A EL-Mitwalli, M Malkoff
ards, basal ganglia, cardiac, cardio-pulmonary support, care unit, complications, critical care, education, emergency medicine, hemodynamics, hemorrhage, ich, intensive, intensive care medicine, intracerebral, medicine, multiorgan failure, neuro, patient care, pediatric, respiratory failure, stroke, surgical i, therapy, ventilation
A EL-Mitwalli, M Malkoff. Intracerebral Hemorrhage. The Internet Journal of Neurology. 2000 Volume 1 Number 1.
Intracerebral hemorrhage (ICH) is a common cause of stroke, accounting for between 5 and 10% of all strokes 1,2,3. In a consecutive series of 938 stroke patients enrolled into the NINCDS Stroke Data Bank, primary ICH accounted for 10.7% of the cases 4. The age-adjusted annual incidence rates for primary intracerebral hemorrhage range from 11 to 31 per 100,000 population in predominantly Caucasian population based-studies with a high rate of CT scanning 5. The risk of intracerebral hemorrhage in blacks is 1.4 times the risk in whites 6. The most common risk factors in the 403 black patients with ICH were pre-existing hypertension (77%), alcohol use (40%), and smoking (30%). Among the 91 non-hypertensive patients, 21 (23%) were diagnosed with hypertension after onset. Compared with women, men had a younger age of onset (54 versus 60 years; p < .001) and a higher frequency of alcohol use (54% versus 22%; p < .001) and smoking (39% versus 17%; p < .001). ICH secondary to hypertension (n = 311) and of undetermined etiology (n = 73) were the most common subtypes in blacks. Patients aged 65 years and older (compared with those aged 15 to 44 years; p = .001) and women (compared with men; p = .02) were more likely to be dependent at discharge11. ICH remains a significant cause of morbidity and mortality in this population.
Moderate drinking of
Causes of ICH
Chronic hypertension produces fibrinoid necrosis, lipohyalinosis, and medial degeneration, which make the vessels susceptible to rupture. ICH that originates in the putamen, thalamus, pons or cerebellum is most likely linked with hypertension. ICH at these sites are often referred to as “
Table 1: Causes of ICH
Cerebral amyloid angiopathy (CAA)
Acute changes in blood pressure and blood flow
Stimulation of the trigeminal nerve
Posterior fossa operative procedures
Following carotid endarterectomy
ICH after migraine attack
Sympathicomimetic agents and illegal drug abuse
Delayed post-traumatic hemorrhage
Silastic dural substitute
Idiopathic hypereosinophilic syndrome
Abrupt, dramatic increase in blood pressure in normotensive patients has been documented to precipitate ICH. Their autoregulatory functions have not adjusted to high blood pressure in contrast to chronically hypertensive patients 5.
ICH is the most common and least treatable neurological complication of
Another common clinical problem is ICH in a patient with an indication for anticoagulation. Bertram et al 26 reported 15 patients with ICH that occurred under anticoagulation with phenprocoumon, with an international normalized ratio (INR) of 2.5-6.5 on admission. Absolute indications for anticoagulation were double, mitral, or aortic valve replacement, combined mitral valve failure with atrial fibrillation and atrial enlargement, internal carotid artery-jugular vein graft, frequently recurring deep vein thrombosis with risk of pulmonary embolism, and severe nontreatable ischemic heart disease. As soon as the diagnosis of ICH was established, INR normalization was attempted in all patients by administration of prothrombin complex, fresh frozen plasma, or vitamin K. After giving phenprocoumon antagonists (and neurosurgical therapy in four patients) heparin administration was started. Nine patients received full-dose intravenous and six low-dose subcutaneous heparin. The following observations were made: all patients with effective, full-dose heparin treatment with a 1.5- to 2-fold elevation in partial thromboplastin time after normalization of the INR were discharged without complication; three of four patients with only incomplete correction of the INR (> 1.35) experienced relevant rebleeding within 3 days (all patients with an INR higher than 1.5), two of whom were on full-dose heparin; three of seven patients with normalized INR and without significant PTT elevation developed severe cerebral embolism. Although this is based on a retrospective analysis, they support treatment with intravenous heparin (partial thromboplastin time 1.5-2 times baseline value) after normalization of the INR in patients with an ICH and an urgent need for anticoagulation.
