Head injuries are a major cause of death and disability worldwide. Road traffic accidents are the most common cause of head injuries in India. The brain is encased within the rigid skull, so any increase in intracranial volume from bleeding or swelling can rapidly increase intracranial pressure. The document discusses the epidemiology, anatomy, physiology and classification of head injuries as well as guidelines for management including medical therapies to reduce intracranial pressure and criteria for surgical intervention for specific injuries like epidural hematomas.
70% of RTA patients have head injury(HI).
One of the most important public health problems of today.
70% of deaths in RTA are due to HI.
At Risk population
Males 15-24
Infants
Young Children
Elderly
70% of RTA patients have head injury(HI).
One of the most important public health problems of today.
70% of deaths in RTA are due to HI.
At Risk population
Males 15-24
Infants
Young Children
Elderly
polytrauma lecture prepare by three medical student in Kerbala university / college of medicine department of surgery to presented as seminar
for download as ppt
https://drive.google.com/open?id=1bc3HMEeJyhrOwag-AvTFMmPVKi12O1PU
polytrauma lecture prepare by three medical student in Kerbala university / college of medicine department of surgery to presented as seminar
for download as ppt
https://drive.google.com/open?id=1bc3HMEeJyhrOwag-AvTFMmPVKi12O1PU
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.
"Trouma" is not a term or concept that I am familiar with. It's possible that you might be referring to something specific or using a term from a different context. Could you please provide more information or clarify your question?
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.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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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.
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.
2. Epidemology
Head injury
Number One Killer in Trauma
25% of all trauma deaths
50% of all deaths from MVC
200,000 people every year in
the world live with the
disability caused by these
injuries
3. Indian Head Injury Foundation
India – highest rate of head injuries in the world
Yearly 1,00,000 lives lost with 1 million suffering from
severe head injury
1 out off 6 trauma victim dies in India ; in USA the
figure is 1 out off 200
RTA (road traffic accidents) most common cause
followed by falls and assault
Motorcylist and pedesticians most common victims of
RTAs
4. In the year 2050
India will have the highest number of automobiles on
the planet , overtaking USA
5. Etiology
Road traffic accidents (RTA) – most common cause
Falls
Sports injury
Assault
Gun shot wounds to head
6. Basic Anatomy
Scalp
Skull
Meninges
Dura Mater
Arachnoid
Pia Mater
Brain Tissue
CSF and Blood
17. Dictates that “the total volume of
the intracranial contents MUST
remain constant”
The MONROE KELLIE doctrine
18. Brain Physiology
Brain Metabolism :
1.Brain oxygen consumption (CMRO2, cerebral
metabolic rate for oxygen) – 3.5 ml per 100 g per min
2.90% of energy from blood glucose
Cerebral blood flow (CBF) :
CBF is 55 ml per 100g per min
autoregulated over mean arterial pressure range of 50 -
150 mm of Hg
19. Intracranial Pressure
The pressure of the brain contents within the skull is
intracranial pressure (ICP)
The pressure of the blood flowing through the brain is
referred to as the cerebral perfusion pressure (CPP)
The pressure of the blood in the body is the mean arterial
pressure (MAP)
Cerebral Perfusion Pressure (CPP) can be determined by
the following formula:
CPP = MAP - ICP
24. Primary Brain Injury :
-occurs at the time of impact
- mechanical damage which is irreversible
- causes permanent mechanical cellular disruption
and microvascular injury.
-includes 1) cerebral contusions
2) diffuse axonal injuries (DAI)
3) cerebral lacerations
PATHOPHYSIOLOGY
25. Secondary Brain Injury
occurs at some time after the moment of impact
often preventable
Prevention of secondary brain injury results in
improved neurological outcome after head injury
may make the difference between independent
survival and dependent survival/death.
26. Brain suffers from traumatic
injury
Brain swelling or bleeding
increases intracranial volume
Rigid cranium allows no room for
expansion of contents so ICP
increases
Pressure on blood vessels within
the brain causes blood flow to the
brain slowly
Cerebral hypoxia and ischemia
occurs
Intracranial pressure continues
to rise. Brain may herniate
Cerebral blood flow decreases
33. Basilar skull fractures
Usually diagnosed on CT imaging or on clinical
evidences
Clinical signs include Battle sign ,Raccoon Eyes and
CSF leak.
May or may not be associated with seventh and eighth
cranial nerve injury
35. INTRACRANIAL LESIONS
Epidural hematoma
Collection of blood & clot b/n dura mater and bones of
the skull
Source Middle Meningeal Artery
Dural Venous Sinuses
C/F Brief loss of consciousness, headache,
drowsiness, dizziness ,nausea, vomitting
Rapid clinical deterioration
36. Classical presentation seen only in 1/3 rd cases
On CT scan lentiform hyper dense lesion between
skull and brain
Associated with mass effect on underlying brain with
or without midline shift.
