Flashcards in RITE answers Deck (44):
What are the neurological presentations of air embolism?
What are the high risk situations for air embolism?
What is seen on imaging?
VAE affects cardiovascular, pulmonary and central nervous system. High level of suspicion required to diagnose. Large bolus of air can lead to right ventricular air lock and immediate fatality
Neuro Sx: Air embolism can cause either global brain damage due to cerebral hypoperfusion or ischaemia from embolism in the case of a patent foramen ovale.
High risk surgeries for VAE are sitting position and posterior fossa neurosurgeries, cesarean section, laparoscopic, orthopedic, surgeries invasive procedures, pulmonary overpressure syndrome, and decompression syndrome. RITE EXAMPLE: cardiopulmonary bypass. Can also be caused from trauma and neursurgeries when the head is operated on above the level of the heart.
Ix: The transesophgeal echocardiography is the most sensitive device which will detect smallest amount of air in the circulation.
On the CT, air can be seen diffusely within the cerebral vessels.
Rx: Treatment of VAE is to prevent further entrainment of air, reduce the volume of air entrained and haemodynamic support.
Mortality of VAE ranges from 48 to 80%.
What did the ECASS 3 trial show?
The ECASS 3 trial demonstrated the benefit of IV tPA between 3 and 4.5 hours after symptom onset when compared to placebo.
Despite an increased incidence of intracranial hemorrhage, there was no mortality benefit.
What is this sign? What does it suggest?
A round or triangular area of hyperdensity at the posterior aspect of the superior sagittal sinus on a noncontrast head CT is called a delta sign and may be an indicator of a sagittal sinus thrombosis.
Risk factors include oral contraceptives, pregnancy, malignancy or a hypercoagulable disorder. Most evidence suggests that the best treatment for cerebral venous thromboses is intravenous heparin or low molecular weight heparins (enoxaparin).
Why is glucose monitoring important prior to TPA?
Hypoglycaemia can mimic an acute stroke and cause focal neurology thus needs to be excluded prior to thrombolysis
What does cerebral amyloid angiopathy commonly cause in elderly patients?
Cerebral amyloid angiopathy usually affects the elderly (age >60) and accounts for up to 10% of intracranial haemorrhages
Typical location: superficial (lobar) with extension into the subarachnoid space
Pathology: the deposition of beta amyloid protein in the vessels int the cortex and leptomeninges (the media and adventitia of small meningeal and cortical vessels) results in lobar haemorrhages. It appears histologically as waxy, pink material in the vessel walls. The material may resemble the hyaline change of arteriolosclerosis. Congo red staining with apple green birefringence on polarization confirms that the material is amyloid.
Cerebral amyloid angiopathy is a common cause of spontaneous lobar intracerebral hemorrhage in elderly patients. This is best seen on gradient echo - chronic microbleeds on gradient echo MRI.
Typically patients have a history of dementia and evidence of multiple tiny old haemorrhages.
There is no current treatment
How does cerebral vasospasm present?
When is cerebral vasospasm likely to occur post subarachnoid haemorrhage?
Cerebral vasospasm is a serious complication of subarachnoid hemorrhage typically occurring between the 4th and 14th day after hemorrhage. It often presents with focal neurologic deficits and drowsiness.
What is the management of BP when thrombolysing? (what are the guidelines)
This has an acute stroke and is evaluated rapidly in an emergency setting. She appears to be a potential candidate for receiving IV t-PA based on her stroke scale, time window, and absence of contraindications to the drug; however, her blood pressure exceeds the guidelines for use of t-PA and IV labetalol would be indicated.
What is the most appropriate medication for someone with multiple strokes 2 AF?
In the absence of clear contraindications, anticoagulation with warfarin is the most appropriate agent for the prophylaxis against recurrent strokes in a patient with atrial fibrillation.
What are the symptoms of Right ACA infarct
unilateral contralateral motor weakness (leg/shoulder > arm/hand/face)
minimal sensory changes (two-point discrimination) in the same distribution as above
left limb apraxia
This patient has a cerebral infarct in the distribution of the right anterior cerebral artery. If contrast is administered, subacute infarcts commonly enhance, usually with a gyriform pattern.
