This document discusses decompressive craniectomy for refractory intracranial hypertension. It provides rationale and indications for decompressive craniectomy, which aims to reduce intracranial pressure by removing part of the skull. Common complications are also mentioned. Guidelines from the American Association of Neurological Surgeons are presented regarding criteria for performing decompressive craniectomy in patients with traumatic brain injury or refractory increased intracranial pressure. Outcomes of decompressive craniectomy are discussed for different patient groups.
Before embarking on an approach, the surgeon should be familiar with both the ventricular anatomy and the options for optimally Accessing lesions in third ventricle is a surgical challenge because of its difficult corridor as well as deeper location, need of neural incision, preservation of vascular, thalamus and hypothalamus and likely risk of fornix injury.
Before embarking on an approach, the surgeon should be familiar with both the ventricular anatomy and the options for optimally Accessing lesions in third ventricle is a surgical challenge because of its difficult corridor as well as deeper location, need of neural incision, preservation of vascular, thalamus and hypothalamus and likely risk of fornix injury.
Pituitary tumor accounts for ~10% ICT. They are common in 3-4 decade and shows association with MEN I.
About 5% of PT are invasive usually with giant tumor (>4cm). Tumor can be classified as functional (hormone secreting) or non functional. This slides details the algorithmic approach in management of pituitary tumors.
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.
Pituitary tumor accounts for ~10% ICT. They are common in 3-4 decade and shows association with MEN I.
About 5% of PT are invasive usually with giant tumor (>4cm). Tumor can be classified as functional (hormone secreting) or non functional. This slides details the algorithmic approach in management of pituitary tumors.
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.
Trial of decompressive craniectomy for traumatic intracranial hypertension1Dr fakhir Raza
The New England Journal of Medicine, Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension, Extended Glasgow Outcome Scale (GOS-E), vegetative state, lower severe disability, traumatic brain injury, RESCUEicp,
Head injuries top the list of trauma patienrts coming to the casualty. The condition has to be immediately assessed and investigated. Depending upon the findings prompt medical or neurosurgical treatment has to be administered.
Research guru and PI for the ARISE study, college examiner and semi-professional forrest-based carpenter, Anthony always gives a fascinating talk. This time he gives an intelligent and considered breakdown on the nebulous topic of cerebral protection.
Austin Biomarkers & Diagnosis is a peer-reviewed, open access journal published by Austin Publishers. It provides easy access to high quality Manuscripts covering aspects of measure and evaluation to examine normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention. It also focus upon aspects of dynamic and powerful approaches in understanding the spectrum of disease with applications in observational and analytic epidemiology, randomized clinical trials, screening and diagnosis.
Austin Publishing Group is a successful host of more than hundred peer reviewed, open access journals in various fields of science and technology with intent to bridge the gap between academia and research access.
Austin Biomarkers & Diagnosis accepts original research articles, review articles, case reports, mini reviews, rapid communication, opinions and editorials on all the related aspects of biomarkers involved in normal biological processes, pathological process, and pharmacological responses as well as in diagnosing diseases.
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.
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!
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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.
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.
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
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
1. Decompressive Craniectomy ForDecompressive Craniectomy For
Refractory Intracranial Hypertension:Refractory Intracranial Hypertension:
Rationale, Indications andRationale, Indications and
complications.complications.
Khaled abdeen M.d.*, hishaMKhaled abdeen M.d.*, hishaM
aboul-enein M.d*, Yasser orzaboul-enein M.d*, Yasser orz
M.d*, shahira a el-MetainY M.d**.M.d*, shahira a el-MetainY M.d**.
*Department of Neurosurgery – Alexandria University*Department of Neurosurgery – Alexandria University
** Department of Anesthesiology – Alexandria University** Department of Anesthesiology – Alexandria University
2. Malignant brain edema is a state of severe,Malignant brain edema is a state of severe,
progressive and diffuse cerebral edema thatprogressive and diffuse cerebral edema that
causes rapid clinical deterioration which doescauses rapid clinical deterioration which does
not respond to aggressive treatment .not respond to aggressive treatment .
Clinically, malignant brain oedema isClinically, malignant brain oedema is
manifested by herniation syndrome in the formmanifested by herniation syndrome in the form
of rapid deterioration of consciousness andof rapid deterioration of consciousness and
pupillary changes .pupillary changes .
Radiologically , there are compression of theRadiologically , there are compression of the
ventricles, poor grey white matter differentiation ,ventricles, poor grey white matter differentiation ,
obliteration of the basal cisterns , and loss ofobliteration of the basal cisterns , and loss of
normal gyral pattern .normal gyral pattern .
3. The American Association ofThe American Association of
Neurological SurgeonsNeurological Surgeons
has recommended decompressive craniectomy forhas recommended decompressive craniectomy for
patients with traumatic brain injury (TBI) and refractorypatients with traumatic brain injury (TBI) and refractory
IH if some or all of the following criteria were met:IH if some or all of the following criteria were met:
1) Diffuse cerebral swelling on cranial CT imaging.1) Diffuse cerebral swelling on cranial CT imaging.
