Presentation on theme: "Neurosurgery Case 3: Subarachnoid Hemorrhage 3Med – C UST-FMS."— Presentation transcript:
Neurosurgery Case 3: Subarachnoid Hemorrhage 3Med – C UST-FMS
57 y/o housewife Admission Few minutes PTA Sudden right-sided headache Bout of vomiting, progressive deterioration in LOC
Physical Exam – Restless, disoriented and non-communicative – BP: 198/102 – Afebrile – (+) nuchal rigidity – Ptosis of right eyelid – Fundoscopy: “suspicious hemorrhage”
Past Medical History – Had previous milder headache 3 days prior – Recently under initial treatment and observation for hypertension Personal & Social History – Former smoker – Took OCPs during premenopausal yrs
Ancillary Procedures – LP and/or cranial CT: confirmed earlier impression of subarachnoid hemorrhage – Angiogram: presence of aneurysm and a complicating vasospasm
Salient Features 57 y/o female Sudden severe headache Vomiting Progressive deterioration in LOC HTN (198/102 mmHg) Afebrile (+) nuchal rigidity ptosis of right eyelid Fundoscopy: “suspicious hemorrhage” Smoker Oral contraceptive use Recent episodes of hypertension CT scan: SAH Angiogram: aneurysm with complicating vasospasm
Causes of Subarachnoid Hemorrhage: Bleeding from a cerebral aneurysm (85%) Bleeding from an arteriovenous malformation (AVM) Bleeding disorder Head injury (Traumatic SAH) Unknown cause (idiopathic) Use of blood thinners (anticoagulant therapy)
Risks include: Fibromuscular dysplasia (FMD) and other connective tissue disorders associated with aneurysm or weakened blood vessels High blood pressure History of polycystic kidney disease polycystic kidney disease Smoking strong family history of aneurysms
SAH Clinical presentation Hypertensive on admission – History of poorly controlled hypertension Lethargy or obtundation Depressed mental status – results from brain shift and herniation secondary to mass effect from the hematoma in deep structures Gradual decline in neurologic function as hematoma expands Schwartz’s Principles of Surgery, 9 th Ed
Rupture of cerebral aneurysm Results in SAH Sudden, severe “thunderclap” headache Hunt-Hess grading system categorizes patients clinically Schwartz’s Principles of Surgery, 9 th Ed
Diagnostic Tests CT scan of the Head – modality of choice generally required to confirm or exclude bleeding.
Diagnostic Test Lumbar Puncture – mandatory in people with suspected SAH if imaging is negative – if an elevated number of RBCs is present equally in all 3 bottles this indicates SAH
CSF sample is also examined for xanthochromia more sensitive is spectrophotometry for detection of bilirubin Diagnostic Test
Angiography – Used after the SAH is confirmed, it origin needs to be determined
Diagnostic Test ECG – QT prolongation, Q waves, cardiac dysrhythmias and ST elevation - mimics a heart attack
HUNT & HESS SCALE FOR GRADING SUBARACHNOID HEMORRHAGE
GradeMotor Deficit 0Intact Aneurysm 1 Asymptomatic. Mild headache and slight nuchal rigidity. 1aNo acute meningeal/brain reaction but with fixed neurological deficit. 2 Cranial nerve palsy. Moderate to severe headache. Nuchal rigidity. 3 Mild focal deficit. Lethargy or confusion. 4 Stupor. Moderate to severe hemiparesis. Early decerebrate rigidity. 5 Deep coma. Decerebrate rigidity. Moribund appearance.
