ECG changes occur in a large precentage of patients with SAH including changes that can be confused with myocardial ischaemia such as ST segment and T wave changes and even rarely Q waves and are more frequent in those with severe neurologic impairment.
The most common are inversion of the T-wave and depressed of the ST segment and premature ventricular complex.
The ECG abnormalities occur within 48 hours of the SAH and may last up to six weeks.These may be life threatening in 5% of patients in the first 48 hrs after SAH.The onset of arrhythmia is most frequently within the first seven days after SAH,the peak occurence is between days 2 and 3 and may return to normal in 10 days or the abnormalities may persist for up to six weeks.
The abnormalities may also changes from one day to the next and may occur intra or postoperatively.
The exact etiology of these ECG abnormalities is unknown.
They have been attributed to post SAH injury to the posterior hypothalamus which release of nor epinephrine from adrenal medulla and sympathetic cardiac afferents and resultant ischemic subendocardial changes.
This relation to hypothalamic injury is supported by the coexistence of high urinary catecholamine,ECG changes
hypertension and hypothalamic and cardiac lesion including subendocardial hemorrhage and myocytolysis.
Electrolyte imbalance such as hypokalemia may also play
a role in the genesis of ECG changes after SAH. Most ECG abnormalities are neurogenic rather than cardiogenic in origin although some patients do have myocardial infarction after SAH.This is often difficult to differentiate especially in patients with coexisting cardiac disease,an echocardio-
graphy and /or pulmo-nary artery catheter may be valuable in these patients. Although non spesific ECG changes not accompanied by symptoms or signs of myocardial dysfunc-
tion are probably insignificant, it's probably prudent to wait as long as possible before proceeding with surgery in those patients with changes suggestive of myocardial infarction as the risk of malignant dysrhythmia is high.
The benefit of early surgery have to be weighed against possible perioperative mycardial ischemia.
May be better to wait at least 72 hrs unless there are mass effects or the patient's condition allows 10-14 days wait.
The prophylactic administration of beta adrenergic blocking drugs or autonomic antagonist has improved cardiac outco-
me in some patients after SAH but not in others.
In acute ECG changes occur in the operating room in conjunction with hypertension or tachycardia and require treatment it is likely appropriate to use beta blockers as first line therapy with NTG reserved for those cases in which clinical judgement dictates that myocrdial disturbance is resulting from coronary artery diseases.
Diltiazem or verapamil may also be reasonable choices if heart rate is an issue and beta blockers are unavailable ,contra indicated or ineffective.
NEUROLOGIC ASSESSMENT:(1,2)
A detailed examination to assess the level of conciousness and the presence of focal neurological deficits should be performed.
Conciousness may be lost temporarily (or longer) because acute rise in ICP,followed by headache and stiffneck as a result of SAH.
Focal or generalized neurologic deficits may be the result of hematoma edema or vasospasm.
Evidence of raised ICP,cerebral vasospasm,hydrocephalus,
and intracranial mass effect should be sought.
If ICP is severely elevated, control hypotension should not be used,to the extent that cerebral perfusion is further compromised.
The time for peak incidence of vasospasm is from about day 4 to day 14 after bleeding, it does not mean that vasospasm cannot occur at other times.
The etiology of vasospasm is under intense investigation and nitric oxide endothelium and the inflamatory response appear to be intimately involved in its pathogenesis.
Calcium channel blocking drugs including nicardipine and nimodipine are currently inwise use for the prevention of delayed ischemic deficit after SAH.
Nimodipine diminishes the myoplasmic calcium in smoot muscle cells and impedes the entry of of extracellular calcium necessary for the contraction of the smooth muscle.The administration of nimodipine to all patients within 96 h of SAH has reduced the incidence of poor outcome by 40 to 70%.
