Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
Nursing management of the client with increased intracranial pressureANILKUMAR BR
The rigid cranial vault contains brain tissue (1,400 g), blood (75 mL), and CSF (75 mL)
The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP.
ICP is usually measured in the lateral ventricles; normal ICP is 10 to 20 mm Hg. Increased ICP is a syndrome that affects many patients with acute neurologic conditions.
This is because pathologic conditions alter the relationship between intracranial volume and pressure. Although an elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumours, subarachnoid haemorrhage, and toxic and viral encephalopathies
Nursing management client with Increased intracranial pressure ( ICP)ANILKUMAR BR
The rigid cranial vault contains brain tissue (1,400 g), blood (75 ml), and CSF (75 ml)
The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP.
ICP is usually measured in the lateral ventricles; normal ICP is 10 to 20 mm hg.
The Monro-kellie hypothesis states that because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others.
Increased ICP is a syndrome that affects many patients with acute neurologic conditions.
This is because pathologic conditions alter the relationship between intracranial volume and pressure.
Although an elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, and toxic and viral encephalopathies.
Antibiotic Stewardship by Anushri Srivastava.pptxAnushriSrivastav
Stewardship is the act of taking good care of something.
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
WHO launched the Global Antimicrobial Resistance and Use Surveillance System (GLASS) in 2015 to fill knowledge gaps and inform strategies at all levels.
ACCORDING TO apic.org,
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
ACCORDING TO pewtrusts.org,
Antibiotic stewardship refers to efforts in doctors’ offices, hospitals, long term care facilities, and other health care settings to ensure that antibiotics are used only when necessary and appropriate
According to WHO,
Antimicrobial stewardship is a systematic approach to educate and support health care professionals to follow evidence-based guidelines for prescribing and administering antimicrobials
In 1996, John McGowan and Dale Gerding first applied the term antimicrobial stewardship, where they suggested a causal association between antimicrobial agent use and resistance. They also focused on the urgency of large-scale controlled trials of antimicrobial-use regulation employing sophisticated epidemiologic methods, molecular typing, and precise resistance mechanism analysis.
Antimicrobial Stewardship(AMS) refers to the optimal selection, dosing, and duration of antimicrobial treatment resulting in the best clinical outcome with minimal side effects to the patients and minimal impact on subsequent resistance.
According to the 2019 report, in the US, more than 2.8 million antibiotic-resistant infections occur each year, and more than 35000 people die. In addition to this, it also mentioned that 223,900 cases of Clostridoides difficile occurred in 2017, of which 12800 people died. The report did not include viruses or parasites
VISION
Being proactive
Supporting optimal animal and human health
Exploring ways to reduce overall use of antimicrobials
Using the drugs that prevent and treat disease by killing microscopic organisms in a responsible way
GOAL
to prevent the generation and spread of antimicrobial resistance (AMR). Doing so will preserve the effectiveness of these drugs in animals and humans for years to come.
being to preserve human and animal health and the effectiveness of antimicrobial medications.
to implement a multidisciplinary approach in assembling a stewardship team to include an infectious disease physician, a clinical pharmacist with infectious diseases training, infection preventionist, and a close collaboration with the staff in the clinical microbiology laboratory
to prevent antimicrobial overuse, misuse and abuse.
to minimize the developme
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QA Paediatric dentistry department, Hospital Melaka 2020Azreen Aj
QA study - To improve the 6th monthly recall rate post-comprehensive dental treatment under general anaesthesia in paediatric dentistry department, Hospital Melaka
Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
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2. • Brain tissue, which is composed of 80% water, is separated from the systemic circulation by a
complex series of interfaces.
• The major site is the endothelial cells that are a component of the neurovascular unit
• Cells that form these interfaces have specialized proteins that form tight junctions; some have
carrier proteins that shuttle essential molecules, and multiple electrolyte pumps on cell
membranes.
• Cellular membranes preserve the compartmental structure with water in extracellular and
intracellular spaces.
INTRODUCTION
Bradley’s Neurology in Clinical Practice,6th
4. Interface Tight-Junction
Location
Functional Aspects
Blood-CSF Choroid plexus
cell
Active secretion of CSF
via ATPase and carbonic
anhydrase
CSF-blood Arachnoid
membrane
Arachnoid granulations
absorb CSF by one-way
valve mechanism
Blood-brain Capillary
endothelial cell
Active transport of ISF
via ATPase; increased
mitochondria and
glucose transporters in
capillary endothelial
Bradley’s Neurology in Clinical Practice,6th
ATPase, Adenosine triphosphatase; CSF, cerebrospinal fluid; ISF, interstitial fluid.
