I LOVE NEUROSURGERY INITIATIVE: Cranio-cerebral Injuries part 1walid maani
A comprehensive presentation about the primary injuries of the scalp, skull and brain occurring in head injuries. Directed to medical students and junior hospital doctors.
I LOVE NEUROSURGERY INITIATIVE: Spinal Tumorswalid maani
A comprehensive presentation about spinal tumors. Some concentration on anatomy. Discussion of presentation, diagnosis and management. Plenty of images.
I LOVE NEUROSURGERY INITIATIVE: Cranio-cerebral Injuries part 1walid maani
A comprehensive presentation about the primary injuries of the scalp, skull and brain occurring in head injuries. Directed to medical students and junior hospital doctors.
I LOVE NEUROSURGERY INITIATIVE: Spinal Tumorswalid maani
A comprehensive presentation about spinal tumors. Some concentration on anatomy. Discussion of presentation, diagnosis and management. Plenty of images.
A short talk about two of the traumatic intracranial bleeds, namely extra and subdural hematomas. Directed to med students moving from basic into clinical teaching.
I am a Neurosurgeon with advanced training in Interventional vascular Neurosurgery(FINR) from Zurich, Switzerland, and FMINS-Fellowship in minimally invasive and Endoscopic Neurosurgery from Germany.
I am presently working in Columbia asia hospitals, Bangalore.
My areas of interest are Vascular Neurosurgery, Stroke specialist, interventional neuroradiology, Endoscopic and minimally invasive Neurosurgery, Endoscopic spine surgery.
Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
I LOVE NEUROSURGERY INITIATIVE: INTRACRANIAL TUMORS.pptwalid maani
A complete presentation to help medical students and junior neurosurgical residents to understand the topic of intracranial tumors. Complete with Illustrations and imaging.
A short talk about two of the traumatic intracranial bleeds, namely extra and subdural hematomas. Directed to med students moving from basic into clinical teaching.
I am a Neurosurgeon with advanced training in Interventional vascular Neurosurgery(FINR) from Zurich, Switzerland, and FMINS-Fellowship in minimally invasive and Endoscopic Neurosurgery from Germany.
I am presently working in Columbia asia hospitals, Bangalore.
My areas of interest are Vascular Neurosurgery, Stroke specialist, interventional neuroradiology, Endoscopic and minimally invasive Neurosurgery, Endoscopic spine surgery.
Intracerebral hemorhage Diagnosis and managementRamesh Babu
About ICH - Diagnosis and management, Discussed the clinical presentation, evaluation, radiological features and management including recent guidelines
I LOVE NEUROSURGERY INITIATIVE: INTRACRANIAL TUMORS.pptwalid maani
A complete presentation to help medical students and junior neurosurgical residents to understand the topic of intracranial tumors. Complete with Illustrations and imaging.
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.
Defines intracranial pressure, cerebral perfusion pressure and mean arterial pressure. Depict formula for caculating ICP, CPP& MAP. Enumerate both pathological and non- pathological causes for increased ICP. Explain Monroe Kellie hypothesis, pathophysiology of increase Intracranial pressure medical, surgical and nursing management of Increased intracranial pressure.
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
CRANIO CEREBRAL INJURIES FOR MEDICAL STUDENTSwalid maani
This is a simple outline of traumatic injuries which occures to the scalp, skull and brain with some simplified classifications and outlined management
Established In 1984 by Prof. Walid Maani, Started with one Neurosurgical Resident. Today it had graduated 20 of the 50 neurosurgeons practicing in Jordan
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdf
I LOVE NEUROSURGERY INITIATIVE: Increased Intracranial Pressure
1. I_ _NEUROSURGERY INITIATIVE
INCREASED INTRACRANIAL PRESSURE
WALID S. MAANI MD, FRCSEd.