Since calcium antagonist tend to reduce patient's blood pressure patients may need hydration immediately before induction of anesthesia and careful attention to fluid balance intra and post operatively. The intrathecal use of recombinant tissue plasminogen activator (RTPA)
has been shown to resolve subarachnoid clots thereby preventing vasospasm in primates and human,reduced the severity of angiographic vasospasm and improved the clinical neurologic grade of the patients.
Alternatively the superselective intraarterial infusion of papaverine(2mg over 10 s)has been to be effective in dilating spesific vessels not accesible to angioplasty technique.
Blood in the subarachnoid space may occlude the aracnoid villie and lead to the development of hydrocephalus which the mortality is higher.
Symptoms include headache,drowsiness,confusion and agitation. If hydrocephalus develops before the aneurysm has been secured a ventriculair drain may improve the neurological state of the patient.
The CSF should be drained to 15-20 cmH20 to avoid excess ventricular decompression which may cause the aneurysm to re-rupture.
Because the decrease in ICP can theoretically cause rupture of an unstable aneurysm by increasing pressure across the aneurysm wall,remember that transmural pressure = MAP - ICP. Futhermore,herniation through the foramen magnum could also occur if a large intracranial mass effect exist from blood,edema and hydrocephalus seizures can occur following SAH and lead to acute increase in blood pres-
sure and rebleeding.When present seizures should be controlled with anti convulsants but there is currently no evidence to support the prophylactic use of anticonvulsants in patients following SAH and hence they are not rutinely
administered at some institution.
PULMONARY EVALUATION:(1,2,3)
Respiratory dysfunction common after SAH can be result of poor ventilation drive,decreased level of conciousness and aspiration of stomach contents or neurologic pulmonary edema,therefore thorough evaluation of the respiratory system must include examination of evidence of pulmonary edema,basal atelectasis and aspiration pneumonia.
The oxygen and ventilatory requirements,arterial blood gases and chest X ray are assessed.
The obtunded patient with an SAH may have retention of secretions with subsequent atelectasis and propensity to airway hyperirritability.
Chest physical therapy and vigorous coughing are probably not to encourage in a patient with fresh clot in a ruptured aneurysm but deep breathing and gentle cleaning of accumulated pulmonary secretions are reasonable.
Although anti cholinergic are not required should be recomended their perioperative use in this situation to minimize the further impact secretions.
In addition to making atelectasis more likely secretions may predispose to laryngospasm,bronchospasm and continued outpouring of saliva that can potentially loosen the securement even of a carefully taped endotracheal tube.
The dislodgement of the airway in a prone position with a pin head an exposed posterior fossa is a true neuroanes-
thetic nightmare.
If oxyenation appears to be impaired by secretion or atelectasis the old fashion used of of several large sigh volumes(two times the usual tidal volume) followed by reasonably large tidalvolume(12 to 15 ml/kg) along with appropriate suction is generally curative.
Pulmonary complication including cardiogenic and neuro-
genic pulmonary edema and pneumonia were the most common non neurologic cause of death in patients after SAH and as such,were responsible for 50% of all deaths from medical complication at three months.
Pneumonia and adult respiratory distress syndrome(ARDS)(28%)and pulmonary emboli(16%) led the list of fatal pulmonary complications.
The frequency of pulmonary edema increased in patients older than 30 years. Poor clinical grade at the time of admission also correlated with a higher frequency of respiratory dysfunction,suggesting neurologic influence (e.g.sympathetic discharge after initial hemorrhage)
The significance of Solenski's study is that it substantiate the need to prevent,recognize,and treat potential medical complication of SAH,especially pulmonary problems to reduce the overall mortality rate.
Patients need high levels of inspired oxygen and positive end expiratory pressure to maintain borderlines arterial blood gases should have their operation postphoned until the respiratory function improves.
Avoiding secondary hypoxaemia insults is important.
OTHER MEDICAL COMPLICATIONS:
Hepatic dysfunction including hepatic failure and hepatitis numbers among the medical complications after SAH.
A total 24% of 455 patients in Solenkie's series had hepatic dysfunction either at the time admission or during the first 14 days after SAH.