MANAGEMENT : SUBARACHNOID HEMORRHAGE MORALEDA FRANCIS B
ANEURYSM RUPTURE = SAH The major cerebral vessels, and therefore aneurysms (focal dilatation of the vessel wall), lie in the subarachnoid space. Rupture results in SAH. The aneurysmal tear may be small and seal quickly, or it may not. SAH may consist of a thin layer of blood in the CSF spaces, or thick layers of blood around the brain and extending into brain parenchyma, resulting in a clot with mass effect. Meningeal linings of the brain are sensitive, SAH usually results in a sudden, severe "thunderclap" headache. A patient will classically describe "the worst headache of my life." Schwartz's Principles of Surgery, 9e
Presenting neurologic symptoms may range from mild headache to coma to sudden death. The Hunt-Hess grading system categorizes patients clinically. Schwartz's Principles of Surgery, 9e
MANAGEMENT Patients with symptoms suspicious for SAH should have a HEAD CT immediately. – CT is rapid, noninvasive, and approximately 95% sensitive. In patients with suspicious symptoms but negative head CT, a LUMBAR PUNCTURE (LP) should be performed. – An LP with xanthochromia and high red blood cell counts (usually 100,000/mL), which do not decrease between tubes 1 and 4, is consistent with SAH. Negative CT and LP essentially rules out SAH. Patients diagnosed with SAH require four-vessel cerebral ANGIOGRAPHY within 24 hours to assess for aneurysm or other vascular malformation. – Catheter angiography remains the gold standard for assessing the patient's cerebral vasculature, relevant anomalies, and presence, location, and morphology of the cerebral aneurysms. Schwartz's Principles of Surgery, 9e
Acute SAH appears as a bright signal in the fissures and CSF cisterns around the base of the brain Subarachnoid hemorrhage is visible as HYPERDENSE signal in the: interhemispheric fissure (1) Bilateral Sylvian fissures (2 shows the left fissure) in the ambient cisterns around the midbrain (3). This gives the classic five-pointed-star appearance of a subarachnoid hemorrhage. Visible temporal tips of the lateral ventricles indicate hydrocephalus.
TREATMENT SAH patients should be admitted to the neurologic ICU. Hunt-Hess grade 4 and 5 patients intubation and hemodynamic monitoring and stabilization. The current standard of care for ruptured aneurysms requires early aneurysmal occlusion. Schwartz's Principles of Surgery, 9e
THE MEDICAL MANGEMENT OF SAH Focuses on: – Protecting the airway – Managing blood pressure before and after aneurysm treatment – Preventing rebleeding prior to treatment – Managing vasospasm – Treating hydrocephalus – Treating hyponatremia – Preventing pulmonary embolus. Harrison's Principles of Internal Medicine, 17e
COMPLICATIONS AND TREATMENT ANEURYSMAL REBLEEDING May be secondary to uncontrolled hypertension or aneurysmal clot fibrinolysis. Surgical clipping or endovascular coiling is strongly recommended to reduce the rate of rebleeding. SEIZURE Because seizures increase the risk of rebleeding after an SAH, prophylactic use of an anticonvulsant, for example, intravenous fosphenytoin or phenytoin, 15–20 mg/kg, is recommended CURRENT Diagnosis & Treatment: Emergency Medicine, 6e
COMPLICATIONS AND TREATMENT HYPOVOLEMIA AND HYPONATREMIA Hypovolemia and hyponatremia can occur secondary to the syndrome of inappropriate secretion of antidiuretic hormone. Treatment involves intravenous hydration with isotonic crystalloid. A central intravenous monitor is desirable. CURRENT Diagnosis & Treatment: Emergency Medicine, 6e
COMPLICATIONS AND TREATMENT ACUTE OBSTRUCTIVE HYDROCEPHALUS This form of hydrocephalus occurs in about 20% of patients after SAH. Ventriculostomy is recommended, although it may increase the risk of rebleeding or infection. CHRONIC COMMUNICATING HYDROCEPHALUS This form of hydrocephalus is a frequent occurrence after SAH. A temporary or permanent cerebrospinal fluid diversion is recommended in symptomatic patients. CURRENT Diagnosis & Treatment: Emergency Medicine, 6e
COMPLICATIONS AND TREATMENT VASOSPASM Vasospasm, or delayed cerebral ischemia, remains a frequent complication with high morbidity and mortality rates. Nimodipine, 60 mg orally every 4 hours, is strongly recommended. HYPERTENSION The acute management of elevated blood pressure in SAH is controversial. There is no evidence that lowering blood pressure decreases rebleeding or the rate of cerebral infarction. However, lowering systolic blood pressure to 160 mm Hg and/or maintaining a mean arterial pressure of 110 mm Hg is associated with lower risk of rebleeding and a decreased mortality rate. Antihypertensive therapy should be reserved for severe blood pressure elevations with evidence of end-organ deterioration. CURRENT Diagnosis & Treatment: Emergency Medicine, 6e Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 6e
COMPLICATIONS AND TREATMENT NEUROSURGICAL CONSULTATION Seek neurosurgical consultation for definitive management, which may include surgical clipping or endovascular coiling depending upon the resources available. CURRENT Diagnosis & Treatment: Emergency Medicine, 6e
TWO OPTIONS FOR OCCLUSION OPTION 1: CLIP IT The patient may undergo craniotomy with microsurgical dissection and placement of a titanium clip across the aneurysm neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel. – Thereby eliminating the risk of rebleeding – craniotomy and brain retraction are associated with neurologic morbidity. Schwartz's Principles of Surgery, 9e Harrison's Principles of Internal Medicine, 17e
Intraoperative surgical images of a large intracranial aneurysm (A) successfully treated by placing an aneurysm clip around the neck of the aneurysm (B).
