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sickle cell crisis | sickle cell anemia

Stroke

Stroke-

Presentation of stroke-
  • Sudden onset focal deficit of cerebral function is the most common presentation.
  • Alternative presentation include apparent confusion ( due to dysphasia or visualpatial impairment), seizures, declining level of consciousness or global loss of brain function and coma .
  • If the symptoms last for >24 hrs ( or lead to death) and there is no apparent cause other than a vascular event,the diagnosis is most likely to be a stroke.if the symptoms last < 24 hrs and after adequate investigation, are presumed to be due to thrombosis or embolism, the diagnosis is a TIA.( Transient ischemic attack)

CAUSE:

  1. Thrombosis or embolism causing cerebral infarction ( 80%)
  2. Primary inter cerebral haemorrhage (15%)
  3. Subarachnoid haemorrhage (5%)
  4. Cerebral venous thrombosis (1%)

RISK FACTOR:

  • GLOBAL

  1. Increasing age
  2. Hypertension
  3. Diabetes
  4. Family history
  5. Dyslipidemia
  6. Homocysteinaemia
  • LIFESTYLE

  1. Drug abuse
  2. Smoking
  3. Oral contraceptives pills
  4. Neck trauma or manipulation
  5. Hormones replacement therapy
  • CEREBRAL

  1. Cerebralvascular diseases
  2. Berry aneurysm
  3. Cerebral amyloid
  4. Cerebral AV malformation
  • CARDIAC

  1. Atrial fibrillation
  2. MI
  3. Left ventricular aneurysm
  4. IHD
  5. Cyanotic heart disease
  6. Endocarditis
  • HAEMATOLOGICAL

  1. Hyper coagulation states
  2. Polycythaemia
  3. Sickle cell disease
  4. Warfarin ( haemorrhage)
  5. Thrombolysis
  • PERIPHERAL VASCULAR

  1. Carotid stenosis
  2. Pulmonary AV malformations
  3. Type IV - carotid dissection
  • In general, a stroke commences suddenly and the deficit is at its peak and established within 24 hrs .
  • If the evolution of symptoms is longer or progresses in a stuttering way over day or weeks , a space occupying lesion must be suspected.
  • If there is a variable depression of consciousness, the diagnosis of SAH should be entertained, and pyrexia at presentation should be alert one to the possibility of cerebral abscess.
  • Seizure occurs in 5-10 % cases of stroke at their onset although they are frequent sequelae.
  • Papilledema would be extremely unusual in arterial stroke but may be present in CVST.
  • Consider this in patient who may have dehydrated and young women with headache and seizures with or without focal signs.
  • Dissection of the internal carotid or vertebral arteries should always be considered, particularly in young patient who may experienced mild neck injury.Carotid dissection may be accompanied by a Horner syndrome, vertebral dissection presents with symptoms associated with brainstem stroke.
PATHO PHYSIOLOGY:
  • The pathophysiology of stroke is complex, and involves excitotoxicity mechanisms, inflammatory pathways, oxidative damage, ionic imbalances, apoptosis, angiogenesis and neuroprotection.
  • The ultimate result of ischemic cascade initiated by acute stroke is neuronal death along with an irreversible loss of neuronal function.

ISCHEMIC STROKE:

  • Ischemic stroke may manifest in the form of thrombotic stroke (large vessel and small vessel types); embolic stroke (with/without known cardiac and/or arterial factor); systemic hypoperfusion (Watershed or Border Zone stroke); or venous thrombosis.
  • Irrespective of the cause, compromised vascular supply to the brain is the primary event in majority (85–90%) of acute strokes.
  • Low respiratory reserve and complete dependence on aerobic metabolism make brain tissue particularly vulnerable to effects of ischemia.
  • A spectrum of severity is generally observed in the affected region of the brain, owing to the presence of collateral circulation.
  • Thus, part of the brain parenchyma (core) undergoes immediate death, while others may only be partially injured with potential to recover.

HEMORRHAGIC STROKES:

  • This form of stroke occurs due to rupture of a blood vessel in the brain. Its harmful effects are a resultant of: (a) hypoxia due to disrupted vascular supply; (b) irritant effect of released blood on brain parenchyma and vasculature; and (c) raised ICP due to continued bleeding, which may further restrict cerebral blood flow.
  • In this respect, hemorrhagic strokes are more dangerous than ischemic strokes. There are two types of hemorrhagic stroke: intracerebral hemorrhage (generally occurs in small arteries or arterioles and is commonly due to hypertension, trauma, bleeding disorders, amyloid angiopathy, illicit drug use like amphetamines or cocaine, and vascular malformations), and subarachnoid hemorrhage (due to rupture of aneurysms from the base of the brain and bleeding from vascular malformations near the pial surface).
  • It constitutes only 10–15% of all strokes.