ICHs during treatment with acetylsalicylic acid
Stroke as a sudden, non-conclusive, focal neurologic deficit is not difficult to diagnose but it is not easy to diagnose or to treat a stroke patient depending only on the clinical diagnosis. Before CT scan, there were many patients diagnosed clinically as ICH but were found to have infarction on autopsy.
General clinical manifestations
ICH occurs characteristically during activity (rarely during sleep). It has been given its own name “apoplexy”. The prototype is an obese, plethoric, hypertensive, male who, “while sane and sound, fall senseless to the ground- impervious to shouts, shaking, and pinching-, breathes stentorously, and dies in a few hours” 1.
Manifestations of increased intra-cranial pressure (ICP) in a Mohr 32 study show headache is reported in about 36% and vomiting in about 44% of patients alert enough to report the symptoms. Although the absence of headache or vomiting does not rule out the diagnosis of ICH, presence of these symptoms is in favor of ICH or SAH as it is reported in less than 10% of occlusive strokes. Seizures are uncommon at the onset in 7% of cases but are found in 32% of lobar hemorrhages.
Hypertension is frequent (91% of cases) 32 and correlates with other physical signs indicative of hypertension such as left ventricular hypertrophy, and hypertensive retinopathy. The presence of subhyaloid hemorrhage is virtually diagnostic of SAH (ruptured aneurysm).
Topographic localization of ICH on clinical examination (see pictures 1-5):
The most common form of ICH is the putaminal hemorrhage. The classical presentation is described by the massive hemorrhages, with rapidly evolving unilateral weakness accompanied by sensory, visual, and behavioral changes. Headache (depends on the patient’s conscious level to complain of it) and vomiting are common within few hours from onset. Although the onset is abrupt, there is often a gradual worsening of both focal deficit and the level of consciousness in the following minutes or hours. In a fully developed syndrome, the neurological examination shows a dense flaccid hemiplegia with a hemisensory syndrome, homonymous hemianopia, conjugate deviation of the eyes toward the side of the lesion, and global aphasia in the dominant hemisphere hematomas, or hemi-inattention in non-dominant lesions. In the smallest putaminal hematomas the patient is alert with hemiparesis, contralateral hemisensory deficit, and has normal gaze. The full picture of the large hematomas can occur even when the hematoma remains small with lateral extension (in dominant hemisphere causing aphasia and hemi-inattention in the nondominant hemisphere). Prominent inattention and neglect syndromes are seen in cases of vertical extension of the putaminal hematomas in nondominant hemisphere 33,34.
Caudate hemorrhage represents approximately 5 to 7% of cases of ICH. Clinical findings include gaze preference towards the side of the lesion, contralateral hemiparesis sometimes accompanied by transient hemisensory syndrome. Other findings include
Thalamic hemorrhage accounts for 10 to 15% of parenchymal hemorrhage. A typical presentation features a rapid onset of unilateral sensorimotor deficit, and
Lobar (white matter) Hemorrhage
Ropper and Davis 38 described 26 cases of spontaneous lobar hemorrhage. Occipital hemorrhage (11 cases) caused severe pain around the ipsilateral eye and dense hemianopia. Left temporal hemorrhage (7 cases) began with mild pain in or just anterior to the ear, fluent dysphasia with poor auditory comprehension but relatively good repetition, and a visual deficit subtending less than a hemianopia. Frontal hemorrhage (4 cases) caused a distinctive syndrome beginning with severe contralateral arm weakness, minimal leg and face weakness, and frontal headache. Parietal hemorrhage (3 cases) began with anterior temporal (“temple”) headache and hemisensory deficit, sometimes involving the trunk to the midline. One patient had a right temporal hemorrhage. Spontaneous lobar hemorrhage and branch artery embolism in the same region produce similar clinical syndromes. Headache is a first and most prominent symptom. A rapid but not instantaneous onset over several minutes, when combined with one of the typical syndromes, suggests lobar hemorrhage rather than other types of stroke. Ancillary investigations (including CT scanning, angiography in 11 patients, and autopsy in 4) disclosed 2 patients with bleeding diatheses due to warfarin, 2 with arteriovenous malformations, and 1 with metastatic tumor. Only 8 of the 26 patients had chronic hypertension (blood pressure greater than 130/85 mm Hg), suggesting that hypertension is not a common etiological factor. In another study of 22 cases, most hematomas were found in the parietotemporal region. Common physical findings were hemiparesis, hemisensory syndrome, and visual field defects. Seizures occurred in 23% of the patients, and coma was infrequent at onset 39.