TWO OPTIONS FOR OCCLUSION OPTION 2: COIL IT The second option is to "coil" the aneurysm via an endovascular approach. The patient is taken to the interventional neuroradiology suite for placement of looped titanium coils inside the aneurysm dome. The coils support thrombosis and prevent blood flow into the aneurysm. – Endovascular techniques involve placing platinum coils, or other embolic material, within the aneurysm via a catheter that is passed from the femoral artery. The aneurysm is packed tightly to enhance thrombosis and over time is walled-off from the circulation Schwartz's Principles of Surgery, 9e
Conventional angiogram following coil embolization of the aneurysm, whereby the aneurysm body is filled with platinum coils delivered through a microcatheter navigated from the femoral artery into the aneurysm neck.
FACTORS FAVORING… CRANIOTOMY AND CLIPPING VIA NEUROSURGEON Young age Good medical condition Broad aneurysm necks. COILING VIA ENDOVASCULAR SURGEON Age Medical comorbidities Narrow aneurysm necks. Schwartz's Principles of Surgery, 9e
WHICH IS BETTER? Due to coil migration or compaction over time, surgical clipping is believed to result in a more definitive cure. The decision to clip or coil is complex and should be fully explored. The International Subarachnoid Aneurysm Trial researchers suggested that endovascular occlusion resulted in better outcomes for certain types of cerebral aneurysms, although this trial was marred by poor selection and randomization techniques, and the validity of its conclusions have been questioned. – Centers that combine both endovascular and neurosurgical expertise likely offer the best outcomes for patients, and there are good data showing that centers that specialize in aneurysm treatment have improved mortality rates. Long-term outcomes may be better in younger patients with clipped aneurysms. Debate also continues regarding optimal care for unruptured intracranial aneurysms. SAH patients often require 1 to 3 weeks of ICU care after aneurysm occlusion for medical complications that accompany neurologic injury. Schwartz's Principles of Surgery, 9e
FAMILIAL INTRACRANIAL ANEURYSMS Families with two or more affected persons should have all members screened. Both autosomal and recessive patterns of inheritance may occur. Clinical Neurology
Aneurysm rupture of an aneurysm of one of the arteries of the base of the brain is the most common cause of spontaneous subarachnoid hemorrhage.
Saccular (“berry”) aneurysms found at points of bifurcation of the intracranial arteries. form on the basis of a prior lesion of the vessel wall, which is either a (usually congenital) structural defect, or an injury due to hypertension.
Saccular (“berry”) aneurysms Anterior communicating artery (40 %), Lateral wall of the internal carotid artery (at the origin of the ophthalmic or posterior communicating artery) (30%) Bifurcation of the middle cerebral artery in the sylvian fissure (20 %) Basilar tip (10%)
Saccular (“berry”) aneurysms Aneurysms can produce neurological deficits by pressing on neighboring structures even before they rupture. E.g. an aneurysm of the posterior communicating artery can compress the oculomotor nerve, causing a third nerve palsy (the patient complains of diplopia).
Fusiform aneurysms elongated (“spindle-shaped”) enlargement of a vessel preferentially involve the intracranial segment of the internal carotid artery, the main trunk of the middle cerebral artery, and the basilar artery. usually caused by atherosclerosis and/or hypertension, and they are only rarely a source of hemorrhage.
Fusiform aneurysms Large fusiform aneurysms of the basilar artery can compress the brainstem. Slow flow inside a fusiform aneurysm can promote intra- aneurysmal clot formation, with subsequent embolic stroke or cut-off of perforating vessels by the direct extension of thrombus. These aneurysms usually cannot be treated neurosurgically, because they are elongated enlargements of normal vessels, rather than pathological structures (like saccular aneurysms) making no contribution to the cerebral blood supply.
Mycotic aneurysms Aneurysmal dilatations of intracranial blood vessels are sometimes the result of sepsis with bacterially induced damage to the vascular wall. preferentially found on small arteries of the brain. The treatment consists of treatment of the underlying infection. Mycotic aneurysms sometimes regress spontaneously; they very rarely cause subarachnoid hemorrhage.
