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random
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Posting #21: Mon Jan 28th, 2008 09:51 |
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I suddenly feel the urge to pee after so many 
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Moolah
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Posting #22: Mon Jan 28th, 2008 09:59 |
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madviruz wrote: Moo,
I'm sure many love cincau.
Its just some can't make good cincau.
- the flavour is lost in translation.
So you really don't like cincau?
So what kind of cincau concoction have you discovered lately?
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madviruz
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Posting #23: Mon Jan 28th, 2008 12:34 |
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On the reality front, I have tasted chincau with durian and santan.
It is heavenly.
Its not bull.
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madviruz
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Moolah
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Posting #24: Tue Jan 29th, 2008 00:43 |
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madviruz wrote: On the reality front, I have tasted chincau with durian and santan.
It is heavenly.
Its not bull.
Durian wif santan?
Ok.. I gotta try this!
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prophet
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Posting #25: Tue Jan 29th, 2008 01:38 |
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madviruz wrote: Would you please not say Cincau is mambo jambo? Please?
Cows do need something to believe in, yes? Without believes.. what reasoning is left to be si lembu?
Moo, I am happy to inform you that this is an unknown unknown so you can continue to drink and believe.
... In ze mediocal world, how would you recommend handling a stroke vic?
Prophet, I will not listen to a soothsayer who prophesies a known quakery but sent him to the hospital.
For those who are interested, please do continue,
Spontaneous intracerebral hemorrhage: Prognosis and treatment
Guy Rordorf, MD
Colin McDonald, MD
UpToDate performs a continuous review of over 375 journals and other resources. Updates are added as important new information is published. The literature review for version 15.3 is current through August 2007; this topic was last changed on September 09, 2007. The next version of UpToDate (16.1) will be released in March 2008.
INTRODUCTION — Intracerebral hemorrhage (ICH) is the second most common cause of stroke, trailing only ischemic stroke in frequency.
This topic will discuss the prognosis and treatment of spontaneous intracerebral hemorrhage. Other aspects ICH are discussed separately. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis").
PROGNOSIS — The 30-day mortality from ICH ranges from 35 to 52 percent [1-5]; one-half of these deaths occur within the first two days [3,6]. Furthermore, only a small number of patients function independently after the event. In a prospective study of 166 patients with spontaneous ICH from a large US metropolitan area, only 12 percent were normal or minimally handicapped at 30 days [7]. In a population-based cohort of patients hospitalized after ICH in the Greater Cincinnati/Northern Kentucky area, the ten-year survival was 18 percent [5].
The prognosis for functional recovery from ICH depends upon the location of hemorrhage, size of the hematoma, level of consciousness, patient age, and overall medical health and condition [3,4,6,8,9]. In addition, preceding oral anticoagulation therapy, and possibly antiplatelet therapy, appears to be associated with worse outcomes after ICH [6,10].
Long-term survival after primary ICH also appears to be decreased compared with controls from the general population matched for age and sex, as illustrated by two studies from Finland. A retrospective cohort study identified 411 patients with first ever ICH and found that the annual risk of dying compared with controls was increased 4.5-fold during the first year after ICH and 2.2-fold during years two to six [4]. A subsequent longitudinal prospective cohort study evaluated patients who had survived the first three months after ICH and observed that the mortality at seven years was significantly higher than controls (32.9 versus 19.4 percent) [11].
Initial ICH volume and level of consciousness — The ICH volume on initial head CT scan and level of consciousness on admission may be particularly important prognostic indicators. This point is illustrated by a study of 188 patients with ICH that analyzed predictors of 30-day mortality [3]; the following observations were made: An ICH volume of 60 cm3 or greater on initial CT and a Glasgow coma scale score (show table 1) of eight or less predicted a 30-day mortality of 91 percent. An ICH volume less than 30 cm3 and a Glasgow coma scale score of nine or more predicted a 30-day mortality of 19 percent.
Hematoma growth — Hematoma growth is also an independent predictor of mortality and poor outcome. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on Hemorrhage enlargement).
Supporting evidence comes from a meta-analysis of 218 patients with spontaneous ICH who had head CT scan within three hours of onset and follow-up head CT within 24 hours [12]. Each 10 percent increase in ICH growth was associated with increased mortality (hazard ratio 1.05, 95% CI 1.03-1.08) and worse outcome as measured by the modified Rankin scale (mRS) (odds ratio 0.84, 95% CI 0.75-0.92). That is, for each 10 percent increase in hematoma volume, patients were 5 percent more likely to die and 16 percent more likely to increase one point on the mRS (show table 2).
