Case Report Session

INTRACEREBRAL HEMMORHAGE

Created by: Dian Yashifa 06120134

Preseptor: Prof. dr. H. Basjiruddin A, Sp.S (K)

NEUROLOGY DEPARTMENT MEDICAL FACULTY OF ANDALAS UNIVERSITY RSUP DR. M. DJAMIL PADANG 2011

CASE REPORT A 68 year old woman, was hospitalized on October 4th 2011, initially came with loss of consciousness. Alterations in the level of consciousness happened 4 hours before patient transferred into hospital, sudden onset while doing an activity. Other symptoms were an intense occipital cephalgia and three times vomit (brownie fluid). Weakness of the right limb was presenced with shift to the left mouth. She had an uncontrolled hypertension within 2 years, and a family history of cerebrovascular diseases (stroke and hypertension). She is a housewife, never smoke or drink coffe. The physical examination revealed a somnolent patient (GCS 11, E3M5V3) with a high value of arterial blood pressure (180/100 mmHg), a cardiac sinus rhythm of 79/min, respiration rate, 24 breaths per minute. Pulmonal examination results were normal. Border line of heart was wider to inferolateral, 1 finger to lateral from linea midclavicula sinistra of VI intercosta space, pure heart sound and regular rhythm. The complete blood cell count revealed normal Hb, Ht and trombocyte (Hb: 12,8 gr%, Ht: 38%, trombocyte: 304.000/mm3) and a slight increase of leucocyte (12.000/mm3). Biochemical blood tests revealed slight increase glucose levels (148 mg/dL), electrolyte was normal (Na: 148 mEq/l, K: 3,5 mEq/l, Cl: 109 mEq/l), ureum and creatinin also in normal limits (Ureum: 15 mg/dL, creatinin: 0,7mg/dL) Neurologic assesment: GCS 11 (E3M5V3), somnolent patient. There were no sign of meningeal excitation as revealed by negative result in the examination of stiffness of neck, brudzinski I & II sign, and kernig sign. There were neither sign of increasing intracranial pressure. Cranial nerve examination: sense of smell (nerve I) cant be done; Direct light reflex positive in both eyes (nerve II); pupil isochor 3mm/3mm, direct and indirect light reflex positive in both eyes (nerve III); doll eyes manuever was moving (III, IV, VI); korneal reflex positive in both eyes (nerve V), asymmetrical face with flattening on the right side of plicanasolabialis (nerve VII); oculoauditoric reflex positive, no nistagmus (nerve VIII); vomit reflex positive (nerve IX); symmetry of arcus pharyngmovement, uvula in center (nerve X); shoulder girdle muscles (nerve XI) cant be examined; tongue deviation negative, no atrophy nor fasciculation (XII). Coordination testing cant be done. The motor system was hypoactive (the right limb was hypoactive than left limb), eutonus, and eutrophy; fallen limb test

shows lateralization to the right, right limb fallen first. The sensory system had a response with moderate pain of impulse. Otonom function: pee using catheter. Physiology reflex (Biseps, Triseps, KPR, APR) is positive two in both side of limb, patholgical reflex (Babinsky, Gordon, Chaddock, and oppenheim) is positive one in right side of inferior limb. Mental status examination cant be done. Three poin in algoritm of gajah mada score were found in this patient; deterioration of consciousness level, cephalgia, and positive babinsky sign; indicates a hemmorhage stroke. Siriraj stroke score result +4.5 also leads to hemmorhage stroke. The CT cerebral scan without contrast performed at the admission revealed a hyperdense lesion in left basal ganglia, obliterate left lateral ventricle, no midline shift, bleeding 90 cc with perifocal oedema. pons, CPA and cerebellum were well. Sulci and gyri extended. This finding led us to standard further investigations appropriate in such a clinical situation. A chest X-ray was performed and revealed cardiomegaly but Electrocardiography shows sinus rhythm and SV1+SV6 <35 mm. funduscopy ocular dextra et sinistra shows fundus of hypertension grade II. Clinical diagnosis : deterioration level of consciousness + hemiparese dextra + parese N. VII sinistra central type; topic diagnosis : subcortex cerebri hemispher sinistra; etiology diagnosis : intracerebral hemorrhage, secondary diagnosis : hypertension grade II + stress ulcer. General supportive medical care: elevation of head 300, 02 3 litre/minutes, fasting, nasogastric tube spooling per 6 hour with NaCl 0,9%, IVFD RL: Triofushin: Panamine = 1:2:1 (6 hours per kolf), and urine catheter for monitoring fluid balance. The patient received brain act 2 x 250 mg, tranexamic acid 6x1 gr, Omeprazole 1x1 ampules, ranitidine 2x50 mg, and manitol kir 20%. Second day of hospitalized, GCS still 11 (E3M5V3) the patient was somnolent. NGT filled with brownie fluid, therapy continued. Third day of hospitalized, GCS increase to 12 (E3M6V3), patient got fever (T=38,80C) NGT still in brownie fluid, blood pressure was increased to 200/120 mmHg, and patient was response with light pain of impulse, therapy added with herbesser to manage the high blood pressure, controlled per 15 minutes and anti-piretic agent for high temperature.

