Tag Archives: ICH


Early surgery for intracerebral haemorrhage

ICHgraphicIconTo operate or not to operate on patients with an intracerebral haematoma? Deep ones can be tricky and risk damage to surrounding brain, so superficial ones may be more likely to benefit.

These patients with superficial lesions were assessed in STICH II, an international prospective randomised controlled trial comparing early surgery with conservative treatment.

Inclusion criteria were strict:

  • spontaneous lobar intracerebral haemorrhage on CT scan (≤1 cm from the cortical surface of the brain) with a volume of between 10 mL and 100 mL
  • within 48 h of onset
  • had a best motor score on the Glasgow Coma Score (GCS) of 5 or 6, and had a best eye score of 2 or more (ie, were conscious at randomisation).

The primary outcome was a Glasgow Outcome Scale-based evaluation of recovery (‘favourable’ vs ‘unfavourable’), which did not significantly differ between groups.

A predefined subgroup of patients with a poorer prognosis (using a score based on age, haematoma size and GCS) may have a better outcome with surgery. Some patients randomised to conservative therapy subsequently underwent delayed surgery. Thanks to appropriate intention-to-treat analysis they would have remained in the conservative treatment group which may have contributed to an underestimation of the benefit of surgery.

So, overall a negative trial, and patients with small lesions and higher GCS scores won’t benefit from surgery. Patients in poorer prognostic groups might benefit, but that remains unproven.

Some other ICH trials to be aware of are Clear III and MISTIE III, which are investigating thrombolytic agents in combination with clot removal, including with minimally invasive techniques.

Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial
Lancet. 2013 Aug 3;382(9890):397-408


BACKGROUND: The balance of risk and benefit from early neurosurgical intervention for conscious patients with superficial lobar intracerebral haemorrhage of 10-100 mL and no intraventricular haemorrhage admitted within 48 h of ictus is unclear. We therefore tested the hypothesis that early surgery compared with initial conservative treatment could improve outcome in these patients.

METHODS: In this international, parallel-group trial undertaken in 78 centres in 27 countries, we compared early surgical haematoma evacuation within 12 h of randomisation plus medical treatment with initial medical treatment alone (later evacuation was allowed if judged necessary). An automatic telephone and internet-based randomisation service was used to assign patients to surgery and initial conservative treatment in a 1:1 ratio. The trial was not masked. The primary outcome was a prognosis-based dichotomised (favourable or unfavourable) outcome of the 8 point Extended Glasgow Outcome Scale (GOSE) obtained by questionnaires posted to patients at 6 months. Analysis was by intention to treat. This trial is registered, number ISRCTN22153967.

FINDINGS: 307 of 601 patients were randomly assigned to early surgery and 294 to initial conservative treatment; 298 and 291 were followed up at 6 months, respectively; and 297 and 286 were included in the analysis, respectively. 174 (59%) of 297 patients in the early surgery group had an unfavourable outcome versus 178 (62%) of 286 patients in the initial conservative treatment group (absolute difference 3·7% [95% CI -4·3 to 11·6], odds ratio 0·86 [0·62 to 1·20]; p=0·367).

INTERPRETATION: The STICH II results confirm that early surgery does not increase the rate of death or disability at 6 months and might have a small but clinically relevant survival advantage for patients with spontaneous superficial intracerebral haemorrhage without intraventricular haemorrhage.

Lowering the BP rapidly in ICH

ICH-iconIn our retrieval service case reviews, one thing that is that sure to generate discussion is what to do about the blood pressure in patients who present with intracranial haemorrhage and hypertension. We don’t want the bleeding to be worsened by higher blood pressure, but we don’t want to decrease cerebral perfusion pressure in patients who have raised intracranial pressure. Consensus guidelines exist for spontaneous intracerebral haemorrhage and subarachnoid haemorrhage, but they’re not based on strong data.

Here’s a study that attempted to provide more information. Intensive lowering to a target systolic of 140 mmHg within 1 hour was compared with lowering to a target of 180 mmHg. There was no significant reduction in the rate of the primary outcome of death or severe disability. The skeptic in me is disappointed there was no placebo arm. An ordinal analysis of modified Rankin scores favoured the intensive BP-lowering intervention, which means this study can be used by both those for and against intensive BP lowering to support their views.