5. • Brain edema is a common term to describe events related to brain insults.
• When shifts in water from one compartment to another occur under pathological
conditions, swelling in the various compartments leads to increased intracranial pressure
(ICP).
• Edema represents a serious, often life threatening consequence of many common brain
disorders including stroke, trauma, tumors, and infection.
• Cerebral edema is the end result of many neurological diseases. Excess fluid can
accumulate in the intracellular or extracellular spaces.
Bradley’s Neurology in Clinical Practice,6th
6. CLASSIFICATION
• A convenient (though simplified) classification separates brain edema into
Cytotoxic or cellular swelling , and Vasogenic or vascular leakage (Klatzo, 1967).
• Another proposed category is Interstitial edema , which represents the
accumulation of fluid in interstitial spaces in hydrocephalus (Fishman,1975).
Bradley’s Neurology in Clinical Practice,6th
7. ETIOLOGY
Type Cause
Cytotoxic Ischemia, trauma, toxins, metabolic
diseases
Vasogenic Infections, brain tumors, hyperosmolar
states, inflammation
Interstitial Hydrocephalus with transependymal
flow
Bradley’s Neurology in Clinical Practice,6th
8. MOLECULAR CASCADE IN INJURY
• Cytotoxic edema, which results from pathological processes that damage cell
membranes, constricts the extracellular spaces, constraining movement of fluid
between the cells.
• Disruption of the BBB leads to vasogenic edema, which expands the extracellular
space. Vasogenic edema moves more readily in between the linearly arranged fibers
that form the white matter. The gray matter restricts water movement because of the
dense nature of the neuropil.
• Because of the lack of cell damage in vasogenic edema, once the damage to the
blood vessel resolves, there may be a return to normal in the edematous tissue. This is
generally not the case in cytotoxic edema, which is due to direct injury to cells.
Bradley’s Neurology in Clinical Practice,6th
10. CYTOTOXIC EDEMA
• Stroke, trauma, and toxins induce cytotoxic edema. After a stroke, brain water
increases rapidly owing to energy failure and loss of ATP. Cytotoxic edema is seen
between 24 and 72 hours after the stroke, when the danger of brain herniation is
greatest.
• Damage to the blood vessels, resulting in vasogenic edema, occurs at multiple times
after the insult. In brain trauma, there is an early opening of the BBB along with
extensive damage to the brain tissue, and a mixture of cytotoxic and vasogenic edema
leads to severe brain edema in the early stages after injury.
• Greater damage occurs in transient ischemia, because the restoration of blood flow
returns oxygen and white blood cells to the region, enhancing the damage.
Reperfusion injury particularly damages the capillary, with disruption of the BBB.
Bradley’s Neurology in Clinical Practice,6th
11. VASOGENIC EDEMA
• Occurs when there is damage to the capillary and subsequent disruption of the
BBB.
• Tight junctions in the endothelial cells are the first line of protection.
• Protein and blood products enter brain tissue, increasing the oncotic pressure in
the brain and exposing brain cells to toxic products from the blood.
• Bacterial meningitis initiates an inflammatory response in the meninges caused by
the invading organisms and by the secondary release of cytokines and
chemokines. The secondary inflammatory response may aggravate the infection.
Bradley’s Neurology in Clinical Practice,6th
12. BLOOD PRESSURE AND OSMOLALITY CHANGES ON
BRAIN EDEMA
• Cerebral blood pressure is tightly regulated in the waking state to ensure
adequate flow to the brain. Loss of autoregulation occurs at both the lower and
upper extremes of blood pressure, with resulting syncope and hypertensive
encephalitis, respectively.
• Rapid elevation of blood pressure causes hypertensive encephalopathy. In
experimental animals, hyperemia is present, suggesting that the blood vessels are
dilated and have increased permeability,
• MRI shows vasogenic edema, primarily in the posterior white matter of the brain,
a condition referred to by some as reversible posterior leukoencephalopathy
syndrome,
Bradley’s Neurology in Clinical Practice,6th
13. BLOOD PRESSURE AND OSMOLALITY CHANGES ON
BRAIN EDEMA
• Another cause of cerebral edema is a rapid change in serum osmolality.