PROFESSOR OF NEUROSURGERY
JORDAN UNIVERSITY HOSPITAL AND MEDICAL SCHOOL
1
5. PHYSIOLOGY 5
INTRACRANIAL PRESSURE FACTS
o Normally 0-140 mm CSF (0-10 mm Hg)
o There are normal regular waves due to pulse and respiration
o With increased pressure “pressure waves” appear
o With continued rise of ICP the Perfusion of the brain falls
o When perfusion falls the blood flow is reduced
o Electrical cortical activity fails if the cerebral blood flow is less than
20ml/100gm/min
o When intracranial pressure reaches mean arterial pressure circulation to
the brain stops.
6. Monroe-Kellie doctrine
• The intracranial pressure is the sum of the pressures
exerted upon the wall of the skull by its contents.
• Any increase in one of these contents and/or the
addition of any mass will lead to increase in the
pressure, unless a similar volume is removed (the
Monroe-Kellie doctrine).
6
12. PHYSIOLOGY
• COMPENSATORY MECHANISMS
• Push CSF out to spinal theca
• Compress venous sinuses and push blood out
• ONCE COMPENSATORY MECHANISMS FAIL then brain
herniations occur.
• Push cerebral hemisphere to other side
(midline shift and Cingulate (subfalcine
herniation)
• Push brain down
• Uncal and Central (transtentorial herniation)
• Tonsillar (transforaminal herniation)
12
13. PHYSIOLOGY
CEREBRAL PERFUSION PRESSURE (CPP)
Cerebral Perfusion Pressure (CPP)=
Mean Arterial pressure – intracranial pressure
MAP (120+80) / 2 =100 mm Hg
ICP = 15 mm Hg
CPP = 100 – 15 = 85 mm Hg (60-120 is good)
13
15. PHYSIOLOGY
• TO MAINTAIN PERFUSION AND FLOW there are
two AUTOREGULATORY MECHANISMS
1. Elevate blood pressure by peripheral
vasoconstriction.,
2. Dilate cerebral vessels by CO2 retention.
15
17. PHYSIOLOGY
The ICP finally rises to the level of the mean arterial
pressure which it self begins to increase, accompanied by
bradycardia or other disturbances of respiratory rhythm
(Cushing response). This is accompanied by dilatation of
small pial arteries and some slowing of venous flow
which is followed by pulsatile venous flow.
17
19. CLINICAL PICTURE
The rise in ICP disturbs brain function by:
• (1) Reduction in CBF
• (2) Transtentorial or foramen magnum
herniation resulting in selective compression
and ischemia in the brain stem.
19
20. CAUSES
Increases in the ICP could be due to:
a) Increase in volume of the normal intracranial
constituents.
b) Any added volume due to an abnormal
condition like a space occupying lesion.
20
21. CAUSES
Increase in Normal Constituents
A) Brain
1) Cerebral edema
2) Idiopathic increased ICP
B) CSF
Hydrocephalus
C) Blood
Vasodilatation due to hypercapnia
21
23. CLINICAL PICTURE
The clinical picture is due to one of the following or a combination.
• Due to the ICP itself
• Due to the herniations
• Due to the causative lesion
23
24. CLINICAL PICTURE
• Early:
• Headache, projectile vomiting and visual
manifestations.
• Late:
• Change in the level of consciousness.
• Loss of motor and sensory functions.
• Pupillary changes (compression of Cranial Nerve III).
• Vital sign changes including widening pulse
pressure, bradycardia and irregular respirations,
• Posturing :decorticate rigidity
• Changing and irregular respiratory patterns
24
25. THE HEADACHE
• Morning headache.
• Ordinary with no specific character.
• Responds to simple analgesia.
D.D.
Migraine
25
26. THE VOMITING
• Morning vomiting.
• Projectile (not preceded by nausea).
D.D.
Pregnancy
Migraine
26
27. THE VISUAL MANIFESTATIONS
Called also amaurosis fugax or obscurations of vision.
• Diminished acuity of vision
• Scotomas
D.D.
