- Head injuries can range from minor bumps on the skull to severe brain injuries. The most common causes are road traffic accidents, falls, and assaults.
- CT scans are important for diagnosis and can reveal traumatic intracranial hematomas like epidural hematomas, which require urgent surgery if detected, as they accumulate in the space between the bone and dura and can expand rapidly.
- Management of head injuries focuses on stabilizing the patient's airway, breathing, and circulation. Additional treatment depends on the severity and type of injuries found upon further examination and investigation.
HEAD INJURY- AN OVERVIEW
Dear viewers,
Greetings from “Surgical Educator”
Today I have uploaded a video on Head injury- an important topic in trauma because 50% of trauma deaths are due to head injuries. I haven’t talked elaborately but have included the essential minimum an undergraduate medical student should know. I have talked about pathophysiology, clinical approach, symptoms, signs, investigations, different individual types of head injuries and management of all the varieties of head injuries. My aim is after watching this video all of you should be able to arrive at a correct working diagnosis of the type of head injury and should also be able to institute immediate lifesaving treatment to the patients if there is a need. You can watch the video in the following links:
Surgicaleducator.blogspot.com
Youtube.com/c/surgicaleducator
Thank you for watching the video.
Presentation by Dept of Surgery Eko Hospitals, Ikeja, Lagos Nigeria on the 1st of July 2015. Prepared by Dr. Ajayi Babajide (Junior Resident Family Medicine.)
HEAD INJURY- AN OVERVIEW
Dear viewers,
Greetings from “Surgical Educator”
Today I have uploaded a video on Head injury- an important topic in trauma because 50% of trauma deaths are due to head injuries. I haven’t talked elaborately but have included the essential minimum an undergraduate medical student should know. I have talked about pathophysiology, clinical approach, symptoms, signs, investigations, different individual types of head injuries and management of all the varieties of head injuries. My aim is after watching this video all of you should be able to arrive at a correct working diagnosis of the type of head injury and should also be able to institute immediate lifesaving treatment to the patients if there is a need. You can watch the video in the following links:
Surgicaleducator.blogspot.com
Youtube.com/c/surgicaleducator
Thank you for watching the video.
Presentation by Dept of Surgery Eko Hospitals, Ikeja, Lagos Nigeria on the 1st of July 2015. Prepared by Dr. Ajayi Babajide (Junior Resident Family Medicine.)
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
- 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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
2. HI :-
– A head injury is any trauma that leads to injury of the scalp, skull, or brain
– The injuries can range from a minor bump on the skull to severe brain injury
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3. 12/28/2023 gkg 3
EPIDEMIOLOGY
• Number one killer in trauma
• 25% of all trauma deaths
• 50% of all deaths from MVA
• 200,000 people in the world live with the disability caused
by these injuries
• 50% in ages b/n 15 and 35
4. 12/28/2023 gkg 4
ANATOMY
• Anatomy of the ’’SCALP’’
Skin
Firmly bound to the 3rd layer by perpendicular
fibers
Connective tissue
Contain blood vessels of the scalp
Aponeurosis
fibrous sheet, found over much of the vertex
Attaches occipitalis to frontalis m
It is in this layer that - the surgeon mobilizes the scalp.
5. • Loose connective tissue
– Accounts for the mobility of the scalp
– Blood tracks freely in this layer
– bilateral orbital edema following sever head injury or cranial operation
• Periosteum
– Adheres to the suture lines of the skull
– Collection of blood beneath this layer
• Outlines the affected bone
• Cephalohematoma (children)
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6.