Cerebellar hemorrhage appears with an average frequency of 10%. It may present with a spectrum of clinical manifestations, from a benign course with little to no neurologic deficit to a rapidly fatal course with hydrocephalus and brainstem compression. In patients with clinical deterioration, ventricular drainage and surgical evacuation of the clot may be life-saving 40. Patients with medial ventral cerebellar peduncular hemorrhages presented with a characteristic syndrome of ipsilateral ataxia, lower motor neuron type facial weakness, and ipsilateral gaze paresis. The gaze paresis can not be overcome with a doll’s head maneuver. The findings are explained by compression of the facial colliculus, with involvement of the sixth nerve nucleus and the middle cerebellar peduncle 41. Three cases of cerebellar hemorrhage and 5 of cerebellar infarction, diagnosed by brain CT, were examined from the early phase of the onset. All cases were mild to moderate in severity. Dizziness and nausea were the most common symptoms and cerebellar and other CNS signs could be detected only for a short period in some of the cases. Although neuro-otological examinations especially gaze nystagmus, eye tracking and positional nystagmus tests, were useful for diagnosing the central vestibular lesions, no definitive signs could be used to differentiate between cerebellar hemorrhage and infarction. Therefore, it is considered difficult in such mild cerebellar strokes to establish correct diagnosis by physical examinations alone 42. Symptoms usually develop during day while the patient is active. Occasionally a single prodromal episode of dizziness or facial numbness may precede hemorrhage. The most common symptom is an inability to stand or walk. Vomiting, dizziness, occipital-occasionally in one side of the head, frontal or associated with neck and shoulder pain mimicking SAH and headache are very frequent symptoms while, dysarthria, tinnitus, and hiccups are less frequent. At least 75% of cases presented with two of the characteristic triad of appendicular ataxia, ipsilateral horizontal gaze palsy, and peripheral facial palsy 43.
Brain stem Hemorrhage
Patients with brain stem lesion usually present with
Spontaneous, nontraumatic mesencephalic (
Before the introduction of CT scanning, the examination of the
Computerized tomography (CT) followed with magnetic resonance imaging (MRI) several years later enabled first the direct visualization of extravascular blood and products of its degradation. The protein component of hemoglobin is over 90% responsible for the hyperdensity of CT image in the case of a hemorrhage, whereas paramagnetic properties of hemoglobin derivatives are responsible for signal changes in MRI. CT is only able to diagnose accurately an acute hemorrhage. The lesion becomes hypodense in 3 weeks and eventually forms a posthemorrhagic pseudocyst. Differentiation of a posthemorrhagic pseudocyst from old contusions, ischemic lesions or even astrocytomas may be difficult. CT has thus a “short memory” for hemorrhage. MRI can differentiate 5 stages of hemorrhage according to the time schedule: hyperacute, acute, subacute stage I, subacute stage II, and chronic. Sequelae of hemorrhage are detectable even years later. The development of intracranial hemorrhage in daily routine MR imaging is described and documented to serve as a guide of the model situation for the use of the physician 46.
The value of
Course and prognosis
The prognostic value of clinical characteristics and CT scan findings in 50 patients of intracerebral hemorrhage (ICH) has been examined. Follow up has been done over a 6 month period. Each patient has been individually followed for 8 weeks. At the end of the follow up period 34% of the patients died, 36% were dependent on outside help for daily living, while 30% were capable of independent existence. Age of more than 60 yrs, Glasgow Coma Scale (GCS) Score of 6 or less at the time of admission, ICH volume greater than 30 ml, midline shift in CT scan of more than 3 mm and presence of intraventricular hemorrhage (IVH) and hydrocephalus all had an adverse impact on outcome. Young age, GCS score of more than 8, ICH volume of less than 20 ml, presence of lobar hemorrhage and absence of IVH/hydrocephalus were associated with relatively favorable outcome 47.