What are the sx of a lateral medullary syndrome? Where is the lesion?
This patient has a lateral medullary syndrome caused by occlusion of the posterior inferior cerebellar artery.
Ipsilateral signs include loss of pain and temperature on the face, Horner syndrome, and cerebellar signs. Patients also develop contralateral hemibody anesthesia. Nausea and vertigo are related to involvement of the vestibular nuclei. Dysphagia and a diminished gag reflex are associated with nucleus ambiguus. Also associated with hiccups
What are the symptoms of a carotid dissection?
The syndrome characterized by ipsilateral Horner syndrome and neck pain with contralateral hemiparesis is most suggestive of a carotid dissection. Dissections often occur in the setting of neck trauma and disorders of connective tissue including fibromuscular dysplasia.
What is the most important modifiable RF for stroke?
Although diabetes, hypertension, smoking, and hyperlipidemia clearly increase stroke risk, hypertension is the most important risk factor, and hypertension control is the most important intervention in this patient to reduce his future risk of cerebral ischemia.
What does the CT show?
The CT head demonstrates a hyperdensity of the right middle cerebral artery (MCA), consistent with a thrombus or very slow flow. The cerebral angiogram demonstrates tapering narrowing (the flame sign) of the extracranial, right internal carotid artery with features classic for carotid dissection.
What is the likely aetiology of 3rd nerve palsies?
Divide into pupillary sparing and non-sparing.
Pupillary sparing: most likely related to diabetes or small brainstem infarct.
Pupillary involvement: "surgical" PICOM - A posterio communicating artery aneurysm, an extrinsic mass
What are fundoscopy findings of arteritic acute ischaemic optic neuropathy?
"This patient has arteritic acute ischemic optic neuropathy, in which the findings are typically a swollen disc and
retinal pallor. The mechanism is likely to be giant cell arteritis based on his clinical history."
What is Anton's syndrome?
Anton's syndrome is denial of blindness / cortical blindness
It is a result of severe acute bilateral injury to the medial occipital lobes and adjacent association cortex, usually due to ischemia in the distribution of the posterior cerebral arteries.
The syndrome has also occurred after traumatic injury to the optic nerve with
associated bifrontal lobe contusions."
Vertebral dissection: what are the symptoms and the RFs
This disorder is more common is women. It often follows neck trauma. When occurring spontaneously, it is often associated with a disorder of connective tissue, such as
Dominant posterior cerebral artery syndrome?
"In the syndrome of alexia without agraphia, a complete right homonymous hemianopsia is present in many
cases, but there are exceptions.
Impaired naming and understanding of color names in the presence of intact or
nearly intact color vision is common, although some patients suffer from an actual impairment of color vision.
Mild anomia is common but not always present. In most cases, there are no other aphasic disturbances or
abnormalities of the primary motor or sensory systems. The most frequently reported pathology is occlusion of
the dominant (left) posterior cerebral artery."
Where is the lesion?
- Right hemiplegia
- Eyes deviated to the left that conjgately cross the midline with the doll's eye maneuver
Most likely has a left frontal lesion
Antiplatelet / anticoagulation post stroke?
Patients with acute ischemic stroke presenting within 48 hours of symptom onset should be given aspirin up to
325 mg/day to reduce stroke mortality and decreased morbidity,
Heparin, warfarin, methylprednisolone, and mannitol have not been shown to reduce morbidity or mortality in acute stroke."
Bilateral ischemia in the mesial inferior occipitotemporal cortex? what are the sx?
This patient has color agnosia and prosopagnosia most likely due to bilateral ischemia in the mesial inferior occipitotemporal cortex.
Sx of a haemorrhageic lesion of the pituitary?
Bitemporal visual field deficit
"A hemorrhagic lesion of the pituitary involving the chiasm would explain the sudden visual field deficit, somnolence, and
hypotension. Elevated intracranial pressure or bilateral cavernous sinus lesions could explain the bilateral sixth nerve palsies with
pituitary apoplexy. The other diagnoses listed are not associated with a bitemporal visual field deficit and the clinical description
What are frequent early signs of sagittal sinus thrombosis? RFs? CT findings?
