVENTION :(1,3,4)


Includes : 


1.Save airway management
2.Cricoid pressure
3.Gastric tube the compression
4.Chemoprophylaxis
   - Clear citrate antacids
   - H2 receptor histamine antagonist
   - Proton pump inhibitors
   - Gastro prokinetic agents


Careful and skill airway management is very needed to reduced pulnary aspiration.


Cricoid pressure(Sellick's manouver) when properly applied can prevent the passage of gastric contents into oropharynx, however it may also provokes active vomiting in an unanesthetized patient.


In addition backward pressure on the cricoid cartilage facilitate laryngoscopy in some patients but interference with it in others. Infact in some patients pushing the larynx posteriorly,cephalad and to the right provides the best view of vocalcord but can also impede mask or larygeal mask airway ventilation.


Cricoid pressure during active vomiting has the potential to cause oesophageal rupture, Nasogastric tube permits gastric decompression,it also prevent lowoesopageal sphincter (LES) closure.    


Chemoprophylaxis :


Antacids: Many investigators have demonstrated that particulate antacids are effective in raising gastric fluid pH in reasonably high precentage in both elective and emergent situation.


Indeed their effectiveness in raising fluid pH depends on :


1.The volume and pH of the gastric contents present at the time of their administration.
2.The frequency and timing of antacid administration.
3.The type and amount of antacid given.
4.What manouvers it any are done to promote mixing of antacid with gastric contents.
5.The intrinsix gastric motility present at the time of antacid administration.
6.The rate of ongoing gastric acid production.


The First :


Their administration may increase gastric volume. As example routine of 2-4 hour dosing with antacid became common practice on many obstetrical wards because of the unpredictability of emergency induction of anesthesia as well as concern over acid rebound(a decrease in pH over basal levels four or more hours following antacid neutralization). In the laboring patient(particularly those receiving narcotic for pain) gastric motility is slowed.


Thus such a practice could lead to significant increases in gastric volume.


The second :


Major criticism is that particulate aspirates result not only in as significant of initial pulmonary derangement as a highly acidic aspirate but also in histologic abnormalities that were present as long as one month following aspiration.


These chronic granulomatous response were not noted in groups with acid aspirates.


Particulate antacids are hazardous to the lungs and are therefore contra indicated preoperatively.


Because of these concerns an intense interest has been sparked in soluble antacids.


The propenderance of evidence suggest that soluble antacids are as effective  as particulate antacids in raising gastric fluid pH in both elective or emergency surgical patients if given within 15-60 minute of induction of anaesthesia(4).


Work has demonstrated that soluble antacids mix with gastric contents more readily than particulate antacids. 


Sodium citrate 0.5-1 ml/kg (30 ml max;1 hour preoperatively may increase gatric volume,but decreases gastric fluid pH and no changes in LES tone).


It must be kept in perspective that antacids remain the most rialable pharmacologic method of neutralizing gastric acid in emergent situation.


HISTAMINE  H2 RECEPTOR ANTAGONIST :


(e.g.cimetidine,ranitidine and famotidine)(1,4).


The H2 blockers decrease gastric acid production by competitively inhibiting the action of histamine on the H2 receptor of gastric pariethal cell. In contrast they have no apparent effect on gastric emptying time or the lower esophageal sphincter(LES) pressure. Administration  of cimetidine intravenously one hour before induction of anesthesia in patients presenting for elective surgery has been shown to signifantly decrease the acidity of gastric contents in samples taken immediately following the induction of anesthesia.


A delay onset of cimetidine ,60-90 minutes  following intravenous administration limit its usefulness in emergence situation.


The cimetidine has been reported to inhibit the mixed function oxydase system and to decrease liver blood flow.
Co administration of cimetidine will prolonge the elemination half life of warfarin,diazepam,theophylline,phenythoin and propranolol.


That cimetidine therapy can agravate bronchospasm in asthmatics by allowing histamine to have an opposed H1 effect.


Rapid intravenous administration of relatively large doses(600 mg) of cimetidine in critically patients has been reported to cause hypotension and significant dysrythmia.


Ranitidine has greater potency, longer duration of gastric anti secretory effect (six to eight hours) than cimetidine (four to six hours) and lower incidence of side effects and lesser degree of inhibition of mixed function oxydase system but their clinical utility is limited in truly emergent surgical patients since its onset of action is no more rapid than that of cimetidine 45-60 minutes following intravenous administration.


Famotidine is propanimidamide derivative is the lattest H2 receptor antagonist. Clinical used dosages supress acids production for 10 to 12 hours intravenous administration may be ascociated with slightly faster onset of anti
secretory effect (30 minutes) compared to other H2 receptor antagonist thus offering a limited advantage of famotidine in emergent situation.


Systemic effect of famotidine in the CNS,cardiovascular,respiratory or endocrine system have been negligible to date and minimal drug interactions 
have been identified in clinical trials.


PROTON PUMP INHIBITOR 
(e.g omeprazole,lansoprazole,pantoprazole).


Similarly effective in reducing further gastric acids production but they have no demonstrable advantage over the H2 histamine receptor antagoinist. For aspiration prophylax.


GASTRO PROKINETIC (e.g.metoclopropamide).


