Hemorrhagic Stroke Guidelines Pdf
Joke Grinman
Hemorrhagic stroke is due to bleeding into the brain by the rupture of a blood vessel. Hemorrhagic stroke may be further subdivided into intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). Hemorrhagic stroke is associated with severe morbidity and high mortality. Progression of hemorrhagic stroke is associated with worse outcomes. Early diagnosis and treatment are essential given the usual rapid expansion of hemorrhage, causing sudden deterioration of consciousness and neurological dysfunction. This activity highlights the role of the interprofessional team in the evaluation and treatment of hemorrhagic stroke.
Objectives:
- Summarize the pathophysiology of hemorrhagic stroke.Identify the most common causes of hemorrhagic stroke and the most common site of the bleeding.Review the common presentations of this hemorrhagic stroke.CT scan is the initial investigation of choice. Prompt medical, sometimes surgical (in indicated cases), management is needed for recovery from hemorrhagic stroke.
Cerebrovascular accident (CVA), otherwise called a stroke, is the third major cause of morbidity and mortality in many developed countries. Stroke can be either ischemic or hemorrhagic. Ischemic stroke is due to the loss of blood supply to an area of the brain. It is a common type of stroke.
Hemorrhagic stroke is due to bleeding into the brain by the rupture of a blood vessel. Hemorrhagic stroke may be further subdivided into intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). ICH is bleeding into the brain parenchyma, and SAH is bleeding into the subarachnoid space. Hemorrhagic stroke is associated with severe morbidity and high mortality.[1] Progression of hemorrhagic stroke is associated with worse outcomes. Early diagnosis and treatment are essential given the usual rapid expansion of hemorrhage, causing sudden deterioration of consciousness and neurological dysfunction.
The usual causes of spontaneous subarachnoid hemorrhage (SAH) are ruptured aneurysm, arteriovenous malformation, vasculitis, cerebral artery dissection, dural sinus thrombosis, and pituitary apoplexy. The risk factors are hypertension, oral contraceptive pills, substance abuse, and pregnancy.
Hemorrhagic stroke contributes to 10% to 20% of strokes annually.[4][1][5] The percentage of hemorrhage in stroke is 8-15% in the United States of America, the United Kingdom, and Australia, and 18% to 24% in Japan and Korea. The incidence is around 12% to 15% of cases per 1,00,000 per year. The incidence is high in low and middle-income countries and Asians. The incidence is more common in men and increases with age. The global incidence is increasing, predominantly in African and Asian countries. Japanese data have shown that control of hypertension reduces the incidence of ICH. The case fatality rate is 25% to 30% in high-income countries, while it is 30% to 48% in low- to middle-income countries. The ICH fatality rate depends on the efficacy of critical care.
Secondary injury is contributed to by inflammation, disruption of the blood-brain barrier (BBB), edema, overproduction of free radicals such as reactive oxygen species (ROS), glutamate-induced excitotoxicity, and release of hemoglobin and iron from the clot.
Usually, the hematoma enlarges in 3 hours to 12 hours. The enlargement of hematoma occurs in 3 hours in one-third of cases. The perihematomal edema increases within 24 hours, peaks around 5 to 6 days, and lasts up to 14 days. There is an area of hypoperfusion around the hematoma. The factors causing deterioration in ICH are an expansion of hematoma, intraventricular hemorrhage, perihematomal edema, and inflammation.[1] Cerebellar hematoma produces hydrocephalus by compression of the fourth ventricle in the early stage.
Non-aneurysmal spontaneous subarachnoid hemorrhage may be either perimesencephalic or non-perimesencephalic SAH. In perimesencephalic SAH, bleeding is mainly in the interpeduncular cistern. Physical exertion, such as the Valsalva maneuver producing increased intrathoracic pressure, and elevated intracranial venous pressure, is a predisposing factor for perimesencephalic nonaneurysmal SAH (PM-SAH).[8] There is diffuse blood distribution in non-perimesencephalic SAH (NPM-SAH).[9]
The common presentations of stroke are headache, aphasia, hemiparesis, and facial palsy.[10] The presentation of hemorrhagic stroke is usually acute and progressing. Acute onset headache, vomiting, neck stiffness, increases in blood pressure, and the rapidly developing neurological signs are the common clinical manifestations of hemorrhagic stroke.[5] Symptoms can lead to the extent and location of hemorrhage.
Cerebellar hemorrhage produces symptoms of raised ICP, such as lethargy, vomiting, and bradycardia. Progressive neurological deterioration indicates the enlargement of hematoma or an increase in edema.
The clinical features of subarachnoid hemorrhage are severe headache described as a thunderclap, vomiting, syncope, photophobia, nuchal rigidity, seizures, and decreased level of consciousness.[8][9] Signs of meningismus such as the Kernig sign (pain on straightening the knee when the thigh is flexed to 90 degrees) and Brudzinski sign (involuntary hip flexion on flexing the neck of the patient) may be positive.