No association between hepatic dysfunction and age,use of alcohol 24h before admission,or use of non steroid anti inflamatory drugs,anti convulsant drugs or histamine -2 receptor blocking drugs.
Almost 8% patients develops renal dysfunction after SAH and 15% of those have severe dysfunction. Nearly 20% of the renal failure patients had sepsis.
During the first 14 days after SAH,4% of patients were reported to develop thrombocytopenia and 35% of those had sepsis.
Other reported hematologic disorders include desseminated intravascular coagulation and leukocytosis.
TIMING OF SURGERY AND SURGICAL CONSIDERATION:(2,3)
Rebleeding is an obvious and serious cause of morbidity and mortality in the population with SAH and is most likely to occur soon after the initial rupture.
The time of aneurysm surgery has been a matter of some controversy in the the neurovascular literature.
In the past,surgeons were more likely to wait several weeks before surgery encountered better operating conditions than possible in early surgery and reported that surgical mortality was reduced by waiting.
Unfortunately this finding was a result of operating on a diminished and highly selected population that had survived the demons of rebleeding,vasospasm and medical complica-
tion such as pneumonia and pulmonary embolism which inevitably occur in sick patients lying in hospital beds.
Technical advances in anesthesia and neurosurgery now make the conditions early surgery more tolerable and more tenable, Many surgeons now advocate early (within 72 hrs) surgery before rebleeding,vasospasm and other complica-
tions occur.
Early surgery removes blood that may contribute to the production of vasospasm and allows for more agressive treatment of vasospasm.
An international study performed several years ago found no differences in outcome between early and late (11 to 14 days after bleeding) surgery,but analysis of their result of North American Surgeon found that early surgery had the
advantage.
Operations performed 7 to 10 days after SAH usually disclosed a slack easily manipulable brain and thougher aneurysmal sac that was less likely to rupture during dissection.There were also problems associated with the post-phonement of surgery however,mortality increased to as high as 40% in patients who rebleed during this waiting period.
It was also harzardous to use triple H to treat delayed ischemia from vasospasm before the aneurysm had been secured.
The proponents of early surgery is the first 24 to 48 hrs sfter SAH cite the advantages of the prevention of rebleeding,the reduction in the incidence vasospasm by the removal of blood from subarachnoid space and the ability
to use volume expansion and deliberate hypertension with relative safety to treat vasospasm once the aneurysm has been clipped.
Other considerations favoring early operative intervention include the reduction medical complications (pneumonia,pulmonary embolus,deep thrombosis
electrolyte imbalance ,gastric ulcer),anxiety on the part of the patients and their family and the cost of prolonged hospitalization.
The International Cooperative Study on the Timing of Aneurysm Surgery,a non randomized,prospective study,
tabulated the results of contemporary surgical and medical management of 3521 aneurysm patients in 68 neurosurgi-
cal centers around the world.At the time of admission,75% of the patients were in good conditions.
Surgery was performed in 83% of the patients.
Vasospasm,rebleeding and the effects of the initial hemorrhage were the leading cause of death.
At the end of first 6 month ,58% of the patients had made a complete recovery and 26% were dead.
The neurosurgeons participating in the study noted a 50% incidence of brain swelling or tightness when patients were operated on day 0 or1 after SAH, as opposed to a 20% incidences when surgery was performed on day10 or later.
Despite this reduction in the rate of rebleeding the overall management results indicated a mortality of 20% and good outcome in 60% of patients wether they had early (0 to 3 days) or late (11 to 14 days) surgery.
The similarity of overall morbidity and mortality was attributed primarily to development of vasospasm.
The outcome was least favourable and mortality was highest when surgery was performed 7 to 10 days after SAH which coincided with the peaking of vasospasm.
In alerts patients timing was not a factor at all.
Ofnote is the fact that outcomes reflected considerable variability among the participating centers,related to casemix and patient management.
to be continued
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