Migraine
27
29. CLINICAL PICTURE
Herniation of intracerebral contents
Supratentorial herniation
• Subfalcine: which results in affection of the ACA leading to
contralateral leg weakness
• Uncal (lateral transtentorial): and central transtentorial are the most
frequently noted.
Result in ipsilateral pupil dilatation, decreased level of consciousness,
changes in respiratory patterns, respiratory arrest, and contralateral
hemiplegia. Results in loss of consciousness, small reactive pupils advancing
to fixed/dilated pupils, respiratory changes leading to respiratory arrest and
decorticate posturing advancing to flaccidity.
Infratentorial herniation
• Tonsillar: As a result of a downward herniation the medulla oblongata is
compressed and displaced causing respiratory and cardiac arrest
29
31. MANAGEMENT
We are guided by how high is the pressure and what
effects did it produce on the health of the patient.
o So it is necessary to examine the patient
o Estimate his Glasgow Coma Score (GCS) on the Glasgow coma
scale. AND ALSO GTS
o Find what the pressure is directly or indirectly.
o Do the required imaging.
31
32. MANAGEMENT
The goals of any management should aim at:
1) Normalization of ICP by keeping ICP below 20
mmHg.
2) Maintaining normal CBF, by keeping CPP above 65
mmHg.
3) Relieving herniation.
4) Treatment of the cause.
32
33. IMAGING
Evidence of increased pressure could be seen in different types of imaging
A) Plain skull X-rays:
Thumb impressions (beaten silver or beaten copper appearance) in the inner
bone table of the skull.
Erosion of the posterior clinoid processes.
Widening of the skull sutures.
B) MRI and CT:
Effacement of the cortical sulci.
Compression of the ventricles.
Shifts.
Herniations.
33
35. IMAGING: CT and MRI
CT: Effacement and
midline shift
MRI: Compressed ventricles
and shift
35
36. ICP MEASUREMENT
Intracranial pressure monitoring:
The intracranial pressure could be measured by a variety of methods, for
diagnosis and to help in determining the need for, or the efficacy of
treatment. These methods could be invasive or non-invasive.
• Invasive methods:
1)Lumbar puncture.
2)Intraventricular catheters.
3)Subarachnoid screws.
4)Subdural sensors.
5)Intraparenchymal sensors.
6)Extradural sensors.
36
39. ICP MEASUREMENT
• Non-invasive methods:
1)Ophthalmodynamometry or retinal Venous Outflow Pressure (VOP).
2)Optic nerve sheath diameter.
3)Tympanic membrane displacement.
4)Transcranial doppler.
The lumbar puncture (LP) is the simplest, but one must be careful to
make sure that there are no expanding lesions inside the skull, otherwise
herniation may occur.
39
40. MANAGEMENT
Measures to reduce high ICP
Steps to be taken to reduce or normalize ICP fall into three categories:
general, specific and definitive.
1) General
1) Elevate head of bed 30 degrees.
2) Avoid bending the neck or compressing the jugular veins.
3) Guard against airway obstruction.
4) Maintain a normal blood pressure.
5) Control pain.
6) Drain the bladder.
7) Control headache (codeine phosphate 30-60 mg.)
40
41. MANAGEMENT
2) Specific
1) Infuse Mannitol. Be careful to monitor blood pressure. Loop
diuretics could be used to the same effect. Careful watch
must be kept over the serum osmolarity to avoid elevation.
2) Hyperventilate the patient with the aim of regulating CO2
in the inspired air by maintaining PaCO2 between 35-40
mmHg..
3) Drainage of CSF.
4) Sedation using propofol or barbiturates with the aim of
reducing the metabolic demand of the brain cells.
5) Hypothermia to reduce the metabolic rate.
6) Decompressive craniectomy, craniotomy should be done if
all measures fail.