7. 12/28/2023 gkg 7
• Anatomy of the meninges (DAP)
Dura
Endosteum and true meningeal layer
Forms falx, tentorium, diaphragm
Arachnoid
Vascular membrane
Arachnoid granulations
Pia
Highly vascular
Dips into sulci and fissures
Carries cortical vessels
8. CAUSES OF HEAD INJURY
• Road traffic accident – 80%
• Falls
• Injuries at work place, during sport, or at home
• Assaults
12/28/2023 gkg 8
RTA’s are the most common cause of TBI followed
by falls and assaults
9. CLASSIFICATIONS OF HEAD INJURY
1) Based on cause
– Primary
– Secondary
3) Based on mechanism
– Blunt
– Penetrating
• 2) Based on GCS (severity)
– Mild 14-15
– Moderate 9- 13
– severe 8 and below
• 4) Morphology
– Skull
– Intracranial lesion
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10. • Skull fracture can be
Vault
Basilar
• Vault fracture can also be
– Closed / open
– Linear / communited
– depressed / undepressed
• Basal skull fracture can be
– Anterior
– Middle
– Posterior
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12. • Head Injuries could be:
- Scalp lacerations
- Skull fractures
- Brain injury
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13. Scalp laceration
• Is a common injury.
• The clinician should identify:
– Traumatic force
– Associated symptoms of head injury
– Wound age
– Likelihood of wound contamination
– Potential presence of foreign body
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14. Skull fracture
– They occur when forces striking the head exceed the mechanical
integrity of the calvarium.
– Significant skull fractures are often accompanied by moderate or
severe intracranial injury.
– The parietal bone is most frequently fractured, followed by the
temporal, occipital, and frontal bones…….PTOF
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15. • Skull fractures themselves may or may not indicate the presence of
significant TBI.
• Certain skull fracture types, such as
– Depressed skull fractures
– Basilar skull fractures with associated cerebral spinal fluid (CSF) leak
and
– Fractures of the temporal-parietal bone that traverse the middle
meningeal artery and vein
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17. PRIMARY INJURY TO SCALP
• Hematoma - Usually do not require Rx
- If large aspiration when it liquefies
• Wounds
Abrasions
- Cleaned & exposed
- Dressed - if hemorrhagic or serous exudate
Lacerations
- Cleaned & sutured( LA or GA)
- LA infiltrated into scalp
- Wound closure without tension
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18. PRIMARY INJURY TO SKULL
Can be vault or basal
Vault can be linear, depressed or communitted
Linear fractures
- Do not require Rx
- At temporal area tear MMAEDH
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19. Depressed #s - simple vs open
Surgery indicated in: 3 cs
oCompression (large plate of bone)
oCosmetic area
o Compound/open wound:
Wound debridement
Elevate the depression
Suture dural laceration
20. Basal skull fracture
- Fractures resulting due to blow to the occiput or
sides of the head
Diagnosis
o History - nasal bleeding,…
o Physical examination
Raccoon eyes
Battle sign
Rhinorrhoea
Pupil size and response
Asymmetrical sluggish response
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23. – If the fluid is blood tinged, the "halo" sign (also called the "ring"
or "target" sign) may be useful to determine the presence of CSF.
– To perform the test, a drop of the fluid is placed on a tissue or filter
paper.
– A rapidly expanding ring of clear fluid around red blood defines a
positive test.
– Of note, the halo test does NOT differentiate among CSF, saline,
saliva, and other clear fluids and has not been formally studied in a
clinical setting.
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24. – CSF can be distinguished from local nasal secretions more
accurately by the presence of beta-trace protein, which is found in
high concentrations in CSF or beta-2 transferrin, which is found
only in CSF, perilymph, and aqueous humor .
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25. PRIMARY BRAIN INJURY
• The damage caused to the brain at the moment of impact
Concussion
Temporary neuronal dysfunction after blunt head trauma
Head CT is normal, &
deficits resolve over minutes to hours
Contusion/laceration
Bruise of the brain
Breakdown of small vessels and extravasation
of blood into the brain
The frontal, occipital, and temporal poles are most often involved.
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26. Diffuse axonal injury
– Damage to axons throughout the brain
– Most frequent finding in patients who die from severe head injury
– Seen in 50% of patients who develop coma after trauma
– Due to rotational acceleration -deceleration.
– Axons may be completely disrupted and then retract.
– Small haemorrhage's can be seen in more severe cases, especially on
MRI.
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27. Mechanisms
Coup & counter-coup injuries
Common sites:-
– Undersurface of frontal lobe
– Tip of temporal lobe
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28. Treatment
–Cerebral contusions rarely require immediate surgical
treatment.
–Pts. must be admitted for observation as these lesions will
tend to mature and expand for 48–72 hours following injury.