• Rapid reduction of plasma glucose and sodium puts patients treated for diabetic
ketoacidosis at risk for edema secondary to water shifts into the brain.
• Cerebral edema is a complication of acute mountain sickness, which in rare
circumstances may be life threatening. Cerebral symptoms are prominent, and
there is an increase in cerebral blood volume related to the hypoxia.
Bradley’s Neurology in Clinical Practice,6th
14. EDEMA IN VENOUS OCCLUSION AND
INTRACEREBRAL HEMORRHAGE
• Occlusion of the venous sinuses draining the brain can cause increased ICP and
venous hemorrhagic infarction.
• Intracerebral hemorrhage (ICH) causes brain edema around the hemorrhagic
mass.
• This edema is both cytotoxic and vasogenic.
• Blood contains coagulation cascade enzymes such as thrombin and plasmin
which can damage cells both directly by their toxic effects and indirectly by
activation of other proteases.
Bradley’s Neurology in Clinical Practice,6th
15. GENERAL MEASURES FOR MANAGING
CEREBRAL EDEMA
1. Optimizing Head and Neck Positions
2. Ventilation and Oxygenation
3. Intravascular Volume and Cerebral Perfusion
4. Seizure Prophylaxis
5. Management of Fever and Hyperglycemia
6. Nutritional Support
Neurosurg Focus 22 (5):E12,2007
16. OPTIMIZING HEAD AND NECK POSITIONS
• 30 ̊elevation of the head in patients is essential for
1. avoiding jugular compression and impedance of venous outflow from
the cranium
2. for decreasing CSF hydrostatic pressure..
• Head position elevation may be detrimental in ischemic stroke, because
it may compromise perfusion to ischemic tissue at risk.
Neurosurg Focus 22 (5):E12,2007
17. VENTILATION AND OXYGENATION
• Hypoxia and hypercapnia are potent cerebral vasodilator
• Patient should be intubated in:
1. GCS scores less than or equal to 8
2. Patients with poor upper airway reflexes be intubated
preemptively for airway protection.
3. Aspiration pneumonitis
4. Pulmonary contusion
5. Acute respiratory distress syndrome.
Neurosurg Focus 22 (5):E12,2007
18. INTRAVASCULAR VOLUME AND
CEREBRAL PERFUSION
• Maintenance of CPP using adequate fluid management in combination with
vasopressors is vital in patients with brain injury
• Hypotonic fluids should be avoided at all cost
• Euvolemia or mild hypervolemia with the use of isotonic fluids (0.9%
saline) should always be maintained through rigorous attention to daily
fluid balance, body weight, and serum electrolyte monitoring.
Neurosurg Focus 22 (5):E12,2007
19. TREATING HYPERTENSION
• Judicious use of antihypertensives
1. Labetalol
2. Enalapril
3. Nicardipine is recommended for treating systemic hypertension.
• Potent vasodilators are to be avoided
• Nitroglycerine
• Nitroprusside
• as they may exacerbate cerebral edema via accentuated cerebral hyperemia
and CBV due to their direct vasodilating effects on cerebral vasculature.
Neurosurg Focus 22 (5):E12,2007
20. CONTROLLED HYPERVENTILATION
• A decrease in PaCO2 by 10 mmHg produces proportional decreases in
CBF resulting in rapid and prompt ICP reduction.
• The vasoconstrictive effect of respiratory alkalosis on cerebral
arterioles has been shown to last for 10 to 20 hours
• Beyond which vascular dilation may result in exacerbation of cerebral
edema and rebound elevations in ICP.
Neurosurg Focus 22 (5):E12,2007
22. OSMOTHERAPY
• The most rapid and effective means of decreasing tissue water and brain bulk.
• Decrease ICP and increase cerebral blood flow.
• Mannitol is the most popular osmotic agent, MOA is unclear,
• IV Mannitol is given in the dosage of 0.25-1.0 g/kg.
• Glycerol is another useful agent given in oral doses of 30 ml every 4-6 hour or
daily IV 50 g in 500 ml of 2.5% saline solution. Used in a dose of 0.5-1.0 g/kg
body weight.