As explained in an accompanying editorial, a number of factors may limit generalisability to Western practice, such as the predominant use of the alpha-blocking agent urapadil in the large numbers of Asian patients, a drug not available in the United States. Future publication of the ATACH-II trial using intravenous nicardipine will shed more light on this topic.

1. Rapid Blood-Pressure Lowering in Patients with Acute Intracerebral Hemorrhage
N Engl J Med. 2013 Jun 20;368(25):2355-65


BACKGROUND: Whether rapid lowering of elevated blood pressure would improve the outcome in patients with intracerebral hemorrhage is not known.

METHODS: We randomly assigned 2839 patients who had had a spontaneous intracerebral hemorrhage within the previous 6 hours and who had elevated systolic blood pressure to receive intensive treatment to lower their blood pressure (with a target systolic level of <140 mm Hg within 1 hour) or guideline-recommended treatment (with a target systolic level of <180 mm Hg) with the use of agents of the physician’s choosing. The primary outcome was death or major disability, which was defined as a score of 3 to 6 on the modified Rankin scale (in which a score of 0 indicates no symptoms, a score of 5 indicates severe disability, and a score of 6 indicates death) at 90 days. A prespecified ordinal analysis of the modified Rankin score was also performed. The rate of serious adverse events was compared between the two groups.

RESULTS: Among the 2794 participants for whom the primary outcome could be determined, 719 of 1382 participants (52.0%) receiving intensive treatment, as compared with 785 of 1412 (55.6%) receiving guideline-recommended treatment, had a primary outcome event (odds ratio with intensive treatment, 0.87; 95% confidence interval [CI], 0.75 to 1.01; P=0.06). The ordinal analysis showed significantly lower modified Rankin scores with intensive treatment (odds ratio for greater disability, 0.87; 95% CI, 0.77 to 1.00; P=0.04). Mortality was 11.9% in the group receiving intensive treatment and 12.0% in the group receiving guideline-recommended treatment. Nonfatal serious adverse events occurred in 23.3% and 23.6% of the patients in the two groups, respectively.

CONCLUSIONS: In patients with intracerebral hemorrhage, intensive lowering of blood pressure did not result in a significant reduction in the rate of the primary outcome of death or severe disability. An ordinal analysis of modified Rankin scores indicated improved functional outcomes with intensive lowering of blood pressure.

2. Blood pressure in intracerebral hemorrhage–how low should we go?
N Engl J Med. 2013 Jun 20;368(25):2426-7

Magnesium doesn’t improve SAH outcome

A multicentre RCT showed intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended.
Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2): a randomised placebo-controlled trial
Lancet 2012 July 7; 380(9836): 44–49 Free full text


Background Magnesium sulphate is a neuroprotective agent that might improve outcome after aneurysmal subarachnoid haemorrhage by reducing the occurrence or improving the outcome of delayed cerebral ischaemia. We did a trial to test whether magnesium therapy improves outcome after aneurysmal subarachnoid haemorrhage.

Methods We did this phase 3 randomised, placebo-controlled trial in eight centres in Europe and South America. We randomly assigned (with computer-generated random numbers, with permuted blocks of four, stratified by centre) patients aged 18 years or older with an aneurysmal pattern of subarachnoid haemorrhage on brain imaging who were admitted to hospital within 4 days of haemorrhage, to receive intravenous magnesium sulphate, 64 mmol/day, or placebo. We excluded patients with renal failure or bodyweight lower than 50 kg. Patients, treating physicians, and investigators assessing outcomes and analysing data were masked to the allocation. The primary outcome was poor outcome—defined as a score of 4–5 on the modified Rankin Scale—3 months after subarachnoid haemorrhage, or death. We analysed results by intention to treat. We also updated a previous meta-analysis of trials of magnesium treatment for aneurysmal subarachnoid haemorrhage. This study is registered with controlled-trials.com (ISRCTN 68742385) and the EU Clinical Trials Register (EudraCT 2006-003523-36).

Findings 1204 patients were enrolled, one of whom had his treatment allocation lost. 606 patients were assigned to the magnesium group (two lost to follow-up), 597 to the placebo (one lost to follow-up). 158 patients (26·2%) had poor outcome in the magnesium group compared with 151 (25·3%) in the placebo group (risk ratio [RR] 1·03, 95% CI 0·85–1·25). Our updated meta-analysis of seven randomised trials involving 2047 patients shows that magnesium is not superior to placebo for reduction of poor outcome after aneurysmal subarachnoid haemorrhage (RR 0·96, 95% CI 0·86–1·08).