In a retrospective report involving 104 patients with acute ICH, the presence of small foci or larger areas of contrast extravasation within the hematoma on CT angiography source images was independently associated with hematoma expansion [13]. Similar results were reported in a smaller prospective study [14].
Early neurologic deterioration — Early neurologic deterioration within 48 hours after ICH onset is not infrequent and is associated with a poor prognosis. Potential mechanisms include hemorrhage enlargement, development of hydrocephalus, and perilesional edema [15]. The inflammatory response to the hemorrhage may also play a role. In a prospective series of 157 patients with ICH, 37 patients (24 percent) died within two days after the onset of symptoms [6]. Factors that independently contributed to two-day mortality were pineal gland displacement on CT of 3 mm or more, blood glucose on admission of 150 mg/dL (8 mmol/L) or more, eye and motor score on the Glasgow coma scale of 8 out of 10 or less, and hematoma volume of 40 cm3 or more. Prognostic indicators for death over the next year included age 70 years or older and severe handicap on day three.
Other reports have also noted that elevated admission blood glucose after ICH is a poor prognostic indicator [4,16,17]. However, it is unclear if elevated glucose directly contributes to poor outcome, or if it alternatively is present secondarily as part of the stress response to severe ICH. In a cohort study of 266 patients with ICH admitted within 12 hours of stroke onset, early neurologic deterioration occurred in 61 (23 percent) and was associated with an eight-fold increase in the probability of a poor outcome (95% CI 2.7-25.5) [18]. Independent predictors of early neurologic deterioration on admission included elevations in body temperature, neutrophil count, and serum fibrinogen level (odds ratios 24.5, 2.1, and 5.6, respectively), all of which could be interpreted as markers of an inflammatory response. Factors measured at 48 hours that were associated with early neurologic deterioration included ICH growth on repeat head CT, intraventricular bleeding, and high systolic blood pressure. In many [6,15,19,20] but not all [18] reports, the initial ICH volume on CT is an independent predictor of early deterioration.
Preceding anticoagulant or antiplatelet use — In the setting of an acute ICH, patients with preceding use of anticoagulants or antiplatelet agents might be expected to have larger initial hematoma volumes or greater hemorrhage enlargement leading to worse outcomes. Accumulating evidence suggests that this notion may be correct, at least with regard to anticoagulants [10,21-24]. However, the issue is not simple, as patients receiving these therapies may be older and have greater comorbidities than those who are not. In addition, the available evidence is mainly observational.
Patients on warfarin have a mortality rate as high as 52 to 73 percent after ICH [10,22,23], and a population-based study from northern Finland reported that warfarin use at the onset of ICH was an independent risk factor for death within three months of ICH (relative risk [RR] 3.2; 95% CI 1.6-6.1) [10].
The evidence regarding preceding antiplatelet use with prognosis after ICH is not as clear, with some [10,21] but not all [23-26] studies reporting worse prognosis or greater hematoma enlargement with ICH. Nonetheless, the more convincing studies do support such a relationship. As an example, the population-based study from Finland reported that regular aspirin use at the onset of ICH was a significant independent risk factor for death within three months of ICH (RR 2.5; 95% CI 1.3-4.6) [10]. However, further evidence is needed to confirm whether antiplatelet therapy is a true independent risk factor for poor prognosis after ICH, or merely a marker for older, sicker patients.
ICH score — A simple six-point clinical grading scale called the ICH score has been devised to predict mortality after ICH [27]. This scale incorporates several clinical components that may be independent predictors of outcome.
The ICH score is determined by adding the score from each component as follows: Glasgow Coma Scale (GCS) score 3 to 4 (= 2 points); GCS 5 to 12 (= 1 point) and GCS 13 to 15 (= 0 points) (show table 1) ICH volume 30 cm3 (= 1 point), ICH volume <30 cm3 (= 0 points) Intraventricular extension of hemorrhage present (= 1 point); absent (= 0 points) Infratentorial origin yes (= 1 point); no (= 0 points) Age 80 (= 1 point); <80 (= 0 points)
Thirty-day mortality rates increased steadily with ICH score; mortality rates for ICH scores of 1, 2, 3, 4, and 5 were 13, 26, 72, 97, and 100 percent, respectively. No patient with an ICH score of 0 died, and none had a score of 6 in the cohort.