Acute Nontraumatic Subarachnoid Hemorrhage caused by the spontaneous rupture of a saccular aneurysm, with escape of blood into the subarachnoid space. Manifestations. – The leading symptom (~45%) of a subarachnoid hemorrhage is a sudden, very intense headache (“the worst headache of my life”). – Meningeal irritation by subarachnoid blood causes nuchal rigidity – Consciousness may be impaired immediately or within the first few hours. – Neck stiffness and vomiting – Cranial nerve palsies and focal neurological signs may be present, depending on the site and extent of the hemorrhage.
Manifestations Focal deficits – Anterior communicating artery or MCA bifurcation aneurysms may rupture into the adjacent brain or subdural space and form a hematoma large enough to produce mass effect. common deficits that result include hemiparesis, aphasia, and abulia. Prodromal symptoms suggest the location of a progressively enlarging unruptured aneurysm. – A third cranial nerve palsy, particularly when associated with pupillary dilatation, loss of ipsilateral (but retained contralateral) light reflex, and focal pain above or behind the eye, may occur with an expanding aneurysm at the junction of the posterior communicating artery and the internal carotid artery.
Manifestations Prodromal symptoms suggest the location of a progressively enlarging unruptured aneurysm. – A sixth nerve palsy may indicate an aneurysm in the cavernous sinus, and visual field defects can occur with an expanding supraclinoid carotid or anterior cerebral artery aneurysm. – Occipital and posterior cervical pain may signal a posterior inferior cerebellar artery or anterior inferior cerebellar artery aneurysm. – Pain in or behind the eye and in the low temple can occur with an expanding MCA aneurysm. – Thunderclap headache is a variant of migraine that simulates a SAH. Before concluding that a patient with sudden, severe headache has thunderclap migraine, a definitive workup for aneurysm or other intracranial pathology is required.
Treatment Aneurysms can be treated with a neurosurgical operation – the neck of the aneurysm is closed with a metal clip. The aneurysm is thereby permanently excluded from the circulation, so that it cannot bleed again. – definitive, but the disadvantage is that it requires operative opening of the skull (craniotomy) and neurosurgical manipulations around the base of the brain that may cause further complications. Surgery should be performed in the first 72 hours after subarachnoid hemorrhage, i.e., before the period of greatest risk for the development of vasospasm
Treatment Early surgery has been shown to improve the prognosis of patients who present with SAH in Hunt and Hess grades 1, 2, or 3. It is the most important form of treatment for the prevention of rebleeding. Filling of the aneurysm with metal coils (“coiling,” a procedure belonging to the field of interventional neuroradiology) – An alternative, less invasive form of treatment – Coils are delivered from the tip of a specialized angiographic catheter, which is inserted transfemorally and advanced to the level of the aneurysm. – Coiling obviates the need for craniotomy, but it may not be an equally reliable method of permanently obliterating the aneurysm.
Clinical Course, Prognosis, and Complications Prehospitalization lethality of aneurysmal SAH is approximately 35%. After the acute event, the patient faces the risk of three potentially fatal complications: Hydrocephalus Rebleeding Vasospasm
Clinical Course, Prognosis, and Complications Hydrocephalus (impaired CSF circulation and/or resorption), – Appears very rapidly after the initial SAH. – Resulting intracranial hypertension often impairs the patient’s consciousness and may also cause focal neurological deficits. Hydrocephalus can be effectively treated by external ventricular drainage. Lumbar drainage is less commonly used.
Clinical Course, Prognosis, and Complications Rebleeding – if it occurs, is more often lethal (50 %) than the initial SAH – risk of rebleeding is 20% in the first 14 days after the initial SAH, – and 50% in the first six months, if the aneurysm has not been obliterated. Rebleeds often produce large intraparenchymal hematomas – because the subarachnoid space around the aneurysm is partly sealed by adhesions resulting from the initial bleed.
Clinical Course, Prognosis, and Complications Vasospasm – occurs a few days later, presumably through the effect of vasoactive substances contained in the extravasated subarachnoid blood. – risk of vasospasm can be reduced by the removal of as much subarachnoid blood as possible during surgery, and by therapeutically induced hypertension. These measures usually suffice to prevent the development of vasospastic infarcts, a much-feared complication. – Vasospasm is a serious impediment to the effective diagnosis and treatment of aneurysmal subarachnoid hemorrhage.