Interpretation Intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended.

Phentolamine for neurogenic pulmonary oedema

A single case report might not be practice changing, but it’s helpful to know about this option:

A patient with acute intracerebral haemorrhage developed hyoxaemia due to neurogenic pulmonary oedema, accompanied by a labile blood pressure and elevated catecholamine levels.

Nicardipine and other antihypertensive agents including metoprolol, hydralazine, and labetalol were tried without benefit, and the patient continued to deteriorate.

Phentolamine was tried. The introduction, withdrawal, and reintroduction of phentolamine and the clinical status of the patient is described convincingly:



a phentolamine infusion was started at 0.17 mg/min and titrated for BP control. Over 6 h, the FIO2 requirements dropped precipitously, gas exchange improved, and the chest radiograph showed improvement of pulmonary edema. When the hospital supply of phentolamine was exhausted, the clinical status deteriorated rapidly. Within just 15 h of the discontinuation of phentolamine, the PaO2 fell from 166 mm Hg to 66 mm Hg, and FIO2 requirements rose from 60% to 100%. When the phentolamine supply was replenished and the infusion restarted, the same rapid improvement was observed and BP stabilized.


Phentolamine is a potent competitive antagonist at both alpha 1 and alpha 2 receptors . Phentolamine causes a reduction in peripheral resistance through blockade of alpha 1 receptors and possibly alpha 2 receptors on vascular smooth muscle.



Abstract
Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant CNS insult. The cause is believed to be a surge of catecholamines that results in cardiopulmonary dysfunction. Although there are myriad case reports describing CNS events that are associated with this syndrome, few studies have identified specific treatment modalities. We present a case of NPE caused by an intracranial hemorrhage from a ruptured arteriovenous malformation. We uniquely document a rise and fall of serum catecholamine levels correlating with disease activity and a dramatic clinical response to IV phentolamine.


Neurogenic Pulmonary Edema: Successful Treatment With IV Phentolamine
Chest March 2012 vol. 141 no. 3 793-795

Cardiac arrest caused by subarachnoid haemorrhage

We know that subarachnoid haemorrhage (SAH) can cause cardiac arrest. Some questions we may have about this are:

Questions
  • What proportion of out-of-hospital cardiac arrests (OOHCA) who achieve return of spontaneous circulation (ROSC) are caused by SAH?
  • What is the usual presenting arrest rhythm – VT/VF or non-shockable rhythms?
  • What is the outcome of these patients – do any survive?
  • Do they have other characteristic cardiac features, such as ECG or echo abnormalities?
  • Should we do a head CT on all survivors of out-of-hospital cardiac arrest of uncertain aetiology?


A recent Japanese article in Resuscitation1 is the third from that country to be published on the topic in three years, the other two2,3 coming from different centres and all demonstrating some consistent answers, as do papers published in recent years from Europe4 and North America5:

Answers
  • Rates of SAH in OOHCA patients who achieve ROSC and make it to CT range from 4-16% (even higher if other sources of intracranial haemorrhage are included).
  • Studies consistently demonstrate VT/VF to be very rare – PEA and asystole are by far the commonest presenting arrest rhythms.
  • Almost no patients with this presentation due to SAH survive to hospital discharge.
  • In the most recent study, all patients who survived long enough to get a 12 lead showed ST-T abnormalities and/or QT prolongation, although echocardiograms were mostly normal.
  • Rates of SAH in OOHCA patients who achieve ROSC seem to be sufficiently high to seriously consider head CT in these patients if there is no obvious alternate explanation for the arrest.


1. Clinical and cardiac features of patients with subarachnoid haemorrhage presenting with out-of-hospital cardiac arrest
Resuscitation. 2011 Oct;82(10):1294-7




Background Subarachnoid haemorrhage (SAH) is known as one of the aetiologies of out-of-hospital cardiac arrest (OHCA). However, the mechanisms of circulatory collapse in these patients have remained unclear.