The ICH score has been validated by retrospective [28] and prospective [29] analysis. A modified ICH score [28] using the National Institutes of Health Stroke Scale (NIHSS) score [30] (show table 3) in place of the GCS score may be a better predictor of good outcome than the original ICH score.
Limiting care — Prognostication for individual patients with acute ICH remains an uncertain science at best, and accumulating data suggest that the inappropriate early use of do not resuscitate (DNR) orders or withdrawal of care may negatively influence outcome in patients with ICH. One study found that physicians tended to be overly pessimistic regarding prognosis for ICH based on information available at the time of patient presentation, potentially leading to a self-fulfilling prophecy [31]. A later study found that in-hospital mortality after ICH was significantly influenced by the rate at which different treating hospitals used DNR orders within the first 24 hours after admission, even after adjusting for case mix [32]. The risk of patient death was not defined solely by DNR status but by an interaction between DNR status and the frequency of early DNR use by hospital. In addition, hospitals in the highest quartile of early DNR use had significantly less frequent use of aggressive procedures such as craniotomy, ventriculostomy, and cerebral angiogram, compared with hospitals in the lowest quartile. These findings suggest that early DNR use might be a surrogate for a nonaggressive approach to treating ICH. A population-based study from Texas identified 270 nontraumatic cases of ICH and noted that 34 percent of patients had DNR orders, withdrawal of care, or deferral of other life-sustaining interventions in the first 24 hours after presentation [33]. These were analyzed together as early combined DNR. After adjustment for known predictors of ICH mortality (age, gender, ethnicity, Glasgow Coma Scale, ICH volume, intraventricular hemorrhage, and infratentorial hemorrhage), early combined DNR was associated with a two-fold increase in the hazard of death both at 30 days (hazard ratio [HR] 2.17, 95% CI 1.38-3.41) and at last (median 417 days) follow-up (HR 1.92, 95% CI 1.29-2.87).
Early DNR orders or limitations to care are not always inappropriate after ICH; the difficulty lies in deciding when such limitations are indeed the most appropriate approach [32].
Current guidelines suggest careful consideration of aggressive full care during the first 24 hours after ICH onset and postponement of new DNR orders during that time [9]. The recommendation does not apply to patients with preexisting DNR orders.
Recurrence — Recurrent hypertensive ICH occurs in as many as 5 percent of patients [34-36]. Recurrence is most common within two years of the first hemorrhage [35], with the most important risk factor being uncontrolled hypertension [34].
TREATMENT — Management of intracerebral hemorrhage (ICH) involves a combination of medical and surgical interventions [9,37]. Guidelines from the American Heart Association/American Stroke Association (AHA/ASA) issued in 2007 recommend that patients with ICH receive monitoring and management in an intensive care unit [9]. This recommendation is based upon the frequent association of ICH with elevations in intracranial pressure and blood pressure, the need for intubation and mechanical ventilation, and multiple medical issues and complications.
General management issues — The initial general management of patients with suspected stroke is briefly summarized here [9]. Sources of fever should be treated, and current guidelines suggest the use of antipyretic medications to lower body temperature to normothermia in febrile patients with stroke [9]. (See "Initial assessment and management of acute stroke", section on Fever). Hyperglycemia in the first 24 hours after stroke is associated with adverse outcomes, and current guidelines suggest insulin treatment for elevated serum glucose >140 to 185 mg/dL (>7.8 to 10.3 mmol/L) [9]. (See "Initial assessment and management of acute stroke", section on Serum glucose). Options for the prevention of venous thromboembolism and deep venous thrombosis in patients with ICH include intermittent pneumatic compression, low-dose subcutaneous low molecular weight heparin, unfractionated heparin, and placement of a vena cava filter [9]. These options are discussed in detail separately. (See "Anticoagulant and antiplatelet therapy in patients with an acute or prior intracerebral hemorrhage"). Early mobilization and rehabilitation are suggested in patients with ICH who are clinically stable [9].
Reversal of anticoagulation — For patients who develop an ICH, all anticoagulant and antiplatelet drugs should be discontinued acutely for at least one to two weeks after the onset of hemorrhage, and anticoagulant effect should be reversed immediately with appropriate agents [9,38].
Aggressive use of intravenous vitamin K, prothrombin complex concentrate, and other factors may be necessary in patients who suffer an ICH while taking warfarin. Reversal of anticoagulation in this setting is discussed in detail separately. (See "Management of warfarin-associated intracerebral hemorrhage", section on Reversing the coagulation defect).