SUMMARY A 68 year old woman, hospitalized on October 4th 2011, initially came with loss of consciousness. She had an uncontrolled hypertension within 2 years. On the physical examination revealed a somnolent patient (GCS 11, E3M5V3) with a high value of arterial blood pressure (180/100 mmHg). There were no sign of meningeal excitation neither sign of increasing intracranial pressure. Cranial nerve examination found impairment in nerve VII, asymmetrical face with flattening on the right side of plicanasolabialis. The motor system was hypoactive (the right limb was hypoactive than left limb), eutonus, and eutrophy; fallen limb test shows lateralization to the right, right limb fallen first. The sensory system had a response with moderate pain of impulse. Patholgical reflex (Babinsky, Gordon, Chaddock, and oppenheim) is positive one in right side of inferior limb. Three poin in algoritm of gajah mada score indicates a hemmorhage stroke. Siriraj stroke score result +4.5 also leads to hemmorhage stroke. The CT cerebral scan without contrast shows a hyperdense lesion in left basal ganglia, obliterate left lateral ventricle, no midline shift, bleeding 90 cc with perifocal oedema, sulci and gyri extended. A chest X-ray shows cardiomegaly but Electrocardiography was normal.

THEORY Intracerebral Hemorrhage

Intracerebral hemorrhage accounts for 8-13% of all strokes and results from a wide spectrum of disorders. Intracerebral hemorrhage is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage. Intracerebral hemorrhage and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes. Depending on the underlying cause of bleeding, intracerebral hemorrhage is classified as either primary or secondary. Primary intracerebral hemorrhage, accounting for 78 to 88 percent of cases, originates from the spontaneous rupture of small vessels damaged by chronic hypertension or amyloid angiopathy. Secondary intracerebral hemorrhage occurs in a minority of patients in association with vascular abnormalities (such as arteriovenous malformations and aneurysms), tumors, or impaired coagulation. Although hypertensive intracerebral hemorrhage remains the most common form of intracerebral hemorrhage, underlying vascular abnormalities should always be considered in appropriate circumstances because of the high risk of recurrent hemorrhage and available treatment options. Nontraumatic intracerebral hemorrhage most commonly results from hypertensive damage to blood vessel walls (eg, hypertension, eclampsia, drug abuse), but it also may be due to autoregulatory dysfunction with excessive cerebral blood flow (eg, reperfusion injury, hemorrhagic transformation, cold exposure), rupture of an aneurysm or arteriovenous malformation (AVM), arteriopathy (eg, cerebral amyloid angiopathy, moyamoya), altered hemostasis (eg, thrombolysis, anticoagulation, bleeding diathesis), hemorrhagic necrosis (eg, tumor, infection), or venous outflow obstruction (eg, cerebral venous thrombosis). Nonpenetrating and penetrating cranial trauma are also common causes of intracerebral hemorrhage. Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis, fibrinoid necrosis, and development of Charcot-Bouchard aneurysms, affecting penetrating arteries throughout the brain including lenticulostriates,

thalamoperforators, paramedian branches of the basilar artery, superior cerebellar arteries, and anterior inferior cerebellar arteries. Predilection sites for intracerebral hemorrhage include the basal ganglia (4050%), lobar regions (20-50%), thalamus (10-15%), pons (5-12%), cerebellum (510%), and other brainstem sites (1-5%).