Methods and results We examined 244 consecutive OHCA patients transferred to our emergency department. Head computed tomography was performed on all patients and revealed the existence of SAH in 14 patients (5.9%, 10 females). Among these, sudden collapse was witnessed in 7 patients (50%). On their initial cardiac rhythm, all 14 patients showed asystole or pulseless electrical activity, but no ventricular fibrillation (VF). Return of spontaneous circulation (ROSC) was obtained in 10 of the 14 patients (14.9% of all ROSC patients) although all resuscitated patients died later. The ROSC rate in patients with SAH (71%) was significantly higher than that of patients with either other types of intracranial haemorrhage (25%, n = 2/8) or presumed cardiovascular aetiologies (22%, n = 23/101) (p < 0.01). On electrocardiograms, ST-T abnormalities and/or QT prolongation were found in all 10 resuscitated patients. Despite their electrocardiographic abnormalities, only 3 patients showed echocardiographic abnormalities.


Conclusions The frequency of SAH in patients with all causes of OHCA was about 6%, and in resuscitated patients was about 15%. The initial cardiac rhythm revealed no VF even though half had a witnessed arrest. A high ROSC rate was observed in patients with SAH, although none survived to hospital discharge.


2. Assessing outcome of out-of-hospital cardiac arrest due to subarachnoid hemorrhage using brain CT during or immediately after resuscitation
Signa Vitae 2010; 5(2): 21 – 24 Full Text




Objectives. The clinical course and outcome of out-of-hospital cardiopulmonary arrest (OHCPA) due to subarachnoid hemorrhage (SAH) is unclear. The objective of this study is to clarify them.


Study design. Single- center, observational study. Setting. We usually perform a brain computed tomography (CT) in OHCPA patients who present without a clear etiology (42% of all OHCPA), such as trauma, to determine the cause of OHCPA and to guide treatment.


Patients. The study included OHCPA patients without a clear etiology, who were transferred to our center and who underwent a brain CT during resuscitation.


Methods of measurement. Patients’ records were reviewed; initial cardiac rhythm, existence of a witness and bystander cardiopulmonary resuscitation efforts (CPR) were compared with patients’ outcomes.


Results. Sixty-six patients were enrolled. 72.7% achieved return of spontaneous circulation (ROSC), 71.2% were admitted, 30.3% survived more than 7 days, and 9.1. survived-to-discharge. In 41 witnessed OHCPA, 87.8% obtained ROSC, 85.4% were admitted, and 14.6% survived-to-discharge. All survivors were witnessed. In 25 non-witnessed OHCPA, 48% obtained ROSC and were admitted, and no patients were discharged. Initial cardiac rhythm was ventricular fibrillation (VF), pulseless electrical activity (PEA) and asystole in 3.0%, 39.4%, and 47.0%. In 2 VF patients 50.0% survived-to- discharge, and there was no survivor with PEA or asystole.


Conclusion. This study shows a high rate of ROSC and admission in OHCPA patients with a SAH, and also reveals their very poor neurological outcome. We conclude that the detection of a SAH in OHCPA patients is important to determine the accurate frequency of SAH in this patient group and to guide appropriate treatment of all OHCPA patients.

3. Subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest: A prospective computed tomography study
Resuscitation. 2009 Sep;80(9):977-80




Aim Aneurysmal subarachnoid haemorrhage (SAH) is a relatively common cause of out-of-hospital cardiac arrest (OHCA). Early identification of SAH-induced OHCA with the use of brain computed tomography (CT) scan obtained immediately after resuscitation may help emergency physicians make therapeutic decision as quickly as they can.


Methods During the 4-year observation period, brain CT scan was obtained prospectively in 142 witnessed non-traumatic OHCA survivors who remained haemodynamically stable after resuscitation. Demographics and clinical characteristics of SAH-induced OHCA survivors were compared with those with “negative” CT finding.


Results Brain CT scan was feasible with an average door-to-CT time of 40.0min. SAH was found in 16.2% of the 142 OHCA survivors. Compared with 116 survivors who were negative for SAH, SAH-induced OHCA survivors were significantly more likely to be female, to have experienced a sudden headache, and trended to have achieved return of spontaneous circulation (ROSC) prior to arrival in the emergency department less frequently. Ventricular fibrillation (VF) was significantly less likely to be seen in SAH-induced than SAH-negative OHCA (OR, 0.06; 95% CI, 0.01–0.46). Similarly, Cardiac Trop-T assay was significantly less likely to be positive in SAH-induced OHCA (OR, 0.08; 95% CI, 0.01–0.61).