There is a risk of creating a prothrombotic state when acutely reversing anticoagulation in a patient with atrial fibrillation; however, the risk of extending the hemorrhage outweighs this potential risk [39].
Protamine sulfate is recommended for urgent treatment of patients with heparin-associated ICH [9]. Protamine sulfate can be administered by slow intravenous infusion (not greater than 20 mg/min and no more than 50 mg over any 10-minute period). The appropriate dose of protamine sulfate is dependent upon the dose of heparin given and the time elapsed since that dose. (See "Therapeutic use of heparin and low molecular weight heparin", section on Use of protamine).
Intracranial pressure control — Increased intracranial pressure (ICP) due to ICH can result from the hematoma itself and from surrounding edema, and may contribute to brain injury and neurologic deterioration. Current guidelines recommend a balanced and graded approach to the management of elevated ICP, beginning with simple measures that include the following [9]: Elevation of the head of the bed to 30 degrees, once hypovolemia is excluded Analgesia and sedation, particularly in unstable, intubated patients
Sedation should be titrated to control pain and minimize ICP elevation, while still permitting clinical evaluation of the patient's neurologic status [9]. Suggested intravenous agents for sedation are propofol, etomidate, or midazolam. Suggested agents for analgesia and antitussive effect are morphine or alfentanil. (See "Use of sedative medications in critically ill patients").
Glucocorticoids should not generally be used to lower the ICP in patients with ICH. A randomized trial found that dexamethasone did not improve outcome but did increase complication rates, primarily infection [40].
Aggressive measures — More aggressive therapies for reducing elevated ICP include osmotic diuretics (eg, mannitol and hypertonic saline solution), ventricular catheter drainage of cerebrospinal fluid, neuromuscular blockade, and hyperventilation [9]. Use of these therapies generally requires continuous monitoring of ICP and arterial blood pressure, with the goal of maintaining cerebral perfusion pressure (CPP) above 70 mmHg [9]. However, the development of cerebral ischemia is still possible even with CPP-guided therapy.
CPP equals mean arterial pressure (MAP) minus ICP. Lowering ICP helps to maintain CPP in an adequate range. (See "Evaluation and management of elevated intracranial pressure in adults"). Intravenous mannitol is the treatment of choice to lower ICP. It is administered as an initial bolus of 1 g/kg, followed by infusions of 0.25 to 0.5 g/kg every six hours. The goal of therapy is to achieve plasma hyperosmolality (300 to 310 mosmol/kg) while maintaining an adequate plasma volume; major side effects include hypovolemia and a hyperosmotic state [9]. Normal saline initially should be used for maintenance and replacement fluids; hypotonic fluids are contraindicated. Mild hypernatremia should be tolerated, but marked hyperosmolality should be avoided to prevent precipitation of acute renal failure [41]. (See "Complications of mannitol therapy" and see "Osmolal gap"). Barbiturate anesthesia can be used if mannitol fails to lower ICP to an acceptable range. Barbiturate coma acts by reducing cerebral metabolism, which results in a lowering of cerebral blood flow and thus decreases ICP [9]. It is of variable benefit for the treatment of elevated ICP from a variety of causes and is associated with a high rate of severe side effects, especially arterial hypotension [42]. Continuous electroencephalogram monitoring is suggested during high-dose barbiturate treatment, with the dose titrated to a burst-suppression pattern of electrical activity [9]. The ICP lowering effect of hyperventilation to a PaCO2 of 25 to 30 mmHg is dramatic and rapid. However, the effect only lasts for minutes to a few hours. Thus, we reserve hyperventilation until the above therapies have been maximized [43]. Neuromuscular blockade is sometimes employed to reduce ICP in patients who are not responsive to analgesia and sedation alone, as muscle activity can contribute to increased ICP by raising intrathoracic pressure, thereby reducing cerebral venous outflow [9]. Drawbacks of neuromuscular blockade include an increased risk of pneumonia and sepsis. In addition, the ability to evaluate the neurologic status is lost once the patient is paralyzed. (See "Use of neuromuscular blocking medications in critically ill patients"). Cerebrospinal fluid drainage by intraventricular catheter placement (ventriculostomy) is an effective means of lowering ICP [9]. However, there are no prospective studies. Ventriculostomy is often used in the setting of obstructive hydrocephalus, which is a common complication of thalamic hemorrhage with third ventricle compression, and of cerebellar hemorrhage with fourth ventricle compression.