Overall mortality rate 18% in all cases but only 2% in
isolated EDH
37.
38. Acute subdural Hematoma
Accumulates in space between dura and arachnoid
Disruption of cortical vessels or brain laceration
produces hematoma
A/w significant primary injury- patients present with
impaired conscious level from the time of injury
CT scan –hyperdense concave lesion spreading across
brain
midline shift disproportionate to size of lesion
Mortality rate as high as 40% in some series
39.
40. Subarachnoid Hemorrhage
Trauma is most common cause followed by Aneurysms
Rarely aneurysmal hemorrhage immediately precedes
trauma.
Most can be managed conservatively
41. Chronic subdural Hemorrhage
Usually occurs in elderly on anti coagulant or anti
platelet agents
h/o minor head injury in weeks or months prior to
presentation
Small bridging veins tear and cause small clinically
silent ASDH ,when hematoma breaks down and
increases in size mass effect is produced
c/f- headache, cognitive impairment, focal
neurological deficit and seizures.
CT scan – acute blood (0-10 days) = hyperdense
- sub acute blood (10-14 days) = isodense
- chronic blood (>2 weeks) =hypodense
42. Acute on chronic SDH
Chronic SDH will more recent hemorrhage in
dependant (posterior) areas.
Treatment is Burr hole evacuation rather than
craniotomy
43. Cerebral contusions
Coup and counter coup injuries
Most commonly affecting inf frontal fossa and
temporal lobes
CT appears heterogeneous with mixed areas of high
and low density
Rarely require immediate surgery
Observation for 48-72 hrs
44.
45. Concussion
Temporary & brief interruption of neurological function
after minor head injury
Due to shearing / stretching of white matter fibres at the
time of impact or temporary neuronal dysfunction
C/o headache, confusion, amnesia
CT/MRI cannot detect
3 grades (Colorado Grading)
grade I- symptoms for 15 mins no LOC , only confusion
grade II-symptoms for > 15 mins ,no LOC, amnesia
gradeIII- LOC present
Medical opinion should be sought in Grade II and III
46. DAI
Diffuse Axonal Injury
Disruption of axons in white matter and brainstem
Injury occurs immediately and is irreversible
Seen after MVC or shaken baby syndrome
Usually have persistent sequlae e.g. cognitive
impairment, spasticity etc.
90% pts with severe DAI will be vegetative
CT usually normal
MRI with multiple, diffuse abnormalities
Hemorrhagic spots classically seen over corpus
callosum, dorsolateral midbrain.
53. Intubation with Cervical inline stabilization
Breathing and ventilation : Intubation precautions
Pre-medicate with Lidocaine, 1mg/kg IV 2 minutes
prior to attempt
Laryngoscopy produces an ICP Spike
64. MANAGEMENT OF
MILD HEAD INJURY (GCS14 -15)
History
General Examination
Limited Neurologic Examination
C-spine and other X-rays as indicated
CT scan??
Discharge with advice
65. Patient can be discharged if following criteria are met
before discharge
1.GCS must be 15/15
2.no focal neurological deficit
3.accompanied by responsible adult
4.verbal and written advice given
66.
67. Aim is prevention of secondary brain injury
Achieved by avoidance of hypoxia and hypotension
CT scan after complete stabilization of patient.
Early neurosurgery consult if intracranial hematoma
seen
Measures to reduce ICP (reverse Trendelenburg) i.e.
head up position by 20-30 degrees ?
ICP monitoring
Mannitol during transport.
MANAGEMENT OF MODERATE HEAD
INJURY(GCS 9-12)
68. MANAGEMENT OF SEVERE HEAD INJURY(3 -
8 )
Primary Survey and Resuscitation
Secondary Survey and ‘AMPLE’ history
Admit to facility – neurosurgical care
Neurologic Re-evaluation
Eye opening
Motor response
Verbal response
Pupillary reaction
69. CT scan only after hemodynamic stabilization
Medical therapy for raised ICP
Immediate neurosurgeon opinion
If needed surgical management
70. MEDICAL THERAPIES FOR HEAD INJURY
Head end elevation – 30 deg
Intravenous fluids:
Maintain normovolemia
Hypotonic/glucose containing fluids
should not be used
Serum sodium levels monitored daily
71. Mannitol
0.25-1g/kg
Osmotic agent- dec ICP, maintains CBF,CPP and brain
metabolism
Dec ICP within 6 hrs.
Expands volume, O2 carrying capacity.