41
42. MANAGEMENT
3) Definitive
The above mentioned general and specific measures could be the
only possible lines of treatment in many cases in which the cause of the
rise in ICP is general as in cases of closed head injury. But if there were
lesions responsible for the elevation of the ICP, then in addition to the
above measures, surgeons resort to removal of the causative lesion; be it
a tumor, contusion or a hematoma. Once the lesion is removed, the ICP
will settle down and all measures will not be needed anymore.
42
43. ICP MEASUREMENT: The waves
• There are 3 waves for ICP
1)A wave
2)B wave
3)C wave
The A wave is the most important and is
called the plateau wave, it has a
sustained ICP of 50 mm of Hg for 20
minutes.
43
44. IDIOPATHIC INTRACRANIAL HYPERTENSION
It is a disease which affects obese women in the childbearing
period, around 40 years of age. There is usually a history of
taking medications like:
1) OCPs,
2) Tetracycline,
3) Nalidixic acid or
4) Vitamins like A.
Sometimes it accompanies other diseases like polycystic kidney,
Bahcet disease, obstructive sleep apnea and hypothyroidism.
44
45. IDIOPATHIC INTRACRANIAL HYPERTENSION
• The patients complain of:
1) Headache and
2) Visual manifestations like scotomas and transient visual loss,
and their visual acuity starts to fail.
3) One may find a sixth nerve palsy.
4) But the striking feature will be the papilledema and in
advanced cases, optic atrophy.
45
46. IDIOPATHIC INTRACRANIAL HYPERTENSION
Diagnosis:
Is usually by exclusion; however, diagnosis depends on the
modified Dandy Criteria (introduced in 1985 after the original in
1937, which include:
1) Signs and symptoms of high ICP.
2) No neurological signs except for 6th. Nerve palsy.
3) Normal CT scan, with normal or small ventricles
4) Increased opening CSF pressure.
5) Normal CSF composition.
46
47. IDIOPATHIC INTRACRANIAL HYPERTENSION
Diagnostic procedures:
1) Visual acuity measurement, visual field charting and
fundoscopic examination.
2) CT to exclude any other pathology.
3) MRV to exclude venous sinus thrombosis.
4) MRI orbital to look at width and shape of optic nerve sheath
and optic nerve respectively.
5) LP to measure pressure and examine CSF composition.
During the performance of the LP and after collecting the
specimen the ICP should be reduced to half of the reading or
to the normal level whichever is higher.
47
48. IMAGING: Normal CT, Tortious optic nerve and wide
sheath, stenosed dural venous sinuses
48
49. IDIOPATHIC INTRACRANIAL HYPERTENSION
Management:
The type of management proposed depends on the seriousness of the
disease as measured by the visual status.
A) The Lumbar puncture itself:
On many occasions, the LP itself will result in dramatic
improvement of the symptoms, which if sustained (the improvement
and the normal pressure reading judged by a second LP, then nothing
more is required.
49
50. IDIOPATHIC INTRACRANIAL HYPERTENSION
B) Medical conservative:
In situations when there is mild to moderate symptoms with no
impending visual loss, the following measures could be used:
Reduction of weight, and maintenance of reduction.
Stopping the OCP, and any other medications thought to be part of the
cause.
Giving medication to reduce CSF production like Acetazolamide
(Diamox).
50
51. IDIOPATHIC INTRACRANIAL HYPERTENSION
C) Surgery
If there is impending visual loss, expanding field loss or development
of a new one, or failure of medical conservative treatment, then the
patient will be offered one of the following to reduce the pressure
inside the cranium and lessen the effects on the optic head, and
consequently preserve vision.
1) Optic nerve sheath fenestration. The CSF will pour inside the
orbit and the lymphatics will absorb it.
2) Lumbo-peritoneal (theco-peritoneal) shunting. The CSF will
be absorbed via the wide peritoneal surface. This shunt has
many complications; like slippage and malfunctioning which
may require revision.
3) Stenting of the stenosed venous sinus.
51