In the subacute phase, the hematoma may be isodense to brain tissue, and magnetic resonance imaging (MRI) may be necessary. The volume of the hematoma can be measured by the formula AxBxC/2, where A and B are the largest diameter and the diameter perpendicular to that.[14] C is the vertical height of the hematoma. Intracerebral hemorrhage with a volume of more than 60 ml is associated with high mortality.[15] The other poor prognostic factors are hematoma expansion, intraventricular hemorrhage, infra-tentorial location, and contrast extravasation on CT scan (spot sign).[5] The paramagnetic properties of deoxyhemoglobin allow early detection of hemorrhage in MRI.[16] Gradient echo (GRE) imaging is as good as CT in detecting acute bleed. MRI can distinguish between the hemorrhagic transformation of infarct and primary hemorrhage. MRI can detect underlying causes of secondary hemorrhages, such as vascular malformations, including cavernomas, tumors, and cerebral vein thrombosis.
Extravasation of contrast in CT angiogram (CTA) indicates ongoing bleeding associated with fatality.[17] Multidetector CT angiography(MDCTA) helps rule out the causes of secondary hemorrhagic stroke such as arteriovenous malformation (AVM), ruptured aneurysm, dural venous sinus (or cerebral vein) thrombosis (DVST/CVT), vasculitis, and Moya-Moya disease.[18] (fig.4).
Four-vessel digital subtraction angiography (DSA) is necessary in the case of SAH. A repeat study is needed to confirm if the DSA is negative for an aneurysm. Repeat angiography is advisable at 1-week and 6-weeks intervals.
Blood investigations such as bleeding time, clotting time, platelet count, peripheral smear, prothrombin time (PT), and activated partial thromboplastin time(aPTT) will detect any abnormality of bleeding or coagulation and any hematological disorder which can cause hemorrhage. Liver function tests and renal function tests are also needed to exclude any hepatic or renal dysfunction as a cause. The investigations to rule out vasculitis are the quantitative evaluation of immunoglobulins, thyroid antibodies, rheumatoid factor, antinuclear antibodies (ANA), anti-double-stranded DNA (ds-DNA antibodies), Histon antibodies, complement, anti-Ro [SS-A] and anti-La [SS-B-] antibodies, cytoplasmic staining and perinuclear staining antineutrophil cytoplasmic antibodies (c- and pANCA), and anti-endothelial antibodies.[22]
There are many different opinions on the treatment of hemorrhagic stroke. There are many trials on the optimal management of hemorrhagic stroke - Antihypertensive Treatment in Acute Cerebral Hemorrhage(ATACH), Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT), Factor VIIa for Acute Hemorrhagic Stroke Treatment (FAST), and Surgical Trial in Intracerebral Haemorrhage (STICH).[23] The role of surgery in hemorrhagic stroke is a controversial topic.
BP should be reduced gradually to 150/90 mmHg using beta-blockers (labetalol, esmolol), ACE inhibitor (enalapril), calcium channel blocker (nicardipine), or hydralazine.[4] BP should be checked every 10-15 minutes. ATACH study observed a nonsignificant relationship between the magnitude of systolic blood pressure (SBP) reduction and hematoma expansion and 3-month outcome.[24] But the INTERACT study showed that early intensive BP-lowering treatment attenuated hematoma growth over 72 hours.[25] It has been found that high SBP is associated with neurological deterioration and death.[20] The American Stroke Association (ASA) recommendation is that for patients presenting with SBP between 150 and 220 mmHg, the acute lowering of SBP to 140 mmHg is safe and can improve functional outcomes. For patients presenting with SBP >220 mmHg, an aggressive reduction of BP with a continuous intravenous infusion is needed.
The initial treatment for raised ICP is elevating the head of the bed to 30 degrees and using osmotic agents (mannitol, hypertonic saline). Mannitol 20% is given at a dose of 1.0 to 1.5 g/kg.[4] Hyperventilation after intubation and sedation to a pCO of 28 to 32 mmHg will be necessary if ICP increases further. ASA recommends monitoring ICP with a parenchymal or ventricular catheter for all patients with Glasgow coma scale (GCS)
Hemostatic therapy is given to reduce the progression of hematoma.[4] This is especially important to reverse the coagulopathy in patients taking anticoagulants. Vitamin K, prothrombin complex concentrates (PCCs), recombinant activated factor VII (rFVIIa), fresh frozen plasma (FFP), etc., are used.[4][20][4] ASA recommends that patients with thrombocytopenia should receive platelet concentrate.[20] Patients with elevated prothrombin time INR should receive intravenous vitamin K and FFP or PCCs. FFP has the risk of allergic transfusion reactions. PCCs are plasma-derived factor concentrates containing factors II, VII, IX, and X. PCCs can be reconstituted and administered rapidly. The FAST trial showed that rFVIIa reduced the growth of the hematoma but did not improve survival or functional outcome.[26] rFVIIa is not recommended in unselected patients since it does not replace all clotting factors.[20]
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