–A small proportion of cerebral contusions will require
delayed surgical evacuation to reduce the mass effect.
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30. DIAGNOSIS
History
– Age
– Loss of consciousness
– Cause, circumstance and mechanism of injury
– Presence of headache & vomiting
– Seizures
– Anticoagulant use,….
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31. ASSESSMENT OF NEUROLOGICAL FUNCTION
AND OF CONCIOUS LEVEL
• Glasgow Coma Score
• Best Eye Response (4)
– No eye opening……………………………1
– Eye opening to pain..…………………….2
– Eye opening to verbal command.……...3
– Eyes open spontaneously…...………….4
• Best Verbal Response (5)
– No verbal response ………………………1
– Incomprehensible sounds. ……………..2
– Inappropriate words. …………………….3
– Confused …………………………………..4
– Orientated …………………………………5
• Best Motor Response (6)
– No motor response.…………………..…..1
– Extension to pain.…………………….…..2
– Flexion to pain.……………………….…...3
– Withdrawal from pain..……………….…..4
– Localizing pain.……….…………….……..5
– Obeys Commands..……………………….6
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32. Exclude other causes of depressed conscious level (causes of
coma)
• No focal signs
– Drugs (alcohol, opiate)
– Circulatory collapse
– Hypothermia
– Hyperthermia
– Concussion
– Meningitis,
– Encephalitis
– Subarachnoid hemorrhage
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36. NICE guidelines for CT
– GCS < 13 at any point
– GCS 13 or 14 at 2 hours
– Focal neurological deficit
– Suspected open or depressed fracture
– Basal skull fracture
– Post-traumatic Seizure
– Persistent Vomiting > 2 episode
– Persistent headache
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37. – Coagulopathy
– Post-traumatic amnesia of >30 minutes
– Significant mechanism of injury
– Severe maxillofacial or spine injury
Urgent CT head scan if none of the above but:
• Age > 65
• Coagulopathy (e.g. on warfarin)
• Dangerous mechanism of injury (CT within 8 hours)
• Antegrade amnesia > 30 min (CT within 8 hours)
38. GENERAL MANAGEMENT OF HEAD INJURY
• ABC rule
Stabilization of airway, breathing and circulation
IV access - maintain normovolemia
- Hypotonic/glucose containing fluids should not be used b/c
hypermetabolic state
• Head end elevation - 300
• Treat co-existing injuries
Chest drain - tension pneumothorax
Cervical collar - # of cervical spine,….
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39. Indications for intubation
– GCS score of ≤8
– Motor score of ≤4
– Loss of protective laryngeal reflexes
– Ventilatory insufficiency
– Hypoxemia(pao2<60mmHg)
– Hypercarbia (arterial co2 tension i.e. paco2>45mmHg)
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40. – Spontaneous hyperventilation causing paco2 <26mmHg
– Respiratory arrhythmia
– Bilateral mandibular fracture
– Copious bleeding in to the mouth
– Seizures
41. Anticonvulsants
• May decrease early post-trauma seizures but no benefit in long term
epilepsy prevention
• Phenytoin
Loading dose = 18 - 20 mg/kg
Maintenance dose = 100 mg TID
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42. Patient approach
• ATLS Protocol
• Primary survey with simultaneous resuscitation
–Identify and treat what is killing the patient.
• Secondary survey
–Proceed to identify all other injuries.
• Definitive care
–Develop a definitive management plan.
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43. Taking a history in head injury
–Mechanism of injury
–Loss of consciousness or amnesia
–Level of consciousness at scene and on transfer
–Evidence of seizure
–Pre-existing medical conditions
–Medications (especially anticoagulants)
–Illicit drugs and alcohol
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44. Examination in head injury
• The general examination
• Vital signs: a combination of
– Hypertension
– Bradycardia and is known as the Cushing reflex
– Irregular respirations
• Pyrexia is seen in medullary lesion.
• Inspection and palpation of the head for skin
• Neck rigidity:
• Signs of spine trauma
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45. Examination in head injury...