"Postpartum women are at increased risk for sagittal sinus thrombosis due to their hypercoagulable state.
Headache, delirium, and focal seizures are frequent early symptoms.
CT may also show hemorrhagic infarction and edema in a non-arterial distribution."
CADASIL- genetic mutation? Sx?
cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) due to a mutation in the Notch3 gene on chromosome 19. This disorder is often associated with progressive focal neurological deficit. Migraine headaches are a common clinical feature as well."
What are contraindications to thrombolysis?
Contraindications to TPA include hemorrhagic stroke, coagulopathy, recent surgery or stroke. Intra-arterial thrombolysis is still considered investigational.
What are contraindications to thrombolysis?
Contraindications to TPA include hemorrhagic stroke, coagulopathy, recent surgery or stroke.
Exclusion criteria include prior intracranial hemorrhage; history of intracranial neoplasm, aneurysm or arteriovenous malformation; stroke or head trauma within the previous 3 months; major surgery or biopsy of a parenchymal organ within preceding 14 days; gastrointestinal or urinary bleeding within the previous 21 days; recent myocardial infarction; seizure at onset of stroke; history of known hereditary of acquired abnormal hemostasis; current use of oral anticoagulants with prothrombin time greater than 15 seconds, use of heparin in previous 48 hours with prolonged partial thromboplastin time; platelet count less than 100,000/mm3, and evidence on CT of major hypodensity or sulcal effacement (greater than one-third of middle cerebral artery territory), and systolic blood pressure greater than 185 mmHg or diastolic blood pressure greater than 110 mmHg, and blood glucose less than 50 mg/dl or greater than 400 mg/dl.
What are the sensitivities for investigating nontraumatic subarachnoid haemorrhage?
The overwhelming majority of patients with aneurysmal subarachnoid hemorrhage (SAH) present with a sudden onset severe headache which may be associated with brief loss of consciousness, seizures, nausea or vomiting or meningismus.
Symptom onset may occur in the setting of physical exertion.
Sudden onset of headache, regardless of severity or prior headache history, should raise the clinical suspicion for SAH and compel a diagnostic evaluation.
Noncontrast head CT using multidetector technique and reformatting acheives greater than 95% sensitivity in the first 24 hours of bleeding onset.
Lumbar puncture is mandatory if there is a strong suspicion of SAH despite a normal head CT. The classic findings are an elevated opening pressure and an elevated red blood cell count that does not diminish from CSF tube one to tube four. Immediate centrifugation of the CSF can help differentiate bleeding in SAH from that due to a traumatic spinal tap. By 1 week, the sensitivity of LP has reduced to around 50% (given CSF circulation and resorption)
Xanthochromia — represents hemoglobin degradation products.
An otherwise unexplained xanthochromic supernatant in CSF is highly suggestive of SAH.
The presence of xanthochromia indicates that blood has been in the CSF for at least two hours; therefore if the CSF is analyzed quickly after a traumatic LP, there will not be xanthochromia. However, if LP is performed within two hours after the onset of SAH, xanthochromia may similarly be absent; the absence of xanthochromia cannot be used as evidence of a traumatic tap if an LP is performed in a SAH of less than two hours duration. For a LP performed several hours after the ictus, a finding of erythrocytosis without xanthochromia is unlikely to be SAH . Xanthochromia can last for two weeks or more
Polyarteritis Nodosa - what is it? Presentation? Causes?
Polyarteritis nodosa (PAN) is a systemic necrotizing vasculitis that typically affects medium-sized muscular arteries, with occasional involvement of small muscular arteries.
PAN is not associated with the presence of antineutrophil cytoplasmic antibodies (ANCA).
Commonly middle-aged or older adults, and the incidence rises with age, with a peak in the sixth decade of life. Patients with PAN typically present with systemic symptoms (fatigue, weight loss, weakness, fever, arthralgias) and signs (skin lesions, hypertension, renal insufficiency, neurologic dysfunction, abdominal pain) of multisystem involvement
Causes: most cases are idiopathic, although hepatitis B virus infection, hepatitis C virus infection, and hairy cell leukemia are important in the pathogenesis of some cases, which are termed secondary PAN.