A chlorbenzamide derivative which possesses three characteristic which make it potentially very useful in anestesia.


It increases the LES pressure,speeds gastric emptying time, and has anti emetic properties. It has no direct effect on gastric fluid pH.


Its action are mediated centrally via antidopaminergic effects and peripherally by facilitation of cholinergic stimulation, an action predominately limited
to the upper gastric intestinal tract.


Diabetes and others with known or suspected gastroparesis are likely the best candidate for gastroprokinetic medication.


A 10 or 20 mg intravenous dose of metoclopropamide can empty the stomach within 10-20 minutes whereas an oral dose taken 30-60 minutes.


But it is contraindicated to attempt to increase gastrointestinal motility in the presence of intestinal obstruction.


In the dose range commonly employed (0,15 to 0,3 mg)kg, metoclopropamide has proven relatively safe.


Higher dosages especially in children has been ascociated with agitation,irritability,confusion and extrapyramidal symptoms(4).


Pharmacologic agents used for the prophylaxis of pulmonary aspiration in children.(3)


Antacids                                                              GV       pH      LES tone
=====================================================================
Sodium citrate        0,5 - 1 ml/kg                            I          I             0
                              (30 ml max;1 hr BS )
Anti cholenergic:
Glycopyrolate    7,5-10 microgram/kg 1 hr BS         ?         ?             0


H2 blocker  :
Cimetidine              7,5 mg/kg (PM/AM)                   D         I             0
Ranitidin                 1,5- 2mg/kg (1-2 hr BS)             0        I             0
Famotidine              0,5 mg/kg (PM/AM)                   D        I             0


Prokinetic agents::
Metoclopropamide:0,1mg/kg (1 hr BS)                     D        0            I


Proton pump inhibitor :
Lansoprazole         1,5 mg/kg (PM/AM)                     D        I            0
Omeprazole           0,3 mg/kg (PM/AM)                     D        1           0
Pantoprazole         1,4 mg/kg    QID                          D        I            0
======================================================================
hr=hour  BS=before surgery  PM=night before  AM=morning of surgery
GV=gastric volume, pH=pH gastric contents  LES=low esophageal sphincter
 I=increase  D=decrease  0=no effect.
======================================================================
Extubation in patient at high risk for pulmonary aspiration should be performed when the patient fully awake and has full return of neuromuscular functions (3).


SUMMARY :


Aspirations of gastric contents to the lungs account for at least 10 percent of deaths attributable to anaesthesia.


The likelihood of pulmonary aspiration is three to four times greater for emergency surgery than the elective surgery.


The preoperative factor most often ascociated with aspiration is gastrointestinal obstruction.


The classic symptoms complex associated with pulmonary aspiration is sudden in onset,with wheezing,shortness of breath, cyanosis and tachycardia.


Pneumonitis aspiration which result from chemically induced damage to lung tissue where pneumonia aspiration is caused by a bacterial infections.


The first periority of treatment is to clear the upper airway and prevent asphyxia. Endotracheal suctioning should be attempt promptly whenever an aspiration is observed.


Brochoscopy is indicated for any patients who shows clinical or rongentnologic signs of large airway obstruction.


Bronchopulmonary lavage is not recomended for acidic aspirate because damage to the lungs occurs within 12 to 18 seconds, in addition more extensive pulmonary damage may occur due to the spread of acidic aspirates to lower regions of the lungs.


The use of prophylactic antibiotics cannot be shown to improve the course of the disease or reduce mortality.


The use of corticosteroid not recomended because the immuno supressant effect of corticosteroid may exacerbate any secondary bacterial pneumonia or sepsis.


Particulate antacids are hazardous to the lungs and therefore contraindicated preoperatively.


The most important measure after pulmonary aspiration is maintainance of pulmonary gas exchange.


REFERENCES 


1.Tasch D.Mark : Pulmonary Aspiration ;Atlee L.John: Complications in Anesthesia,2nd edit,Saunders Elsevier,2007. pp 186-88.


2.Meyer mark : Perioperative Aspiration Pneumonitis ;Atlee l.John: Complications in Anesthesia;2nd edit,Saunders Elsevier,2007. pp 641-43.


3.Schultetin.R.Ray : Aspiration Pneumonitis;Atlee.L.John:Complications in Anesthesia;2nd edit,Saunders Elsevier,2007,pp 157-60.


4.Mc Cammon L.Ri : Aspiration Pneumonitis Prophylaxis and Prevention; International Anesthesia Research Society,Review Course Lectures, San Diego california ,1988,pp.40-44.


5.Spence A.Alastair : Post operative Pulmonary Complication;Nun.FJ,Utting EJ Brown R.Burmell;General Anaesthesia,5th edit;Butterworths ,London,Boston,1989.pp.1153-4.


6.Wynne W.James : Aspiration Pneumonitis;Ravin B.Mark:Problems in Anesthesia; A Case Study Approach;Little Brown and Company,Boston.1981,pp 237-41.


7.Lebowitz W.Philip,:Emergency Complicating Anesthesia.Lebowitz.W.Philip Clark L.John. Clinical Anesthesia Procedures of the Massachusetts General Hospital,Little Brown and Company,Boston, 1978,pp.350-1.

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