Ventriculostomy allows a means of both monitoring ICP and relieving hydrocephalus. Some patients will develop communicating hydrocephalus and require a ventriculoperitoneal shunt. Available evidence suggests its use is associated with high rates of morbidity and mortality [44,45]. Infectious complications include bacterial colonization in 0 to 19 percent of patients [46,47] and bacterial meningitis in 6 to 22 percent [47,48].
Blood pressure control — The mean arterial pressure (MAP) is often elevated in patients with ICH and, by definition, in patients with hypertensive hemorrhage. Severe elevations in blood pressure may worsen ICH by representing a continued force for bleeding. However, the increased MAP may be necessary to maintain cerebral perfusion in some patients, and lowering the arterial pressure (eg, to a systolic blood pressure [SBP] below 130 mmHg) may cause ischemia.
Although prospective data are limited, the evidence regarding blood pressure management in ICH is illustrated by the following observations: The tissue around small to moderate sized hemorrhages is not ischemic and blood pressure can be lowered by at least 15 percent without causing ischemia in the perihemorrhage tissue [49]. This point is supported by a study of 14 patients with relatively small intracerebral hemorrhages, which found that lowering the MAP by 17 percent (143 to 119 mmHg) did not cause a change in global or regional cerebral blood flow [49]. Local cerebral autoregulation appears to be intact in both patients and animals with intracranial hemorrhage [49,50]. An observational study found that a treatment target SBP of 160 mmHg was associated with hematoma enlargement compared with target SBP of 150 mmHg [51]. However, it is uncertain whether higher blood pressure was an effect of hematoma growth or a contributing cause to hematoma growth [9]. In a prospective observational study of 27 patients with acute ICH and hypertension, blood pressure was treated to a target of <160/90 mmHg [52]. While neurologic deterioration and hemorrhagic expansion occurred in 6 and 9 percent of patients, there was a trend toward improved outcome in patients who had blood pressure treated within six hours of ICH onset.
The relationship of hematoma growth and blood pressure in the context of ICH pathogenesis is discussed separately. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on Hemorrhage enlargement).
Guidelines — Current guidelines for managing elevated blood pressure in acute spontaneous ICH are as follows (show table 4) [9]: For patients with SBP >200 mmHg or MAP >150 mmHg, consider aggressive reduction of blood pressure with continuous intravenous infusion of medication accompanied by frequent (every five minutes) blood pressure monitoring For patients with SBP >180 mmHg or MAP >130 mmHg and evidence or suspicion of elevated ICP, consider monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medication to keep cerebral perfusion pressure in the range of 61 to 80 mmHg For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, consider a modest reduction of blood pressure (eg, target MAP of 110 mmHg or target blood pressure of 160/90 mmHg) using intermittent or continuous intravenous medication, and clinically reexamine the patient every 15 minutes
Labetalol, nicardipine, esmolol, enalapril, hydralazine, nitroprusside, and nitroglycerin are useful intravenous agents for controlling blood pressure [9].
Seizure prophylaxis and treatment — The risk of seizures in patients with acute spontaneous ICH ranges from 4.2 to 29 percent. The frequency depends in part on the extent of monitoring, as seizures associated with ICH are often nonconvulsive [9]. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on Clinical presentation).
Appropriate intravenous antiepileptic treatment should be used to quickly control seizures for patients with ICH. The choice of the initial antiepileptic agent depends upon individual circumstances and contraindications. Current guidelines suggest lorazepam or diazepam followed directly by intravenous fosphenytoin or phenytoin [9].
Some experts suggest a brief period of antiepileptic prophylaxis soon after ICH onset as a potential means of reducing the risk for early seizures in patients with lobar hemorrhages [9]. However, this strategy has not been tested prospectively in clinical trials.
Surgery — The indications for surgery in patients with ICH vary with the site of the bleed.
Surgical removal of hemorrhage with cerebellar decompression should be performed for patients with cerebellar hemorrhages greater than 3 cm in diameter who are deteriorating, or who have brainstem compression and/or hydrocephalus due to ventricular obstruction [9,53]. Surgery decreases the risk of brainstem compression and obstructive hydrocephalus. External drainage alone, without posterior fossa decompression, may create the theoretical opportunity for upward herniation of the cerebellar mass.