Conclusion Aneurysmal SAH causes OHCA more frequently than had been believed. Immediate brain CT scan may particularly be useful in excluding SAH-induced OHCA from thrombolytic trial enrollment, for whom the use of thrombolytics is contraindicated. The low VF incidence suggests that VF by itself may not be a common cause of SAH-induced OHCA.


4. Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest
Resuscitation. 2001 Oct;51(1):27-32




Objective: Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest.


Design: We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features.


Results: Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome.


Conclusions: Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.


5. Cranial computed tomography in the resuscitated patient with cardiac arrest
Am J Emerg Med. 2009 Jan;27(1):63-7




Introduction The incidence of out-of-hospital and in-hospital cardiorespiratory arrest from all causes in the United States occurs not infrequently. Postresuscitation care should include the identification of the inciting arrest event as well as therapy tailored to support the patient and treat the primary cause of the decompensation. The application of one particular testing modality, cranial computed tomography (CT) of the head, has not yet been determined. We undertook an evaluation of the use of head CT in patients who were resuscitated from cardiac arrest.


Methods Prehospital (emergency medical services), ED, and hospital records were reviewed for patients of all ages with cardiorespiratory arrest over a 4-year period (July 1996-June 2000). Information regarding diagnosis, management, and outcome was recorded. The results of cranial CT, if performed, and any apparent resulting therapeutic changes were recorded. Patients with a known traumatic mechanism for the cardiorespiratory arrest were excluded.


Results A total of 454 patients (mean age 58.3 years with 60% male) with cardiorespiratory arrest were entered in the study with 98 (22%) individuals (mean age 58.5 years with 53% male) undergoing cranial CT. Arrest location was as follows: emergency medical services, 41 (42%); ED, 11 (11%); and hospital, 46 (47%). Seventy-eight (79%) patients demonstrated 111 CT abnormalities: edema, 35 (32%); atrophy, 24 (22%); extra-axial hemorrhage, 14 (13%); old infarct, 12 (11%); new infarct, 11 (10%); intraparenchymal hemorrhage, 6 (5%); skull fracture, 5 (4%); mass, 3 (2%); and foreign body, 1 (1%). Therapeutic and diagnostic alterations in care were made in 38 (39%) patients—35 abnormal and 3 normal CTs. The following alterations occurred: medication administration, 26; withdrawal of life support, 7; additional diagnostic study, 6; neurologic consultation, 6; and intracranial pressure monitoring. 4. No patient survived to discharge.


Conclusion In this subset of resuscitated patients with cardiac arrest, abnormalities on the head CT were not uncommon. Alterations in management did occur in those patients with abnormalities. The indications and impact of head CT in the population of resuscitated patients with cardiac arrest remain unknown, warranting further investigation.


New ICH Guidelines

A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association on the management of spontaneous intracerebral haemorrhage has been published in Stroke. The full text is available here.

In summary:

Medical Treatment for ICH

  • Patients with a severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement therapy or platelets, respectively
  • Patients with ICH whose INR is elevated due to oral anticoagulants (OAC) should have their warfarin withheld, receive therapy to replace vitamin K–dependent factors and correct the INR, and receive intravenous vitamin K. Prothrombin Complex Concentrates have not shown improved outcome compared with FFP but may have fewer complications compared with FFP and are reasonable to consider as an alternative to FFP.
  • rFVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not routinely recommended as a sole agent for OAC reversal in ICH
  • Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic ICH patients, there is an increase in thromboembolic risk with rFVIIa and no clear clinical benefit in unselected patients. Thus rFVIIa is not recommended in unselected patients. Further research to determine whether any selected group of patients may benefit from this therapy is needed before any recommendation for its use can be made.
  • The usefulness of platelet transfusions in ICH patients with a history of antiplatelet use is unclear and is considered investigational
  • Patients with ICH should have intermittent pneumatic compression for prevention of venous thromboembolism in addition to elastic stockings
  • After documentation of cessation of bleeding, low-dose subcutaneous low-molecular-weight heparin or unfractionated heparin may be considered for prevention of venous thromboembolism in patients with lack of mobility after 1 to 4 days from onset
  • Blood Pressure
    • Until ongoing clinical trials of BP intervention for ICH are completed, physicians must manage BP on the basis of the present incomplete efficacy evidence. Current suggested recommendations for target BP in various situations are listed in an accompanying table and may be considered
    • In patients presenting with a systolic BP of 150 to 220 mmHg, acute lowering of systolic BP to 140 mm Hg is probably safe