About 30% of patients with polyarteritis nodosa will have circulating antibodies to hepatitis B virus.
Diagnosis should be confirmed by biopsy whenever possible. Established PAN is characterized by segmental transmural inflammation of muscular arteries; it does not involve veins, unlike other forms of systemic vasculitis.
What are the findings of acute cerebral infarcts? (macro pathology)
"Acute cerebral infarcts are characterized by swelling, effacement of the gray-white junction, and cracking at the interface between the intact and infarcted brain tissue. The photo illustrates these findings as well as small cortical hemorrhages in this large fresh cerebral infarct in the middle cerebral artery territory."
Epidural Haemorrhage-(epidural haematoma, extradural haematoma) Cause? Classical presentation? Radiological findings? Treatment?
Epidural hematoma (EDH) is caused by bleeding in the potential space between the dura and the skull, usually as a consequence of traumatic injury. Nontraumatic acute EDH is rare. Commonest in young adults, rare above 50
Source of blood: most often arterial, can involve middle meningeal artery - caused by trauma to sphenoid bone associated with tearing of middle meningeal artery - resulting in haemorrhage over the cerebral convexity in the middle cranial fossa.
A typical presentation is of a young patient involved in a head strike (either during sport or a result of a motor vehicle accident) who may or may not lose consciousness transiently. Following the injury, they regain a normal level of consciousness (lucid interval), but usually have an ongoing and often severe headache. Over the next few hours, they gradually lose consciousness- and develop symptoms of blood collection .
Head CT is a fast and accurate method for the detection of acute intracranial hemorrhage. Epidural blood produces a lens-shaped pattern on head CT.
Most patients with focal neurologic signs or symptoms attributable to acute EDH require emergent surgical hematoma evacuation to prevent irreversible brain injury or death caused by hematoma expansion, elevated intracranial pressure, and brain herniation.
What happens at the cellular level during ischaemia?
"Animal studies suggest that brain ischemia causes an excessive increase of extracellular concentration of glutamate, an excitotoxic amino acid, in the central nervous system. In neuronal cells, glutamate receptor activation by excitotoxic glutamate causes the entry of extracellular Ca2+ resulting in intracellular acidification through unknown mechanisms This intracellular
accumulation of the electrolyte calcium thus leads to apoptotic and necrotic cell death by initiating a cascade of events at both the cytoplasmic and nuclear levels."
"Cessation of electrical activity due to hyperpolarization that occurs acutely after an ischemic insult is the result
of activation of potassium (K+) membrane channels."
What is antiphospholipid syndrome? Clinical manifestations? Blood markers?
Antiphospholipid syndrome is a coagulopathy that occurs most commonly in young women.
Associated problems may include migraine, spontaneous abortion, TIA, or stroke in a young adult, and systemic lupus erythematosus (SLE) in a minority of patients.
Detection of anticardiolipin or beta 2-glycoprotein I antibodies helps to establish the diagnosis.
Cavernous Malformations: clinical presentation? Causes? annual bleeding rates? Identification? Management?
Cavernous malformations (cavernous angiomas, cavernomas) may occur as a sporadic or familial condition.
Three genetic loci (CCM1, CCM2, and CCM3) responsible for familial cavernous malformations
Hispanic Americans = CCM1 (Autosomal Dominant)
white non-Hispanic = CCM2 and CCM3
These are thin walled dilated capillaries with a simple endothelial lining. Associated developmental venous anomalies occur in about 25 percent.
They can occur throughout the brain but are most common in the subcortical rolandic and temporal areas.
Clinical presentation can include hemorrhage, seizures, and/or progressive neurologic deficits.
Annual bleeding rates are up to 1 percent per year for supratentorial lesions and up to 3 percent per year for brainstem lesions. Recurrent hemorrhage is more common after an initial bleed and may be as high as 5 percent per year for supratentorial lesions and 21 percent for brainstem lesions.