Vasospasm Narrowing of the arteries at the base of the brain causes symptomatic ischemia and infarction in ~30% of patients – major cause of delayed morbidity and death. – signs of ischemia appear 4–14 days after the hemorrhage, most often at 7 days. – mortality rate of 40-50% – severity and distribution of vasospasm determine whether infarction will occur. Delayed vasospasm is due to direct effects of clotted blood and its breakdown products on the arteries within the subarachnoid space. – the more blood that surrounds the arteries, the greater the chance of symptomatic vasospasm. All of these focal symptoms may present abruptly, fluctuate, or develop over a few days. In most cases, focal spasm is preceded by a decline in mental status.
Grading is characterized by a thin and localized layer of subarachnoid blood Grade I has thick layer in two of three subarachnoid compartments or in one subarachnoid compartment and the cortical surface Grade II is a severe diffuse SAH involving all subarachnoid compartments, or two of three plus the cortical surface. Grade III
Vasospasm detected reliably with conventional x-ray angiography, – invasive procedure – expensive – carries the risk of stroke and other complications. TCD ultrasound – based on the principle that the velocity of blood flow within an artery will rise as the lumen diameter is narrowed. – By directing the probe along the MCA and proximal anterior cerebral artery (ACA), carotid terminus, and vertebral and basilar arteries on a daily or every-other-day basis, vasospasm can be reliably detected and treatments initiated to prevent cerebral ischemia. CT angiography is another method that can detect vasospasm. Severe cerebral edema in patients with infarction from vasospasm – increase the ICP enough to reduce cerebral perfusion pressure. – treatment may include mannitol, hyperventilation, and hemicraniectomy; moderate hypothermia may have a role as well.
Venous Malformation “the abnormal formation or development of blood vessels” usually congenital occur during fetal development Not visible until weeks or even years after birth typically grow in proportion to the growth of the child – growth is usually gradual and steady during the first year of life
Etiology almost always congenital No genetic, demographic, or environmental risk factors identified. Trauma associated with inherited neurological disorders (rare)
AV Malformation most significant lesions masses of arteries and arterialized veins. brain tissue between the vessels, is usually abnormal and often scarred from previous tiny hemorrhages
AV Malformation blood is shunted directly from the arterial system to the venous system. Effects: – the oxygen content of the blood remains high as it enters the vein – the flow is high and the pressure is elevated within the veins contribute to hemorrhages or seizures which occur with AVMs Occur throughout the brain and spinal cord
Capillary Telengectasias small (0.3 to 1.0 cm) lesions composed of tiny blood vessels in the brain clump of enlarged capillary- sized vessels separated from each other by more or less normal appearing brain tissue rarely symptomatic
Cavernous hemangiomas “cavernous angiomas, cavernomas, angiomas” well-defined lesions which may reach significant size made up of fairly large blood- filled channels or "caverns". immediately adjacent to each other and there is no recognizable intervening normal brain tissue "blood sponge”
Cavernous hemangioma Two different modes: – Inherited, multiple and bilateral – solitary and sporadic slow flow lesion, not a shunt may present with either hemorrhage or seizures consists of variable sized vascular spaces that vary between capillaries, sinusoids, and larger cavernous spaces
Venous Malformation most common type of vascular malformation superficial or deep veins that are abnormally formed and dilated natural history is slow, steady enlargement. – surgery, trauma, infection, or hormonal changes associated with puberty, pregnancy, or menopause may cause rapid expansion. skin, mucous membrane, brain, bowel, liver, spleen a deficiency of smooth muscle cells in the vein walls is known to be a critical factor alterations in the genes responsible for the communication of endothelial cells and smooth muscle
Venous Malformations Venous Angioma and the Venous Varix crown of multiple small venules that converge on a larger venous trunk. The venous trunk usually drains into a dural sinus. lack of "bridging veins" connecting the cortex to the dural sinuses – transcortical vein will now drain an unusually large volume of brain, and therefore enlarges The "crown" of veins that converge onto the connecting trunk are "collecting veins" that drain the capillaries from the affected volume – venous pressure within the varix can be elevated – produce the secondary cavernous hemangiomas separated by normal brain tissue very common, very benign best left alone
Venous Malformation Vein of Galen malformations combination of lesions vein of Galen – unsupported by surrounding tissue, lacks a fibrous wall, free within the fluid of the quadrigeminal plate cistern – any increase in venous pressure results in a dilatation of the vein – converting its normal cylindrical shape into a sphere Increased pressure within the deep venous system also interferes with normal venous development, usually producing persistence of embryologic channels that normally regress (e.g. the "falcine vein").