23. CONTRAINDICATIONS FOR MANNITOL
1. Acute tubular necrosis,
2. Anuria
3. Pulmonary edema;
4. Acute left ventricular failure
5. CHF
6. Cerebral haemorrhage.
SIDE EFFECTS:
DEHYDRATION, HYPERKALEMIA, AND HYPERNATREMIA
Neurosurg Focus 22 (5):E12,2007
24. THERAPEUTIC BASIS AND GOAL OF
OSMOTHERAPY
• Fundamental goal of osmotherapy is to create an osmotic gradient to
cause egress of water from the brain extracellular (and possibly
intracellular) compartment into the vasculature
• The goal of using osmotherapy is to maintain a euvolemic or a slightly
hypervolemic state.
• A serum osmolality in the range of 300 to 320 mOsm/L has traditionally
been recommended for patients with acute brain injury
Neurosurg Focus 22 (5):E12,2007
25. HYPERTONIC SALINE
• Unique extraosmotic properties of hypertonic saline
1. Modulation of CSF production resorption
2. Accentuation of tissue oxygen delivery.
3. May modulate inflammatory response.
4. Following brain injury that may act together to ameliorate cerebral edema.
• FORMULATIONS OF HYPERTONIC SALINE
• 2%
• 3% NaCl has 513 mEq/L of Na and Cl.
• 5% NaCl has 856 mEq/L of Na and Cl.
• 7% (1200 mEq/L) and
• 7.5%
• 10%
• 23.4% (approx 4000 mEq/L),
Neurosurg Focus 22 (5):E12,2007
26. DIURETICS
• The osmotic effect can be prolonged by the use of loop diuretics (Furosemide)
after the osmotic agent infusion. Loop diuretics (Furosemide) can be used as an
adjunct. Furosemide (0.7 mg/kg) has been shown to prolong the reversal of blood
brain osmotic gradient established with the osmotic agents by preferentially
excreting water over solute.
Neurosurg Focus 22 (5):E12,2007
27. CORTICOSTEROIDS
• Lower intracranial pressure primarily in vasogenic edema because of their
beneficial effect on the blood vessel,
• Less effective in cytotoxic edema, and are not recommended in treatment of
edema secondary to stroke or haemorrhage.
• Inj. Dexamethasone 4-6 mg IM every 4-6 hours.
• Management of malignant brain tumours, either primary or secondary, as
adjuvant chemotherapy of some CNS tumours and perioperatively in brain
surgery
Neurosurg Focus 22 (5):E12,2007
28. OTHER AGENTS
• Barbiturates, Procaine derivatives, Indomethacin, Propofol and THAM
(Tromethamine), are some other agents which have been tried and used in the
past ,not being used routinely in present practice,
29. PHARMACOLOGICAL COMA -BARBITURATES
• Barbiturates lower ICP, principally via a reduction in cerebral metabolic
activity, resulting in a coupled reduction in CBF and CBV.
• In patients with TBI, barbiturates are effective in reducing ICP but have
failed to show evidence of improvement in clinical outcome.
• Agents used
• Pentobarbital : a barbiturate with an intermediate physiological half life
(approximately 20 hours) is the preferred agent
• Phenobarbital : which has a much longer half- life (approximately 96 hours)
• Thiopental : which has a much shorter half-life (approximately 5 hours)
Neurosurg Focus 22 (5):E12,2007
30. ANALGESIA, SEDATION AND PARALYSIS.
• Pain and agitation can worsen cerebral edema and raise ICP significantly,
and should always be controlled.
• Judicious intravenous doses of
• bolus morphine (2–5 mg)
• fentanyl (25– 100 mcg)
• continuous intravenous infusion of fentanyl (25–200 mcg/hour) can be used for
analgesia.
• A NEUROMUSCULAR BLOCKADE:
• can be used as an adjunct to other measures when controlling refractory ICP.
• Nondepolarizing agents should be used, because a depolarizing agent (such
as succinylcholine) can cause elevations in ICP due to induction of muscle
contraction.
Neurosurg Focus 22 (5):E12,2007
31. THERAPEUTIC HYPOTHERMIA
• Hyperthermia is deleterious to brain injury, achieving normothermia is a
desirable goal in clinical practice.