• Glasgow Coma Score
• Pupil size and response
• Lateralising signs
• Signs of basal skull fracture
– Bilateral periorbital edaema (raccoon eyes)
– Battle’s sign (bruising over mastoid)
– CSF rhinorrhoea or otorrhoea
– Hemotympanum or bleeding from ear
• Full neurological examination: tone, power, sensation, reflexes
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46. Neuro sign chart every 30 min
Hx
Seizure
Headache
Vomiting
PE
BP, PR, RR, and Temperature
GCS
RBS
Oxygen saturation
Pupil size & reactivity
Limb movement
In put and out put
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47. • The following criteria must be met before discharge:
– GCS of 15
– No focal neurological deficit
– Accompanied by a responsible adult
– Should not be under the influence of alcohol or other drugs
– Verbal and written HI advice must be given
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48. Mild HI…
– Some pts. with mild HI are at significant risk of intracranial
hematoma and require CT SCAN.
– The National institute for health and clinical excellence(NICE) has
published some guidelines when to carry out a CT SCAN in a pt. with
mild HI.
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49. Traumatic Intracranial Hematomas
• Contribute to death and disability.
• Hematomas can expand rapidly and cause brain shifting and
subsequent herniation.
• Could be;
– Epidural hematoma
– Subdural hematoma
– Intraparanchymal
– Subarachnoid
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50. 1)Epidural hematoma
– Is a neurosurgical emergency.
– Also called Extradural haematoma
– The skull fracture is associated with tearing of a meningeal artery.
– Hematoma accumulates in the space between bone and dura.
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54. EPIDURAL HEMATOMA………..
• Usually from torn MMA (85-90%) and/or vein (10%)
• Other causes:
Torn dural sinuses(e.g: sagittal sinus)
Oozing from diploe bone & stripped Dura
• Uncommon but serious,1- 4% of TBI
• Highest among adolescents and young adults
• Skull fractures in 75-95%
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55. • The most common site is temporal, as the pterion is the thinnest part of
the skull & overlies the middle meningeal artery.
• It can also occur in other regions such as frontal & posterior fossa.
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57. • Clinical presentation
Lucid interval (in 1/3 of cases) associated with headache vomiting,
drowsiness, confusion, aphasia, seizures and hemiparesis
• Patient initially complains of a headache but is fully alert and orientated
with no focal deficit.
Epidural hematoma due to venous bleeding neurologic decline is
slower but in arteries its rapid
Posterior fossa EDH - elevated ICP
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58. 12/28/2023 gkg 58
• Diagnostic evaluation
CT scan: Lentiform ( biconvex) hyper dense
lesion
• With or without midline shift.
• Areas of mixed density may be seen in a lesion that
is actively bleeding.
• Does not cross sutural margins, but does cross
dural attachments.
59. Treatment
• Immediate surgical evacuation.
• Craniotomy / ?burr hole
Evacuation
• Prognosis-mortality -10%
• Indications for evacuation (craniotomy)
– Larger than 30 mL in volume regardless of GCS score;
– Maximum thickness >=10 mm.
– Mid-line shift >=5 mm
– EDH and coma (GCS score ≤8) who have pupillary abnormalities
(anisocoria)
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60. 2) SUBDURAL HEMATOMA
Accumulates in the space between the dura and the arachnoid.
Pathophysiology
Result from the tearing of bridging veins crossing the subdural space
or hemorrhage from severe cerebral contusions
Spread more diffusely over the hemisphere than extradural and are often
associated with diffuse swelling of the underlying hemisphere
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62. Clinical manifestations - depends on type
– ASDH is nearly always associated with a significant primary brain
injury.
– Patients usually present with an impaired conscious level from the
time of injury, but further deterioration can occur.
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63. ACUTE SUBDURAL HEMATOMA
• 1-2 days after onset
Coma in (56%)
Lucid interval (12-38%)
Posterior fossa SDH - signs of increased ICP
• Result from:
Torn bridging veins
Cortical lacerations
Torn dural sinuses (common) ?