Surgical hematoma evacuation for supratentorial ICH is controversial [9,54-61]. A meta-analysis published in 1997 found insufficient data to draw conclusions regarding the risk/benefit ratio of surgery [54] In a small trial (n = 20), patients with ICH assigned to early surgery (the median time from onset of symptoms to surgery was 8.5 hours) showed a nonsignificantly higher rate of good outcome at three months than patients treated medically (56 and 36 percent) [62]. In addition, surgery was associated with a statistically significant improvement in one of the secondary outcomes, the National Institutes of Health Stroke Scale (NIHSS) score (4 versus 14). Another small study of ultra early surgical evacuation was stopped prematurely because surgery within four hours of ICH symptom onset showed a trend towards increased rebleeding compared with surgery within 12 hours (40 versus 12 percent, respectively) [56]. Postoperative rebleeding was significantly associated with increased mortality. In the International Surgical Trial in Intracerebral Haemorrhage (STICH), patients assigned to early surgical hematoma evacuation (n = 503) were slightly more likely to have a favorable outcome at six months compared with initial conservative treatment (n = 530), but the trend did not reach statistical significance [60]. Benefit from early surgery was nonsignificantly more likely in patients who had craniotomy as opposed to alternate techniques, and in those with hematoma located 1 cm or less from the cortical surface.
Although the STICH trial was designed to investigate the effectiveness of early surgery (within 24 hours of randomization), the STICH trial does not address the effectiveness of very early surgery in the first 12 hours after ICH onset [61,63,64]. First, considerable delay to surgery was possible in the "early surgery" group, since patients were randomly assigned within 72 hours after hemorrhage onset and then treated within 24 hours after randomization; the median time to surgery in this group was 30 hours. In addition, the trial design permitted crossover to surgery in patients initially assigned to conservative medical management; such crossover occurred in 26 percent of the conservative group, mainly because of neurologic deterioration, at a mean time of 60 hours. Therefore, the trial more accurately assessed the surgical removal of ICH at about 30 hours versus initial medical management with or without delayed surgery [64].
Open craniotomy is the most widely studied surgical techniques in patients with supratentorial ICH [9]. Other methods include endoscopic hemorrhage aspiration, use of fibrinolytic therapy to dissolve the clot followed by aspiration, and CT-guided stereotactic aspiration.
Because of the questionable efficacy of surgery, it should only be considered as a life saving procedure to treat refractory increases in ICP; even in these instances, decisions should be addressed on a per patient basis: Surgery should not be considered for patients who are either fully alert/intact or deeply comatose. Patients with intermediate levels of arousal (obtundation-stupor) are more appropriate candidates. Features that support performing surgery include a recent onset of hemorrhage, ongoing clinical deterioration, involvement of the nondominant hemisphere, and location of the hematoma near the cortical surface. Features in favor of less aggressive therapy include serious concomitant medical problems, advanced age, stable clinical condition, remote onset of hemorrhage, involvement of the dominant hemisphere, and inaccessibility of the hemorrhage
For patients with supratentorial ICH, current guidelines suggest consideration of standard craniotomy only for those who have lobar clots within 1 cm of the surface [9]. No other patient group is recommended for surgery, and no surgical method other than standard craniotomy is supported. The routine evacuation of supratentorial ICH in the first 96 hours is not recommended.
Hemostatic therapy — Hemostatic therapy offers the potential to improve outcome by stopping ongoing hemorrhage and preventing hemorrhage enlargement. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on Hemorrhage enlargement).
The agent that has been most studied for use in ICH is activated recombinant factor VIIa (rFVIIa), which promotes hemostasis at sites of vascular injury [65]. (See "Plasma derivatives and recombinant DNA-produced coagulation factors", section on Recombinant coagulation products).
While preliminary studies suggested that treatment with rFVIIa was safe and effective for ICH [66,67], results from the multicenter double-blind phase 3 clinical trial, not yet published, were disappointing [68]. The trial randomly assigned 821 patients with spontaneous ICH (confirmed by head CT scan within three hours of symptom onset) to receive either rFVIIa or placebo within four hours of symptom onset [68]. Compared with placebo, treatment with rFVIIa was associated with a significant reduction in hematoma growth and with improvement in neurologic and functional outcome at day 15. However, rFVIIa treatment was not associated with improvement in the primary outcome measures, mortality or severe disability, at day 90.
In contrast, the earlier multicenter phase 2B study evaluated 399 patients with spontaneous ICH and found that treatment significantly reduced the risk of severe disability or death compared with placebo at 90 days (absolute risk reduction of 16 percent) [67].