• External cooling devices
• air-circulating cooling blankets
• iced gastric lavage
• surface ice packs
Neurosurg Focus 22 (5):E12,2007
32. OTHER ADJUNCT THERAPIES
• HYPERBARIC OXYGEN:
• For the treatment of cerebral edema, based on a clinical trial (100% oxygen at
1.5 atmospheres for 1 hour every 8 hours) that demonstrated enhanced
survival in patients with TBI
• INDOMETHACIN:
• Although the mechanisms are poorly understood, indomethacin treatment has
been shown to attenuate increases in ICP in Traumatic Brain Injury and fever
prevention
Neurosurg Focus 22 (5):E12,2007
33. SURGERY
• Surgical treatment is occasionally recommended for large hemispherical infarcts
with edema and life threatening brain-shifts.
• Temporary ventriculostomy or craniectomy may prevent deterioration and may
be lifesaving.
• Decompressive craniectomy in the setting of acute brain swelling from cerebral
infarction is a life saving procedure and should be considered in younger patients
who have a rapidly deteriorating neurological status.
• Severe Hydrocephaus- Ventriculo Peritoneal shunt.
Bradley’s Neurology in Clinical Practice,6th
34. REFERENCES
• Bradley’s Neurology in clinical practice 6th Edition
• Medical Journal Of Armed Forces Of India
• Brain Trauma Foundation Guidelines
• Neurosurg Focus 22 (5):E12,2007
Neurons, astrocytes and pericytes form the Neurovascular Unit.
On the abluminal surface of the endothelial cells is a thin layer of basal lamina composed of type IV collagen, fibronectin, heparan sulfate, laminin, and entactin.
Basal lamina provides structure through type IV collagen, charge barriers by heparan sulfate, and binding sites on the laminin and fibronectin molecules. Within the basal lamina reside the pericytes, which are a combination of smooth muscle and macrophage. Astrocyte foot processes surround the basal lamina. Neurons complete the group of cells that comprise the neurovascular unit
Tight junctions (TJ) between the endothelial cells maintain the electrical resistance. A large number of mitochondria are seen in the capillary. Amino acid and glucose transporters are present. Around the cell is a basal lamina composed of type IV collagen, laminin, fibronectin, and heparan sulfate. Astrocytic end-feet surround cells. Pericytes, which are embedded in the basal lamina, are macrophage-like cells that have macrophage and smooth muscle functions in the perivascular space.
Headache
Nausea, Vomiting
Altered mental status
Dizziness, Fainting
Blurred vision, Diplopia
Urinary incontinence
Seizures
Coma
Cytotoxic: TBI, SAH, ischemic stroke and ICH,and severe toxic–metabolic derangements (hyponatremia and fulminant hepatic encephalopathy),severe hypothermia, Reye’s Syndrome
Vasogenic: Primary and metastatic neoplasms, inflammatory diseases (meningitis, ventriculitis, cerebral abscess, and encephalitis),
Area in the nervous system composed of mostly unmyelinated axons, dendrites and glial cell processes that forms a synaptically dense region containing a relatively low number of cell bodies.
1)Cellular and blood vessel damage follows activation of an injury cascade. The cascade begins with depletion of energy and glutamate release into the extracellular space which occurs during a hypoxic, ischemic, or traumatic injury and causes cytotoxic damage. Release into the extracellular space of excessive amounts of the excitatory neurotransmitter, glutamate, opens calcium channels on cell membranes, allowing extracellular calcium to enter the brain.
2)The removal of excess calcium from the cell, causes a buildup of sodium within the cell, creating an osmotic gradient that pulls water into the cell. While the cell membrane is intact, the increase in water causes dysfunction but not necessarily permanent damage.
Accumulation of calcium ions within the cell activates intracellular cytotoxic processes, leading to cell death. An inflammatory response is initiated by the formation of immediate early genes (e.g., c-fos and c-jun) and cytokines, chemokines, and other intermediary substances. Microglial cells are activated and release free radicals and proteases, which contribute to the attack on cell membranes and capillaries. Irreversible damage to the cell occurs when the integrity of the membrane is lost.
Free radicals are pluripotential substances produced in the ischemic brain and after traumatic injury. The arachidonic acid cascade produces reactive oxygen species such as superoxide ion, hydrogen peroxide, and hydroxyl ion.
3)Release of fatty acids provide supply of damaging molecules.
Opening of the BBB could occur by loosening of tight junctions, development of pinocytotic vesicles in the endothelial cell, or an alteration in the basal lamina surrounding the capillaries.