The most important predictor of the 28-day survival is the level of consciousness on admission, followed by first day MAP. Hypertension is the most important predictor of the first day MAP, followed by age, which had an inverse effect on the MAP level. At all levels of consciousness, high first day MAP (especially if > 145 mm Hg) worsened the 28-day survival rate 48.
Guidelines for the Management of Spontaneous Intracerebral Hemorrhage49
Initial management should first be directed toward the basics of airway, breathing, circulation, and detection of focal neurological deficits. In addition, particular attention should be given to detecting signs of external trauma. A complete examination should also include looking for complications such as pressure sores, compartment syndromes, and rhabdomyolysis, in patients with a prolonged depressed level of consciousness (patients “found down”).
Although intubation is not required for all patients, airway protection and adequate ventilation are critical. Patients who exhibit a decreasing level of consciousness or show signs of brain stem dysfunction are candidates for aggressive airway management. Imminent respiratory insufficiency rather than an arbitrary cutoff such as a specific Glasgow Coma Scale (GCS) score should guide intubation.
Four small randomized trials of medical therapy for ICH have been conducted: steroid versus placebo treatment (2 trials), hemodilution versus best medical therapy (1 trial), and glycerol versus placebo (1 trial). None of the 4 studies showed any significant benefit for the 3 therapies. In the study by Poungvarin et al, patients who were treated with steroids were more likely to develop infectious complications than those treated with placebo. Thus, the medical guidelines below are based on the reported experience of treatment of ICH in clinical series as well as general guidelines for treatment of any acutely ill patient in a neuro-intensive care unit.
Blood Pressure Management
The optimal level of a patient’s blood pressure should be based on individual factors such as chronic hypertension, elevated intracranial pressure (ICP), age, presumed cause of hemorrhage, and interval since onset. In general, recommendations for treatment of elevated blood pressure in ICH are more aggressive than those for patients with ischemic stroke. The theoretical rationale for lowering blood pressure is to decrease the risk of ongoing bleeding from ruptured small arteries and arterioles. A prospective observational study of growth in the volume of ICH did not demonstrate a relation between baseline blood pressure and subsequent growth of ICH, but frequent early use of hypertensive agents in this study may have obscured any relationship. Conversely, overaggressive treatment of blood pressure may decrease cerebral perfusion pressure and theoretically worsen brain injury, particularly in the setting of increased intracranial pressure. To balance these 2 theoretical rationales they recommend that blood pressure levels be maintained below a mean arterial pressure of 130 mm Hg in persons with a history of hypertension (level of evidence V, grade C recommendation). In patients with elevated ICP who have an ICP monitor, cerebral perfusion pressure (MAP–ICP) should be kept >70 mm Hg (level of evidence V, grade C recommendation). Mean arterial blood pressure >110 mm Hg should be avoided in the immediate period. If systolic arterial blood pressure falls below 90 mm Hg, pressors should be given. Nitroprusside, the most commonly used agent for severe elevation of blood pressure, is a vasodilatory agent that theoretically can increase cerebral blood flow and thereby intracranial pressure. This possible disadvantage has yet to be demonstrated in a clinical study.
ICP is considered a major contributor to mortality after ICH; thus, its control is essential. ICP may be managed through osmotherapy, controlled hyperventilation, surgery and other measures. A therapeutic goal for all treatment of elevated ICP is ICP <20 mm Hg and cerebral perfusion pressure (CPP) >70 mm Hg37. Optimal head position can be adjusted according to CPP values. Patients with suspected elevated ICP and deteriorating level of consciousness are candidates for invasive ICP monitoring. The GCS level that requires ICP monitoring should be based on rate of decline (of GCS) and other clinical factors such as CT evidence of mass effect and hydrocephalus. In general, ICP monitors should be placed in (but not limited to) patients with a GCS score of <9 and all patients whose condition is thought to be deteriorating due to elevated ICP (level of evidence V, grade C recommendation). The type of device depends on availability, experience, and situation. Intraventricular ICP monitors and intraparenchymal fiberoptic ICP devices are commonly used methods of monitoring ICP.