Diuretic effect- net intravascular volume is reduced.
72. Furosemide
To reduce ICT in conjunction with mannitol
Dose 0.3 to 0.5 mg/kg
Never use in Hypovolemia
73. Hypertonic Saline
Improves CPP and brain tissue O2 levels
Decreased ICP by 35% (8-10 mm HG)
CPP increased by 14%
MAP remained stable
Greatest benefit in those with higher ICP and lower CPP
Repeated doses were not associated with rebound,
hypovolemia or HTN
30 mL of 23.4% over 15 minutes
74. HYPERVENTILATION
No role as prophylaxis in 24 hrs.
Reducing PaCO2 cerebral vasoconstriction
Maintain PaCo2 25 – 35 mmhg
Last resort for reducing ICP
TEMPORARY MEASURE ONLY.
75. Barbiturates
Effective in reducing ICP – refactory to other measures
Not used in presence of hypotension/hypovolemia
77. Surgical Management of Specific
Head injuries
Various guideline followed
Guidelines For Surgical Management of Traumatic
Brain Injury
Published in 2001
All new reports and literature regularly updated
through Neurosurgical Evidence Based Medicine
Centre ,University Of Washington.
79. Fracture Skull Base
With CSF leaks
no acute surgery required for CSF leak
for first 72 hrs observation (elevation of head)
if leak persists
temporary CSF diversion (lumbar drainage or
ventriculostomy)
Still leak persists surgery to be done
Exploration of floor of frontal fossa with closure of
dural defect
80. EDH
Absolute indications of surgery (regardless of GCS)
1. > 30 ml vol of hematoma
2. > 15 ml thickness of blood clot
3. midline shift >5 mm
4. anisocoria ( > 1mm)
If GCS <8 = immediate surgery
If GCS > 8 = as soon as possible
If size less than above but GCS <8 = surgery
If size less than above but GCS >8 =nonoperative
management can be done
Mean time of EDH for reexpansion is 8 hrs -36 hrs.
81. SDH
Absolute indication of surgery
1. > 10 mm thickness of blot clot
2.Midline shift > 5mm
If size less than above but GCS <8 along with
1. GCS decreased by 2 from time of injury to
admission
2. Pt. with asymmetric or fixed dilated pupils
3.ICP >20 mm of Hg
If size less than above and GCS >8 = non operative
treatment.
If planned surgery should be within first 4 hrs
Craniotomy with duraplasty with or without bone flap
removal
82. Posterior Fossa Lesions
No monitoring possible because of location
Guidelines for evacuation
1. > 3cm clot on CT scan
2. any size of clot with ASDH or EDH
83. Penetrating Brain Injury
Meningitis and abscess most common complications
followed by Seizures
If grossly contaminated wound then craniotomy and
debridement required
Small clean wounds with no scalp devitalization can be
managed conservatively
If open sinus suspected repair should be done
If dural injury suspected repair should be done.
85. Procedure
A burr hole is placed on
the side of the dilating
pupil.
In the absence of a CT
scan, the burr hole is
placed 2 finger widths
anterior to the tragus of
the ear and 3 finger widths
above the tragus of the ear.
86. A vertical incision is made approximately 3
cm long, centered over the entry point all
the way down to the temporalis muscle
dividing the fibers of the muscle vertically.
The periosteum is then cut in the same
manner.
88. If there continues to be excessive bleeding
through the hole, packing the wound should
be tried with Gel foam or by cutting off a piece
of temporalis muscle and stuffing it into the
hole.
89. Decompressive Craniectomy
Controversial
Used in patients without focal lesion and raised ICP
who are refractory to maximum medical management
The operation involves removing a large section of
skull and opening the dura, allowing the swollen brain
to expand underneath the scalp
The bone flap is stored and can be replaced 3–6
months later when the patient has made a good
neurological recovery and the brain swelling has
resolved
90.
91. Long term sequelae of Head Injury
Neurorehabilitation
Neuropsychology – after minor head injuries such as
headache, dizziness, impaired short term memory,
concentration etc.
Seizures –prophylactic anticonvulsants cant prevent long
term seizures
Delayed CSF leak –CT cisternography or CT isotope studies
can be done
92. Seizure Disorder
2% Early post-traumatic incidence
Increased to 30% in children, alcoholics and with
intracranial hematoma
Prophylactic antiepileptics reduce early occurrence
Use not supported by the literature
Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - Cognitive/Memory dysfunction
93. Concussion
Up to 80% may have symptoms at 3 months
15% may have symptoms at 1 year
Persistence of these symptoms is termed Postconcussive
Syndrome
85-90% recover after 1 year
Risk factors:
- Female - Litigation - Low socioeconomic status