    Inpatient Management and Prevention of Secondary Brain Injury

    • Initial monitoring and management of ICH patients should take place in an intensive care unit with physician and nursing neuroscience intensive care expertise
    • Glucose should be monitored and normoglycemia is recommended

    Seizures and Antiepileptic Drugs

    • Clinical seizures should be treated with antiepileptic drugs
    • Continuous EEG monitoring is probably indicated in ICH patients with depressed mental status out of proportion to the degree of brain injury
    • Patients with a change in mental status who are found to have electrographic seizures on EEG should be treated with antiepileptic drugs
    • Prophylactic anticonvulsant medication should not be used

    Procedures/Surgery

    • Patients with a GCS score of ≤8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus might be considered for ICP monitoring and treatment. A cerebral perfusion pressure of 50 to 70 mmHg may be reasonable to maintain depending on the status of cerebral autoregulation
    • Ventricular drainage as treatment for hydrocephalus is reasonable in patients with decreased level of consciousness

    Intraventricular Hemorrhage Recommendation

    • Although intraventricular administration of recombinant tissue-type plasminogen activator in IVH appears to have a fairly low complication rate, efficacy and safety of this treatment is uncertain and is considered investigational

    Clot Removal

    • For most patients with ICH, the usefulness of surgery is uncertain. Specific exceptions to this recommendation follow
    • Patients with cerebellar hemorrhage who are deteriorating neurologically or who have brainstem compression and/or hydrocephalus from ventricular obstruction should undergo surgical removal of the hemorrhage as soon as possible. Initial treatment of these patients with ventricular drainage alone rather than surgical evacuation is not recommended
    • For patients presenting with lobar clots ≥30 mL and within 1 cm of the surface, evacuation of supratentorial ICH by standard craniotomy might be considered
    • The effectiveness of minimally invasive clot evacuation utilizing either stereotactic or endoscopic aspiration with or without thrombolytic usage is uncertain and is considered investigational
    • Although theoretically attractive, no clear evidence at present indicates that ultra-early removal of supratentorial ICH improves functional outcome or mortality rate. Very early craniotomy may be harmful due to increased risk of recurrent bleeding

    Outcome Prediction and Withdrawal of Technological Support

    • Aggressive full care early after ICH onset and postponement of new DNR orders until at least the second full day of hospitalization is probably recommended. Patients with preexisting DNR orders are not included in this recommendation. Current methods of prognostication in individual patients early after ICH are likely biased by failure to account for the influence of withdrawal of support and early DNR orders. Patients who are given DNR status at any point should receive all other appropriate medical and surgical interventions unless otherwise explicitly indicated.

    Prevention of Recurrent ICH

    • In situations where stratifying a patient’s risk of recurrent ICH may affect other management decisions, it is reasonable to consider the following risk factors for recurrence: lobar location of the initial ICH, older age, ongoing anticoagulation, presence of the apolipoprotein ε2 or ε4 alleles, and greater number of microbleeds on MRI
    • After the acute ICH period, absent medical contraindications, BP should be well controlled, particularly for patients with ICH location typical of hypertensive vasculopathy
    • After the acute ICH period, a goal target of a normal BP of <140/90 (<130/80 if diabetes or chronic kidney disease) is reasonable
    • Avoidance of long-term anticoagulation as treatment for nonvalvular atrial fibrillation is probably recommended after spontaneous lobar ICH because of the relatively high risk of recurrence. Anticoagulation after nonlobar ICH and antiplatelet therapy after all ICH might be considered, particularly when there are definite indications for these agents. Avoidance of heavy alcohol use can be beneficial. There is insufficient data to recommend restrictions on use of statin agents or physical or sexual activity

    Rehabilitation and Recovery

    • Given the potentially serious nature and complex pattern of evolving disability, it is reasonable that all patients with ICH have access to multidisciplinary rehabilitation. Where possible, rehabilitation can be beneficial when begun as early as possible and continued in the community as part of a well-coordinated (seamless) program of accelerated hospital discharge and home-based resettlement to promote ongoing recovery

    Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association
    Stroke published online Jul 22, 2010

    Ultrasound of intracranial haematoma

    Using a 2Mhz transducer insonating through the temporal acoustic bone window, Italian physicians detected the expansion of an extradural haematoma. In their discussion they highlight that transcranial sonography of brain parenchyma in adults has been proposed by several authors for the evaluation of the ventricular system, monitoring of midline shift, diagnosis and follow-up of intracranial mass lesions. In one study, of 151 patients, 133 (88%) had a sufficient acoustic bone window. Note that the skull contralateral to the acoustic bone window is visualised.