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64. 12/28/2023 gkg 64
• CT SCAN FEATURES
clot is bright or mixed-density
crescent-shaped (lunate)
may have a less distinct border
Can cross sutural margins, but is limited by dural attachments
does not cross the midline due to the presence of falx ( dural
attachement)
Is hyperdense (acute blood)
Gives diffuse and concave appearance
• Signs of mass effect:
ventricular compression, midline shift and reduction in the size of the
basal cisterns
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SUBACUTE SUBDURAL HEMATOMA
• After approximately 1-2 weeks the subdural collection become isodense to
grey matter
• detection may be challenging & recognized when:
effacement of cortical sulci
deviation of lateral ventricle
midline shift
• Contrast enhancement will often define cortical-subdural interface
66. Treatment
• Evacuation via craniotomy.
• Small haematomas with little mass effect may be managed
conservatively in neurosurgical centres.
• The mortality rate from ASDH is much higher than for EDH
and is as high as 40%.
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67. Indications for Evacuation
• Acute SDH >10 mm in thickness or
• Associated with midline shift >5 mm
• If the GCS score is ≤8 or
• If the GCS score has decreased by ≥2
• The patient is with asymmetric or fixed and dilated pupils, and/or
• ICP measurements are consistently >20 mmHg
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68. 12/28/2023 gkg 68
CHRONIC SUBDURAL HEMATOMA
• after 2 weeks usually post trivial injury
due to injury of small bridging veins
headache, cognitive impairment, apathy, seizures and focal deficits
symptoms are transient and fluctuating
proximal, painless and intermittent paraparesis
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CT features
After 2 weeks, hypodense crescentic collections
Acute-on-chronic SDHs can further complicate the
images, with hyperdense fresh haemorrhage
intermixed, or layering posteriorly, within the chronic
collection
Do not cross the midline
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Management
• Acute SDH - Surgery for symptomatic & unstable pt
Surgery
burr hole
craniotomy
Nonoperative Mx
clinically stable
clot thickness <10mm
no clinical or CT signs of herniation
repeat CT scans 6-8 hrs after initial scan
72. Chronic subdural haematoma
• Usually occur in the elderly, alcholics and are more common in
those on anti-coagulant or anti platelet agents.
• There is usually but not always a history of minor head injury in the
weeks or months prior to presentation.
• It is thought that small bridging veins tear and cause a small ASDH
which is clinically silent.
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73. • As the haematoma breaks down it increases in volume, leading
to a mass effect on the underlying brain.
• Patients present with headache, cognitive decline, focal
neurological deficits and seizures.
• It is important to exclude hypoxic, metabolic and endocrine
disorders in this group of patients.
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74. CT appearance of CSDH
• Acute hematoma (0–10 days) is hyper-dense.
• Subacute hematoma (10 days to 2 weeks) is
iso-dense.
• Chronic hematoma (> 2 weeks) is hypo-dense.
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75. • Treatment of a CSDH and most acute-on-chronic subdural
haematomas is evacuation via burr hole.
• This is an important distinction as burr holes can be easily
performed under local anesthetic in an elderly patient with
extensive co-morbidity.
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76. RAISED INTRACRANIAL PRESSURE
• The three normal contents of the cranial vault are
–brain tissue (80%),
–blood (10%)
–CSF (10%)
• Normal state - ICP normal
4-14 mmHg - normal
>20mmHg – abnormal
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• The Monro-Kellie doctrine states that ’’the cranial vault is a rigid structure, and
therefore, the total volume of the contents determines ICP ’’
• Cerebral Perfusion Pressure (CPP) can be determined by the following formula:
CPP = MAP – ICP
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Symptoms & Signs of increased ICP
• Diminishing level of consciousness
• Headache, vomiting, seizures
• Cushing’s Triad:
• Pupillary changes
• Papilledema – most sensitive
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Management of raised ICP
• Initiated when ICP rises above 20mmHg.
• includes airway protection and adequate ventilation (intubation may be
required)
• a bolus of Mannitol 0.25-1g/kg causes:
free water diuresis
increased serum osmolality and extraction of water from the brain
• require rapid neurosurgical evaluation
• ventriculostomy or craniotomy may be needed for definitive decompression
81. MX of ICP…
In refractory cases;
Barbiturate coma
Induced hypothermia and
Decompressive caniectomy.