ATHEROSCLEROSIS:

  • Atherogenesis is a decade-long process which involves luminal obstruction by cellular and extracellular substances.
  • The pathogenetic process from onset of atherosclerotic changes in cerebrovascular or extracranial circulation to precipitation of acute ischemic stroke with its consequent cell damage is complex.
  • Changes may manifest in the form of:
(a) Fatty streak, earliest lesions seen as yellowish areas of discoloration of intima, due to accumulation of lipid-filled macrophages (foam cells) in approximately 30% children below 5 years
(b) More advanced lesions with massive extracellular lipid at the branching points of arterial vessels
(c) Complicated fibrous plaques: central acellular area of lipid covered by a cap of smooth muscle cells and collagen, seen in the third decade of life .
Persons with risk factors for atherosclerotic disease (e.g., hypertension, hypercholesterolemia, cigarette smoking) tend to have clinically advanced atherosclerotic lesions with increased frequency.
MAJOR CATEGORIES OF STROKE:
Strokes can be classified into two major categories:
1) Ischaemic stroke (87%)
2) Haemorrhagic stroke (13%)
ISCHAEMIC STROKE:
Ischaemic strokes occur when the blood supply to an area of the brain is reduced, resulting in tissue hypoperfusion.
There are several mechanisms which can result in an ischaemic stroke including:
  • Embolism: An embolus from somewhere else in the body (e.g. the heart) causes obstruction of a cerebral vessel, resulting in hypoperfusion to the area of brain the vessel supplies.
  • Thrombosis: A blood clot forms locally within a cerebral vessel (e.g. due to atherosclerotic plaque rupture).
  • Systemic hypoperfusion: Reduced blood supply to the entire brain secondary to systemic hypotension (e.g. cardiac arrest).
  • Cerebral venous sinus thrombosis: Blood clots form in the veins that drain the brain, resulting in venous congestion and hypoxia which damages brain tissue.

HAEMORRHAGIC STROKE:
Haemorrhagic strokes occur when there is a rupture of a blood vessel or abnormal vascular structure within the brain.
There are two sub-types of haemorrhagic stroke:

INTRACEREBRAL HAEMORRHAGE:
Bleeding within the brain itself secondary to a ruptured blood vessel.
Intraparenchymal (bleeding within the brain tissue) Intarparenchyma
aemorrhage Intraventricular (bleeding within the ventricles)

SUBARACHNOID HAEMORRHAGE:

Bleeding that occurs outside of the brain tissue, between the pia mater and arachnoid mater.

INTRACEREBRAL HAEMORRHAGE:

Often has an apoplectic onset with headache,neck stiffness, vomiting and loss of consciousness of acute onset.
Conscious level can be depressed for >24 hrs , may be associated with b/l extensors plantar response and with high BP next 24 hrs .
But features such as these have been integrated scoring systems, difficult to differentiate ischaemic from haemorrhagic stroke on clinical ground alone.A CT scan is required.
BLOOD SUPPLY OF THE CEREBRUM:
  • The anterior, middle and posterior cerebral arteries each supply a specific territory of the brain:The anterior cerebral arteries (ACA)
  • supply the anteromedial area of the cerebrum.The middle cerebral arteries (MCA )
  • supply the majority of the lateral cerebrum.The posterior cerebral arteries (PCA)
  • supply a mixture of the medial and lateral areas of the posterior cerebrum.
BAMFORD CLASSIFICATION OF ISCHAEMIC STROKE:
The most commonly used classification system for ischaemic strokes is the Bamford classificationsystem.
This categorises stroke based on the initial presenting symptoms and clinical signs. This system does not require imaging to classify the stroke, instead, it is a purely clinical diagnosis.
TOTAL ANTERIOR CIRCULATION STROKE (TACS):
A total anterior circulation stroke (TACS) involves a large cortical stroke affecting the areas of the brain supplied by both the middle and anterior cerebral arteries.
All three of the following need to be present for a diagnosis of TACS:
  • Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial disorder)
PARTIAL ANTERIOR CIRCULATION STROKE (PACS):
A partial anterior circulation stroke (PACS) is a less severe form of TACS, in which only part of the anterior circulation has been compromised.

TWO OF THE FOLLOWING NEED TO BE PRESENT FOR A DIAGNOSIS OF PACS:
  • Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial disorder)

POSTERIOR CIRCULATION SYNDROME (POCS):
posterior circulation syndrome (POCS) involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).
ONE OF THE FOLLOWING NEED  TO BE PRESENT FOR A DIAGNOSIS OF POCS:
  • Cranial nerve palsy and a contralateral motor/sensory deficit
  •  Bilateral motor/sensory deficit
  • Conjugate eye movement disorder (e.g. horizontal gaze palsy)
  • Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
  • Isolated homonymous hemianopia
LACUNAR SYNDROME (LACS):
A lacunar syndrome (LACS) involves a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia).
One of the following needs to be present for a diagnosis of LACS:
  • Pure sensory stroke
  • Pure motor stroke
  • Senori-motor stroke
  • Ataxic hemiparesis

WHEN TO SCAN:

  • All suspected patient of stroke should must be scanned as soon as possible, atleast within 24 hrs of onset.
  • CT scan is the investigation of choice in the majority of cases because it is better at detecting bleed in early stages compared with MRI .
  • After 24 hrs and in any case where the stroke is suspected to involve brain stem or cerebellum, MRI is superior.it may reveal area of ischemia or infarct.

URGENT CT SCAN TO BE PERFORMED IN CASES OF:

  • Depressed level of consciousness
  • H/o anticoagulant Treatment or coagulopathy
  • Suspected case of SAH
  • Suspected case of SDH
  • any space occupying lesion
  • Cerebral infection
  • Indication of throbolysis


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