Recombinant factor VIIa has a potential risk of serious side effects from activation of the coagulation system or thrombosis [65]. There was a nonsignificant increase in serious thromboembolic events (mainly myocardial infarction or cerebral infarction) associated with rFVIIa treatment of ICH in the phase 2B study [67]. However, small open-label studies suggest that rFVIIa treatment for ICH is associated with significantly increased rates of troponin elevation and myocardial infarction [69] and higher than expected rates of posthemorrhagic hydrocephalus [70]. (See "Therapeutic uses of recombinant coagulation factor VIIa", section on Safety issues).
Given the available data, we agree with current guidelines that recombinant factor VIIa treatment for acute ICH is investigational and should not be used routinely outside of the context of a clinical trial [9].
Resumption of antiplatelet therapy — A common question is when patients can resume antiplatelet therapy after suffering an ICH. Our extensive experience with the use of aspirin suggests that it is probably safe to resume therapy after the acute phase of ICH provided that blood pressure is well controlled and that the indication for antiplatelet treatment is sufficiently strong that the potential benefit outweighs the increase in risk of recurrent ICH.
Unfortunately, there are no data that we are aware of that specifically address this issue. Therefore, decisions must be made by extrapolating from the limited data regarding antiplatelet therapy and the risk of primary ICH. The best available data comes from meta-analyses of randomized controlled trials; these suggest that aspirin use is associated with an approximately 40 percent relative increase in the risk of initial ICH, which translates into a very small absolute increase in risk [71,72]. (See "Anticoagulant and antiplatelet therapy in patients with an acute or prior intracerebral hemorrhage", section on Aspirin and warfarin therapy).
Although aspirin reduces the risk of ischemic stroke by 25 percent, this benefit is largely negated by the associated increased risk of recurrent ICH, which typically causes more disability than ischemic stroke. Therefore, we do not recommend aspirin or antiplatelets for those patients with only an "average" risk of recurrent ischemic stroke.
What exactly constitutes "average" or "above average" risk is not certain, but we consider hypertension, diabetes, hypercholesterolemia, and the absence of heart disease to be markers of average risk. Atrial fibrillation, cardiomyopathy, large vessel extracranial and intracranial stenoses, and malignancy can be considered as markers for those with "above average" risk who may benefit from long-term antiplatelet therapy after ICH.
We do not recommend resumption of aspirin or antiplatelets for primary prevention of cardiovascular disease. In the few existing primary prevention studies, patients with any prior ICH were excluded. Such patients should avoid aspirin unless a compelling indication for aspirin use develops later on.
Timing and dose — The timing of antiplatelet use after ICH is largely empiric. There is risk of rebleeding and hematoma expansion in the first several hours. At 10 days, rebleeding is unlikely. The AHA/ASA guidelines of 2006 state that antiplatelets should be discontinued for at least one to two weeks [38].
Some experts have argued that aspirin can be used safely as soon as 48 hours after ICH in those who require prophylaxis for venous thromboembolism. We agree, provided neuroimaging has demonstrated a stable ICH. (See "Anticoagulant and antiplatelet therapy in patients with an acute or prior intracerebral hemorrhage", section on Prevention of VTE).
If aspirin is used after ICH, we agree with others that a lower dose (30 to 160 mg daily) is both effective and safer than higher doses. (See "Anticoagulant and antiplatelet therapy in patients with an acute or prior intracerebral hemorrhage").
Resumption of anticoagulation — The question of when to restart anticoagulation in patients at high risk for embolic events who have suffered an ICH has not been definitively answered. For patients who require anticoagulation soon after a cerebral hemorrhage, the AHA/ASA guidelines conclude that intravenous heparin may be safer than oral anticoagulation [38]. In addition, the guidelines suggest that oral anticoagulants may be resumed three to four weeks after onset of the hemorrhage with rigorous monitoring and maintenance of INRs in the lower end of the therapeutic range.
Resumption of anticoagulation is discussed in greater detail separately. (See "Management of warfarin-associated intracerebral hemorrhage", section on Resumption of anticoagulation).
Secondary prevention — Efforts to control blood pressure over the long term are likely to significantly reduce the risk of recurrent ICH. The potential magnitude of this effect was demonstrated in the PROGRESS trial [73]. Among over 6000 patients with prior cerebrovascular events and a mean baseline blood pressure of 147/86, a modest reduction in blood pressure of 9/4 mmHg decreased the rate of ICH by 50 percent (95% CI 26%-67%). In the subgroup of 611 patients with prior ICH, there was a similar 49 percent risk reduction (95% CI 18%-68%) for recurrent ICH.