Cavernous malformations are typically identified on MRI and are often angiographically occult.
Asymptomatic cavernous malformations are followed without intervention. Surgical resection may be indicated for progressive neurologic deficits, intractable epilepsy, and/or hemorrhage. Stereotactic radiosurgery is an option for nonoperable lesions.
What is the MOA of clopidogrel?
Oral antiplatelet agent
An irreversible blockade of the adenosine diphosphate
(ADP) receptor on platelet cell membranes. This receptor is named P2Y12 and is important in platelet aggregation, the crosslinking of platelets by fibrin. The blockade of this receptor inhibits platelet aggregation by blocking activation of the glycoprotein IIb/IIIa pathway.
Dipyridamole inhibits the uptake of adenosine into platelets, endothelial cells and erythrocytes in vitro and in vivo; the inhibition occurs in a dose-dependent manner at therapeutic concentrations (0.5-1.9 g/mL).
This inhibition results in an increase in local
concentrations of adenosine which acts on the platelet A2-receptor thereby stimulating platelet adenylate cyclase and increasing platelet cyclic-3',5'-adenosine monophosphate (cAMP) levels. Via this mechanism, platelet aggregation is inhibited in response to
various stimuli such as platelet activating factor (PAF), collagen and adenosine diphosphate (ADP).
Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (COX) enzyme. Cyclooxygenase is required for prostaglandin and thromboxane synthesis. Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation.
MOA of tPA?
Tissue-type plasminogen activator (tPA) is one of the two mammalian serine proteases that activates plasminogen into plasmin, the primary plasmatic function being fibrinolysis."
MOA of dabigatran?
Dabigatran, an FDA-approved oral anticoagulant, is a direct thrombin inhibitor (DIT) that was demonstrated to reduce the incidence of stroke and systemic emboli compared with dose-adjusted warfarin in patients with non-valvular atrial fibrillation (AF), while concomitantly decreases the risk of bleeding in a pivotal study (Randomized Evaluation of Long-term Anticoagulant Therapy, or RE-LY).
Rivaroxaban and Apixaban MOA?
apixaban and rivaroxaban, inhibit factor Xa, and have also demonstrated non-inferiority with warfarin in patients with AF in prevention of stroke, with a lower bleeding risk.
What are the CT findings of hepatic encephalopathy?
CT head demonstrates generalized cerebral edema and is found in most patients with acute hepatic encephalopathy.
What is the most common cause of non-traumatic CNS haemorrhage?
Hypertension is the most common cause of non-traumatic intraparenchymal central nervous system (CNS) hemorrhage.
While intracerebral deep grey matter is the most common site for rupture of vessels secondary to hypertension, pons and rarely cerebellum also account for some cases.
What is the risk of stroke when holding aspirin or clopidogrel?
Aspirin: there is an increase in platelet aggregation in the first 7 to 10 days after discontinuing aspirin therapy. Clinical studies demonstrate that as many as 4.49% of strokes can be linked to aspirin cessation within the prior 10 days and there is a 3-fold increase in the risk of stroke after discontinuing aspirin.
Clopidogrel: data indicate that clopidogrel withdrawal results in a rebound platelet aggregation, this does not seem to cause an increased risk of stroke, especially if the patient continues aspirin.
What is pituitary apoplexy? What are the clinical symptoms?
Pituitary apoplexy is caused by hemorrhage or infarction of the pituitary gland in the setting of a pituitary adenoma.
The clinical presentation of pituitary apoplexy ranges from relatively mild symptoms to more severe symptoms including acute headache, ophthalmoplegia, decreased visual acuity, change in mental status, adrenal crisis, coma, or even sudden death. Thunderclap headache may be a predominant feature. It may occur acutely or subacutely
Pituitary apoplexy can present with TCH in patients who have normal physical examinations, head CT scans, and cerebrospinal fluid analyses. Pituitary tumors that are isodense to normal brain tissue may be easily overlooked on CT studies, even if hemorrhage is present. Brain MRI has a much higher sensitivity than CT for detecting the tumor and associated blood.