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83. Osmotic therapy
• By osmolar gradient, it decreases interstitial volume and then ICP.
• Mannitol;
Used most consistently to achieve ICP control.
It has also been shown to improve CBF.
It is given in boluses of 0.25 to 1 g/kg every 4 to 6 hrs as needed.
Monitoring of serum osmolality, fluid balance, renal function, and
electrolytes is required.
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84. Hyperventilation
• Control of ventilation helps prevent increases in intrathoracic
pressures that may elevate CVPs and impair cerebral venous
drainage.
• Hyperventilation decreases paco2 thereby leading to cerebral
vasoconstriction,which then results in decreased cerebral
blood volume and ICP.
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85. Hyperventilation…
• However,hyperventilation induced vasoconstriction may also cause
secondary ischemia can also increase extracellular lactate and
glutamate levels that may contribute to secondary brain injury.
• So that, it is recommended to avoid hyperventilation, especially in
the acute phase(the first 24 to 48 hrs) following TBI.
• Mild to moderate hyperventilation can be considered at later
stages, but paco2 of <30mmHg should be avoided.
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86. Sedation
• Sedation lowers elevated ICP by reducing metabolic demand.
• It may also ameliorate ventilator asynchrony and blunt
sympathetic responses of hypertension and tachycardia.
• Pentobarbital remains a RX option for elevated ICP refractory
to other therapies.
• A loading dose of 5 to 20 mg/kg is given as a bolus, followed
by 1 to 4 mg/kg per hr.
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87. Sedation…
• These drugs cause hypotension and cerebral vasodilation.
• Monitor CPP to evaluate unpredictable effects of these agents
on BP and ICP.
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88. Antiepileptic drugs
• Over all,the incidence of early post taumatic seizure is 6 to 10
% but may be as high as 30% in pts with severe TBI.
• About 15 to 25% of pts with coma and severe HI will have
nonconvulsive seizures identified on EEG.
• It has been shown to reduce the incidence of early seizures,
but does not prevent the later development of epilepsy.
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89. Reasons to prevent early seizures include
The risk of status epilepticus, which has a high fatality rate.
The potentials to aggravate systemic injury
Recurrent seizures may increase CBF could there by increase
ICP
Seizures increase a metabolic demand on damaged brain
tissue and aggravate secondary brain injury
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90. MX of Glucose
• Hyperglycemia is associated with worsened outcome in a
variety of neurologic conditions including severe TBI.
• Aggravation of secondary brain injury is by;
Increased tissue acidosis from anaerobic metabolism.
Free radical generation and
Increase BBB permeability.
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91. MX of Glucose…
• To avoid extremes of very high or low blood glucose levels, a
broad target range of upto 140 mgldl or possibly even 180
mg/dl may be appropriate.
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92. Glucocorticoids
• This therapy was found to harmful following head trauma .
DVT
Is difficult MX issue in TBI.
Can be reduced by the use of mechanical thromboprophylaxis or
antithrombotic therapy, but this has to be weighed against the
potential risk of hemorrhage expansion.
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93. Outcomes after HI
Outcome scores
• Glasgow outcome score(GOS)
Good recovery=5
Moderate disability=4
Severe disability=3
Persistent vegetative state =2
Dead =1
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94. Outcome scores…
• GOS 5 does not mean that there is no deficit but implies
independent functioning and the possibility of return to work.
• Pts with GOS 4 remain independent though with disabling deficit.
• Pts with GOS 3 are dependent on others for atleast some of their
care.
• GOS 2 pts are not aware of themselves or their environment.
• This state is not considered permanent until at least 1 yr after TBI.
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95. TECHNIQUES OF BURR HOLE AND CRANIOTOMY
BUR HOLE
Position;
• Shoulder roll,
• Head turned with side to be explored up, and
• Horse shoe head holder.
• The scalp is prepared as usual.
• For each burr hole – a straight incision 4-5cm long is made,
directed towards the vertex.
• These can be incorporated into a scalp flap if this prove necessary
for craniotomy.