1)Proteases and free radicals are the major substances that attack the capillaries. The layer of basal lamina around the capillary, containing type IV collagen, fibronectin, and laminin, is degraded by proteases. The proteases involved include the serine proteases, plasminogen activators/plasmin system, and matrix metalloproteinases (MMPs).
2)Free radicals activate the proteases and attack the membranes directly .Brain cells and infiltrating leukocytes are the sources of proteases and free radicals. Neutrophils contain prepackaged gelatinase B (MMP-9), which is released at the injury site and activated.
1) Common causes of rapid elevations of blood pressure are kidney disease, particularly in children with lupus erythematosus or pyelonephritis, and in the pregnancy-induced syndrome of eclampsia.
Changes may be transient, and complete recovery is possible if treatment is instituted before hemorrhage or infarction occurs.
2) A characteristic pattern of vasogenic edema without cytotoxic edema is present on MRI: there is extensive edema seen in the white matter, generally in the posterior regions, but spread in frontal regions can be seen, and an absence of DWI lesions indicating this is only vasogenic edema.
Long-standing hyperosmolality leads to solute accumulation in the brain to compensate for hyperosmolar plasma levels. These idiogenic osmoles are thought to include taurine and other amino acids.
During treatment of the diabetic ketoacidosis, blood osmolality is reduced, and water moves into brain along the osmotic gradient, resulting in cerebral edema. Rapid reduction of serum hyperosmolality, as in diabetic ketoacidosis, should be avoided to prevent brain edema due to the residual idiogenic osmoles.
Accumulation of blood causes both mass effect on the surrounding tissues and release of toxic blood products into adjacent tissues. Mass effect can lead to herniation.
Target PaCO2 = 35 mm Hg.
Controlled hyperventilation is to be used as a rescue or resuscitative measure for a short duration until more definitive therapiesare instituted and maintained that are tailored toward the particular patient
1)Thought to decrease brain volume by decreasing overall water content, to reduce blood volume by vasoconstriction, to reduce CSF volume by decreasing water content. Mannitol may exert a protective effect against biochemical injury.
2) When Mannitol is used, one should aim for plasma osmolality 300-320 mOsm/L with maintenance of adequate plasma volume
IN PROXIMAL TUBULE:
Retains water isoosmotically in PT dilutes luminal fluid which opposes NaCl reabsorption.
IN LOOP OF HENLE:
Inhibits transport processes in the thick AscLH by an unknown mechanism.
Major site of action is LOOP OF HENLE
The extraosmotic properties of mannitol have been studied extensively and may provide additional beneficial effects in brain injury, including decreases in blood viscosity, resulting in increases in rCBF and CPP, and a resultant cerebral vasoconstriction leading to decreased CBV, free radical scavenging,and inhibition of apoptosis
An ideal osmotic agent is one that produces a favorable osmotic gradient, is inert and nontoxic, is excluded from an intact BBB, and has minimal systemic side effects.
Ability of the intact BBB to exclude a given compound has been quantified (reflection coefficient ). compounds with s approaching 1 (completely impermeable) are considered to be better osmotic agents because they are completely excluded by an intact BBB, and conversely less likely to exhibit “rebound” cerebral edema during withdrawal of osmotherapy.
Mannitol= 0.9 ; HTS= 1
With Mannitol, the potential for rebound cerebral edema exists as a result of a reversal of the osmotic gradient between the brain and the intravascular compartment in areas in which the BBB is disrupted
A common strategy used to raise serum sodium rapidly is to administer an intravenous bolus of furosemide (10 to 20 mg) to enhance free water excretion and to replace it with a 250-ml intravenous bolus of 2 or 3% hypertonic saline.
Precise mechanisms of the beneficial effects of steroids are unknown., steroids decrease tight-junction permeability and, in turn, stabilize the disrupted BBB.
Glucocorticoids, especially dexamethasone, are the preferred steroidal agents, due to their low mineralocorticoid activity
1)Cerebral vasculature is most sensitive to arterial pCO2 changes around the normal level of 40 mm Hg.
2) THAM: tris(hydroxymethyl)-aminomethane, a buffer (pKa ~ 7.8) introduced in the 1960s, which has been shown to ameliorate secondary neuronal injury and cerebral edema, presumably by ameliorating tissue acidosis.
Barbiturates produce a marked decrease in metabolic rate and it seems likely that the fall in cerebral blood flow and ICP is secondary. Complication of barbiturate therapy, in particular systemic hypotension and pulmonary failure.