Intraventricular hemorrhage occurs in one third of intracerebral hemorrhage cases from extension of thalamic ganglionic bleeding into the ventricular space. Isolated intraventricular hemorrhage frequently arise from subependymal structures including the germinal matrix, AVMs, and cavernous angiomas. The clinical symptoms and signs vary depending on the size, location, and rate of expansion of the bleed. Symptoms can evolve over several minutes (10 to 30 minutes) or even hours, contrary to popular belief that the deficit is always maximum at onset. The evolution of symptoms is likely due to hemorrhage expansion.Typical features found in many, but not all, patients include focal neurologic signs, headache, nausea, vomiting, and alterations in the level of consciousness. Elevated blood pressure is found in over 90% of patients acutely, even if they have no prior history of hypertension. Patients with a large hematoma usually have a decreased level of consciousness as a result of increased intracranial pressure and the direct compression or distortion of the thalamic and brain-stem reticular activating system. Decreased central benzodiazepine-receptor binding on cortical neurons in the presence of small, deep lesions may also contribute to altered consciousness. Patients with a supratentorial intracerebral hemorrhage involving the putamen, caudate, and thalamus

have contralateral sensory-motor deficits of varying severity owing to the involvement of the internal capsule. Abnormalities indicating higher-level cortical dysfunction, including aphasia, neglect, gaze deviation, and hemianopia, may occur as a result of the disruption of connecting fibers in the subcortical white matter and functional suppression of overlying cortex, known as diaschisis. In patients with an infratentorial intracerebral hemorrhage, signs of brain-stem dysfunction include abnormalities of gaze, cranial-nerve abnormalities, and contralateral motor deficits. Ataxia, nystagmus, and dysmetria are prominent when the intracerebral hemorrhage involves the cerebellum.Common nonspecific symptoms include headache and vomiting due to increased intracranial pressure and meningismus resulting from blood in the ventricles. In one fourth of patients with intracerebral hemorrhage who are initially alert, a deterioration in the level of consciousness occurs within the first 24 hours after onset of the hemorrhage. The presence of a large hematoma and ventricular blood increases the risk of subsequent deterioration and death. Expansion of the hematoma is the most common cause of underlying neurologic deterioration within the first three hours after the onset of hemorrhage. Worsening cerebral edema is also implicated in neurologic deterioration that occurs within 24 to 48 hours after the onset of hemorrhage. Infrequently, late deterioration is associated with progression of edema during the second and third weeks after the onset. laboratory orders should include complete blood count, coagulation parameters (fibrinogen, PT, PTT, INR), serum electrolytes, and liver function tests. Additionally a type and screen should be sent to the blood bank. Additional labs and diagnostics (chest x-ray and ECG) should be ordered as required by the patients comorbidities. CT scanning remains the gold standard for initial neuroimaging in suspected ICH and will likely remain so in the coming decade. CT imaging not only defines the size and location of the hemorrhage but it can suggest the underlying cause of the hemorrhage and any secondary complications (intraventricular extension, hydrocephalus, and signs of herniation). Additional imaging, such as MRI or cerebral

angiography may be required to further define the cause of the hemorrhage in atypical cases. The treatment of patients with ICH consists of emergency stabilization of the ABCs (airway, breathing, circulation), concurrent management of comorbidities, general supportive medical care with emphasis on neurologic protection and complication prevention, and lastly, targeted therapies to address the hemorrhage itself. Unlike ischemic stroke patients, patients with ICH frequently require acute interventions to maintain their airway and provide mechanical ventilation. A knowledgeable understanding of airway management is critical to minimize delays to intubation and to prevent unnecessary elevation in intracranial pressure associated with intubation. Similarly, hypertension is a common associated finding and many patients require blood pressure management. Optimal blood pressure management remains unsettled. The goal is to balance the belief that hypertension may promote hemorrhage growth with concerns that reducing blood pressure may reduce perihematomal perfusion, especially in the setting of increased intracranial pressure (ICP). Current American Heart Association (AHA) guidelines provide criteria for blood pressure management using agents such as labetalol, enalapril, nitroprusside and nicardipine. Currently blood pressure management is initiated when the systolic blood pressure is greater than 180 mmHg or the diastolic blood pressure is greater than 105 mmHg. In those patients with ICP monitoring, blood pressure should be maintained to ensure cerebral perfusion pressure (CPP=mean arterial pressure- ICP) is maintained above 70 mmHg. While uncommon, hypotension should be managed by correction of any volume deficit first, then complemented with vasopressors, such as phenylephrine or dopamine to maintain systolic blood pressures > 90 mmHg. Unlike AIS, seizures are relatively common in ICH; close to25% of patients develop seizures typically within the first 24 hours from hemorrhage onset. A high index of suspicion must be maintained, especially in comatose patients, as many seizures may be nonconvulsive. Prophylactic anticonvulsants are not recommended. Typical agents to treat ICH related seizures include phenytoin and phenobarbital. Fortunately, most seizures associated with ICH do not require anticonvulsant therapy beyond the first month.