Current guidelines note that treating hypertension in the nonacute setting is the most important step to reduce the risk of ICH, and probably recurrent ICH [9]. Stopping smoking, heavy alcohol use, and cocaine use are also recommended for prevention of recurrent ICH.
SUMMARY AND RECOMMENDATIONS The 30-day mortality from intracerebral hemorrhage ICH ranges from 35 to 52 percent. Among survivors, the prognosis for functional recovery depends upon the location of hemorrhage, size of the hematoma, level of consciousness, patient age, and overall medical health and condition. (See "Prognosis" above). Prognostication for individual patients with acute ICH remains an uncertain science at best. Current guidelines suggest consideration of aggressive full care during the first 24 hours after ICH onset and postponement of new DNR orders during that time. (See "Limiting care" above). Patients with acute ICH should be managed in an intensive care unit. All anticoagulant and antiplatelet drugs should be discontinued acutely, and anticoagulant effect should be reversed immediately with appropriate agents. Sources of fever should be treated. We suggest use of antipyretic medications to lower body temperature to normothermia in febrile patients. We suggest insulin treatment for elevated serum glucose >185 mg/dL (>10.3 mmol/L). (See "Treatment" above and see "General management issues" above and see "Reversal of anticoagulation" above). The prevention of venous thromboembolism and deep venous thrombosis in patients with ICH is discussed separately. (See "Anticoagulant and antiplatelet therapy in patients with an acute or prior intracerebral hemorrhage"). Initial management of elevated intracranial pressure (ICP) includes elevating the head of the bed to 30 degrees and use of analgesia and sedation. Suggested intravenous agents for sedation are propofol, etomidate, or midazolam. Suggested agents for analgesia and antitussive effect are morphine or alfentanil.
More aggressive therapies for reducing elevated ICP include osmotic diuretics (eg, mannitol), ventricular catheter drainage of cerebrospinal fluid, neuromuscular blockade, and hyperventilation [9]. We suggest continuous monitoring of ICP and arterial blood pressure when using these aggressive therapies, with the goal of maintaining cerebral perfusion pressure above 70 mmHg. (See "Intracranial pressure control" above). Severe elevations in blood pressure may worsen ICH by representing a continued force for bleeding.
- For patients with SBP >200 mmHg or MAP >150 mmHg, we suggest aggressive reduction of blood pressure with continuous intravenous infusion of medication accompanied by blood pressure monitoring every five minutes
- For patients with SBP >180 mmHg or MAP >130 mmHg and evidence or suspicion of elevated ICP, we suggest monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medication to keep cerebral perfusion pressure in the range of 61 to 80 mmHg
- For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, we suggest a modest reduction of blood pressure to a target MAP of 110 mmHg or target blood pressure of 160/90 mmHg using intermittent or continuous intravenous medication accompanied by reexamination of the patient every 15 minutes
Labetalol, nicardipine, esmolol, enalapril, hydralazine, nitroprusside, and nitroglycerin are useful intravenous agents for controlling blood pressure. (See "Blood pressure control" above). Appropriate intravenous antiepileptic treatment should be used to quickly control seizures for patients with ICH and clinical seizures. (See "Seizure prophylaxis and treatment" above). For patients with cerebellar hemorrhages >3 cm in diameter who are deteriorating or who have brainstem compression and/or hydrocephalus due to ventricular obstruction, we recommend surgical removal of hemorrhage. Surgery for supratentorial ICH is controversial, and current guidelines suggest consideration of standard craniotomy only for those who have lobar clots within 1 cm of the surface. The routine evacuation of supratentorial ICH in the first 96 hours is not recommended. (See "Surgery" above). Recombinant factor VIIa treatment for acute ICH is investigational and should not be used routinely outside the context of a clinical trial. (See "Hemostatic therapy" above). Treating hypertension is the most important step to reduce the risk of ICH, and probably recurrent ICH. Stopping smoking, heavy alcohol use, and cocaine use are also recommended. (See "Secondary prevention" above).
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WALAU! By the time i gotta end, my friend already comatoasted! 
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madviruz
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Posting #26: Tue Jan 29th, 2008 01:52 |
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WALAU! By the time i gotta end, my friend already comatoasted!
Yes prophet...if you tried to treat.....he is DEAD!!!
not comatose...
Thats the price for play-play doctor or pseudo-scientist.
Last edited on Tue Jan 29th, 2008 01:53 by madviruz
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madviruz
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