    Arrow indicates EDH; asterisk indicates mesencephalon

    Bedside detection of acute epidural hematoma by transcranial sonography in a head-injured patient
    Intensive Care Med. 2010 Jun;36(6):1091-2

    Magnesium for subarachnoid haemorrhage

    Symptomatic cerebral vasospasm occurs in nearly one-third of patients with aneurysmal subarachnoid hemorrhage and is a major cause of disability and mortality in this population.

    Magnesium (Mg) acts as a cerebral vasodilator by blocking the voltage-dependent calcium channels.. Experimental studies suggest that Mg also inhibits glutamate release by blocking N-methyl-D-aspartate receptors, decreases intracellular calcium influx, and increases red blood cell deformability; all these changes may reduce the occurrence of cerebral vasospasm and minimise brain ischemic injury occurring after SAH.

    One hundred and ten patients within 96 hours of admission for aneurysmal subarachnoid haemorrhage (SAH) were randomised to receive iv magnesium or placebo. Nimodipine was not routinely given. Twelve patients (22%) in the magnesium group and 27 patients (51%) in the control group had delayed ischemic infarction – the primary endpoint (p< .0020; odds ratio [OR], 0.28; 95% confidence interval [CI], 0.12– 0.64). Mortality was lower and neurological outcome better in the magnesium group but these results were not statistically significant.

    Larger trials of magnesium in SAH are ongoing.

    Prophylactic intravenous magnesium sulfate for treatment of aneurysmal subarachnoid hemorrhage: A randomized, placebo-controlled, clinical study
    Crit Care Med. 2010 May;38(5):1284-90

    Update September 2012:

    A multicentre RCT showed intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended.
    Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2): a randomised placebo-controlled trial
    Lancet 2012 July 7; 380(9836): 44–49 Free full text


    Background Magnesium sulphate is a neuroprotective agent that might improve outcome after aneurysmal subarachnoid haemorrhage by reducing the occurrence or improving the outcome of delayed cerebral ischaemia. We did a trial to test whether magnesium therapy improves outcome after aneurysmal subarachnoid haemorrhage.

    Methods We did this phase 3 randomised, placebo-controlled trial in eight centres in Europe and South America. We randomly assigned (with computer-generated random numbers, with permuted blocks of four, stratified by centre) patients aged 18 years or older with an aneurysmal pattern of subarachnoid haemorrhage on brain imaging who were admitted to hospital within 4 days of haemorrhage, to receive intravenous magnesium sulphate, 64 mmol/day, or placebo. We excluded patients with renal failure or bodyweight lower than 50 kg. Patients, treating physicians, and investigators assessing outcomes and analysing data were masked to the allocation. The primary outcome was poor outcome—defined as a score of 4–5 on the modified Rankin Scale—3 months after subarachnoid haemorrhage, or death. We analysed results by intention to treat. We also updated a previous meta-analysis of trials of magnesium treatment for aneurysmal subarachnoid haemorrhage. This study is registered with controlled-trials.com (ISRCTN 68742385) and the EU Clinical Trials Register (EudraCT 2006-003523-36).

    Findings 1204 patients were enrolled, one of whom had his treatment allocation lost. 606 patients were assigned to the magnesium group (two lost to follow-up), 597 to the placebo (one lost to follow-up). 158 patients (26·2%) had poor outcome in the magnesium group compared with 151 (25·3%) in the placebo group (risk ratio [RR] 1·03, 95% CI 0·85–1·25). Our updated meta-analysis of seven randomised trials involving 2047 patients shows that magnesium is not superior to placebo for reduction of poor outcome after aneurysmal subarachnoid haemorrhage (RR 0·96, 95% CI 0·86–1·08).

    Interpretation Intravenous magnesium sulphate does not improve clinical outcome after aneurysmal subarachnoid haemorrhage, therefore routine administration of magnesium cannot be recommended.