In addition to the mass effect of the hematoma, secondary hydrocephalus may contribute to elevated ICP. Ventricular drains should be used in patients with or at risk for hydrocephalus. Drainage can be initiated and terminated according to clinical performance and ICP values. Because of infectious complications, external drainage devices must be checked regularly, and duration of placement ideally should not exceed 7 days (level of evidence V, grade C recommendation). Use of anti-infectious prophylaxis is optional (level of evidence V, grade C recommendation). There is some recent evidence to support the use of intrathecal thrombolytics in the treatment of IVH, but this must be replicated in a larger manner.
The beneficial effect of
The complications of both methods include pneumonia (from immobility and immune suppression), hypotension (most pronounced at the time of bolus barbiturate administration), and predisposition to infection. Systemic hypotension results from decreased venous tone, decreased baroreflex tone, and sympathetic activity. Cardiovascular side effects may be aggravated by concomitant dehydration promoted by osmotherapy and diminished cardiac filling pressures. Maximal reduction in cerebral metabolism may be accompanied by electrocerebral silence (continuous EEG recording) and rises in jugular oxygen saturation.
The goal of fluid management is euvolemia. Optimal central venous pressure (CVP) or pulmonary wedge pressure may vary from patient to patient. Fluid balance is calculated by measuring daily urine production and adding for insensible water loss (urine output plus 500 ml for insensible loss plus 300 ml per degree in febrile patients). Electrolytes (sodium, potassium, calcium, and magnesium) should be checked and substituted according to normal values. Acidosis and alkalosis should be corrected according to blood gas analysis.
Seizure activity can result in neuronal injury and worsening of an already critically ill patient and, therefore, must be treated aggressively. Additionally, nonconvulsive seizures may contribute to coma in10% of neuro-critical care patients. In patients with ICH, prophylactic antiepileptic therapy (preferably phenytoin with doses titrated according to drug levels [14 to 23 µg/ml]) may be considered for 1 month. This should be tapered and discontinued if no seizure activity occurs during treatment, although data supporting this therapy are lacking (level of evidence V, grade C recommendation).
Body temperature should be maintained at normal levels, unless deliberate hypothermia is attempted.
Many patients who are delirious or stuporous are agitated. Hyperactivity is distressing to patients, caregivers, and family and may lead to self-injury. If psychological support is insufficient, prudent use of minor and major tranquilizers is recommended. Short-acting benzodiazepines or propofol are preferred. Other drugs such as analgesics and neuroleptics can be added if necessary. Doses and regimen should be titrated to clinical needs.
Pulmonary embolism is a common threat during the recovery period, particularly for bedridden patients. Pneumatic devices and heparin (and related compounds) can decrease the risk of pulmonary embolism. Depending on the patient’s clinical state, physical therapy, speech therapy, and occupational therapy should be initiated as soon as possible.
Guidelines for Surgical Removal of ICH
Patients with small hemorrhages (<10 cm3) or minimal neurological deficits should be treated medically because they generally do well with medical treatment alone (levels of evidence II through V, grade B recommendation). Patients with a GCS score
Patients with cerebellar hemorrhage >3 cm in diameter who are neurologically deteriorating or who have brain stem compression and hydrocephalus from ventricular obstruction should have surgical removal of the hemorrhage as soon as possible (levels of evidence III through V, grade C recommendation). 51
Stereotactic aspiration may be associated with better outcomes than standard craniotomy for moderate-sized cerebellar hemorrhages and at other sites, but this hypothesis has yet to be tested in a randomized study (no recommendation). 52 Young patients with large lobar hemorrhages (
In conclusion, therapy for ICH is largely supportive. Surgery has a definite role in cerebellar ICH and may play an increasing role in supratentorial ICH. Medical management remains supportive and largely untested 49.