While not classically defined as neuroprotection, there is a growing body of literature which suggests tight glycemic control and maintenance of normothermia (<38.5oC) are important adjuncts to general care that minimize secondary neurologic injury. Recent guidelines for AIS call for initiation of insulin administration when serum glucose is above 200 mg/dL. Similarly, it is well known that hyperthermia is detrimental to the acutely injured brain. Induced hypothermia is under investigation as a general neuroprotective strategy. For now, tight glucose control and maintenance of normothermia is recommended. Until recently, targeted hematoma therapies generally involved correction of coagulopathies and coagulation parameters with the administration of blood products (fresh frozen plasma (FFP), platelets, etc). Specific corrections for warfarin associated hemorrhages include administration of vitamin K and FFP. ICH associated with unfractionated heparin should be treated with protamine. Most low-molecular weight heparins can also be treated with protamine. Correction of coagulopathies should be started as quickly as possible. Increased intracranial pressure is a common sequela of ICH and is responsible for much of mortality and morbidity in ICH. Early intervention when ICP is above 20 mmHg is required to prevent often precipitous herniation and death. Osmotherapy remains the first approach to lowering ICP. Osmotic therapy typically consists of mannitol 20% (0.25-0.5g/kg every 4 hours) to maintain a serum osmolality of 310 mOsm/L. Moderate hyperventilation, with a target pCO2 from 30-35 mmHg produces a drop in ICP from 25-30% within 30 minutes. Additional measure to minimize ICP also includes muscle relaxants and adequate sedation for patients receiving mechanical ventilation. Sedation is also important prior to procedures, such as endotracheal suctioning, nasogastric tube placement, etc, which cause transient elevations in ICP. Obstructive hydrocephalus also increases ICP and requires ventriculostomy for drainage of cerebral spinal fluid (CSF). Other therapies have been used in attempts to blunt ICP, but corticosteroids and glycerol have not been shown to be beneficial while barbiturates and hypertonic saline require additional study before their potential benefits become clear. Intraventricular hemorrhage has been associated with worse outcomes, largely through obstruction of normal CSF flow. A ventriculostomy can remove excess CSF and monitor ICP, but have associated risks of infections and catheter tract hemorrhages. Recent pilot trials have also demonstrated faster resolution of

ventricular hematoma with the infusion of fibrinolytics via the ventriculostomy; Surgical removal of hematomas is fairly common despite the lack of compelling evidence that it impacts outcome. Potential surgical candidates, identified in the AHA guidelines, include cerebellar hemorrhages greater than 3 cc associated with clinical deterioration or brain stem compression, ICH associated with structural lesions in patients with a chance for good outcome, and young patients with a moderate or large lobar hemorrhage who are clinically deteriorating. While it is difficult to specifically predict outcome in individual patients, GCS at presentation and volume of ICH have been shown to help predict general outcome. In a study by Broderick and colleagues, patients with an initial ICH volume >60 cc (just 4 tablespoons!) and a presenting GCS < 9 had a 30 day mortality of 91%. Patients with an initial ICH volume of < 30 cc and a presenting GCS 9 had a predicted 30 day mortality of 19%. Additional variables associated with worse clinical prognosis include intraventricular extension, ICH associated with anticoagulation, advanced age, and associated seizures.