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96. Standard burr hole sites
• Frontal -8cm above the superciliary ridge & 3cm
from the midline
• Parietal -on the parietal eminence
• Temporal -1cm in front of the external auditory
meatus, just above the zygomatic arch.
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97. Craniotomy
• First outline the trauma flap with a skin marker.
1. Start at the zygomatic arch <1cm anterior to the tragus.
2. Proceed superiorly and the curve posteriorly at the level of top of
the pinna.
3. 4 to 6 cm behind the pinna it is taken superiorly.
4. 1 to 2 cm ipsilateral to the midline(sagittal suture) curve ateriorly
to end behind the hairline.
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98. 12/28/2023 gkg 98
COMPLICATIONS HEAD INJURY
• Meningitis & brain abscess
• CSF rhinorrhea and otorrhea
• Epilepsy - about 80% arise in 2yrs
• Hydrocephalus- usually due to atrophied white matter
• Amnesia (PTA)
• Postconcussional Sx
• Posttraumatic encephalopathy
• Cranial nerve injury - in up to 30% pts
101. Management
General
• ABC with C –spine protection
• IV line and isotonic fluids
• Catheterization
• NGT feeding
• 100% Oxygen
• GI prophylaxis
• DVT prophylaxis
• Anti pain & antipyretics
• Neuro sign & glucose monitoring
ICP MX
• Head elevation to 30 degree
• Hyperventilation
• Osmotic diuresis
• Hypertonic saline
• Then specific mx
MVA = motor vehicle injury
Periosteum
adheres to the suture lines of the skull
collection of blood beneath this layer
outlines the affected bone
cephalohematoma (children)
C connective tissue -fat lobules bound in tough fibrous septa
-contain blood vessels of the scalp.
-vessels retract when lacerated.
Dips = penetrates
classification
According to the mechanism of injury
1. Blunt head injury
2. Penetrating head injury
-low velocity injury
-stabbing injury
-high velocity injury
-gunshot injury
Skull fractures
Diastatic- fractures that cross sutures
Displaced ( depressed )- fracture which displaces bone into the cranial cavity by a distance greater than the thickness of the bone
Signs of base of skull fracture
■ Bilateral periorbital oedaema (raccoon eyes)
■ Battle’s sign
■ CSF rhinorrhoea or otorrhoea
■ Haemotympanum
Concussion
head injury brought about by a change in the momentum of the head
- movement of the head is arrested by a rigid surface
Instant onset of transient neurologic dysfunction
- loss of consciousness, temporary respiratory arrest, loss of reflexes
Complete neurologic recovery
Amnesia of the event persists
Post concussive syndrome results in some
Direct Parenchymal Injuries
Contusion
Bruising of the brain following transmission of kinetic energy to the brain
Blow to the surface of the brain results in
Rapid tissue displacement
Disruption of vascular channels
Hemorrhage, tissue injury, edema
Common sites are at the tips of the frontal and temporal lobes
Coup and contrecoup injuries
Laceration
Penetration of an object and tearing of tissue
Diffuse Axonal Damage
Seen in 50% of patients who develop coma after trauma
May occur in the absence of cerebral contusion
Mechanical forces damage axons at the node of Ranvier
Common in supratentorial compartment
Corpus callosum, paraventricular and hippocampal areas, cerebral peduncles, brachium conjunctivum, superior colliculi, deep reticular formation)
Coup and Contrecoup injuries
Coup injury
Occurs when head injury occurs while the head is stationary
It is caused by the force of direct impact b/n the brain and the skull at the site of impact
Contrecoup injury
Injury to mobile head
Caused when the brain strikes the opposite inner surface of the skull after sudden deceleration
Lucid Interval
A temporary restoration of consciousness after a person has been rendered unconscious from a blow to the head.
The victim subsequently relapses into COMA.
This is a sign of raised INTRACRANIAL PRESSURE from arterial bleeding and indicates that surgery may be required to control the intracranial haemorrhage.
Lucid Interval
A temporary restoration of consciousness after a person has been rendered unconscious from a blow to the head.
The victim subsequently relapses into COMA.
This is a sign of raised INTRACRANIAL PRESSURE from arterial bleeding and indicates that surgery may be required to control the intracranial haemorrhage.