2) Within 48 hours of injury .2) Within 48 hours of injury .
3) No episodes of sustained ICP > 40 mmHg before3) No episodes of sustained ICP > 40 mmHg before
surgery.surgery.
4) GCS >3 at some point subsequent to injury.4) GCS >3 at some point subsequent to injury.
5) Secondary clinical deterioration.5) Secondary clinical deterioration.
6) Evolving cerebral herniation syndrome.6) Evolving cerebral herniation syndrome.
7) pupillary abnormalities but respond to mannitol .7) pupillary abnormalities but respond to mannitol .
4. Malignant” MCA infarctionMalignant” MCA infarction
is defined as an infarction of at least two thirdsis defined as an infarction of at least two thirds
MCA territory upward . These patients presentMCA territory upward . These patients present
clinically with severe hemispheric strokeclinically with severe hemispheric stroke
syndrome and progressive deterioration ofsyndrome and progressive deterioration of
consciousness within the first 2 days. Thereafter,consciousness within the first 2 days. Thereafter,
symptoms of transtentorial herniation occursymptoms of transtentorial herniation occur
within 2–4 days of stroke onset. These patients’within 2–4 days of stroke onset. These patients’
prognosis is poor and mortality is as high asprognosis is poor and mortality is as high as
80% . So therapy of malignant MCA infarction80% . So therapy of malignant MCA infarction
should be more aggressive .should be more aggressive .
5. Malignant Middle Cerebral ArteryMalignant Middle Cerebral Artery
Infarction SyndromeInfarction Syndrome
Large hemispheric infarction involvingLarge hemispheric infarction involving
>50% of MCA territory associated with a>50% of MCA territory associated with a
massive cerebral oedema and brain-stemmassive cerebral oedema and brain-stem
herniationherniation
Caused by complete/ near completeCaused by complete/ near complete
occlusion of either internal carotid arteryocclusion of either internal carotid artery
(ICA trunk) or proximal middle cerebral(ICA trunk) or proximal middle cerebral
arteryartery
6. MMCAISMMCAIS
Dense pyramidal signs (initial)Dense pyramidal signs (initial)
Neurological deterioration < 24-72 hrNeurological deterioration < 24-72 hr11
duedue
to elevated ICP leading to brain stemto elevated ICP leading to brain stem
herniationherniation
Very high mortality despite maximalVery high mortality despite maximal
medical treatmentmedical treatment
70% (37/ 53 ) died in NICU (33/37 died within70% (37/ 53 ) died in NICU (33/37 died within
first 5 days)first 5 days)22
78% (35/45) died within 1 week78% (35/45) died within 1 week11
1. NG L et al. Stroke 1970
2. Berrouschot J et al. ICM 1998
7. Decompressive craniectomy [DC] hasDecompressive craniectomy [DC] has
been used as a final option in thebeen used as a final option in the
management of refractory intracranialmanagement of refractory intracranial
hypertension . It is a method of givinghypertension . It is a method of giving
room to the swelling brain , can be liferoom to the swelling brain , can be life
saving procedure because it decreasessaving procedure because it decreases
compression of brain stem structures andcompression of brain stem structures and
minimizes herniation .minimizes herniation .
9. Early DCEarly DC
Early DC reduces brain edema
formation by more than 50% and
prevents secondary brain damage
when performed early enough (i.e.,
during the first 3 h after trauma).
(Zweckberger K, et al.; 2006)
10. Does decompressive craniectomy improveDoes decompressive craniectomy improve
outcomes?outcomes?
Survival (mortality)Survival (mortality)
Functional outcomes .Functional outcomes .
Can we predict malignant brainCan we predict malignant brain
oedema?oedema?
Timing: when to operate?Timing: when to operate?
12. Large (10 × 15 cm) frontotemporoparietal craniectomy with the
lower margin from the middle cranial fossa.
In the event of massive cerebral swelling, extensive duraplasty
with internal decompression is performed.
13.
14.
15.
16.
17.
18. Decompressive HemicraniectomyDecompressive Hemicraniectomy
(DH)(DH)
11stst
described by Kocher in 1901 for the treatment ofdescribed by Kocher in 1901 for the treatment of
TBITBI
11stst
reported by Rengachary S et al.reported by Rengachary S et al.11
for the treatementfor the treatement
of MMCAIS in 1981of MMCAIS in 1981
Removal of an ipsilateral bone flap ≥ 12 cm inRemoval of an ipsilateral bone flap ≥ 12 cm in
diameter and including parts of the frontal, parietal,diameter and including parts of the frontal, parietal,
temporal and occipital squama plus Duraplastytemporal and occipital squama plus Duraplasty
To relieve ICPTo relieve ICP
Inadequate craniectomy size is associated withInadequate craniectomy size is associated with
parencymal haemorrhage ± infarction and increasedparencymal haemorrhage ± infarction and increased
mortalitymortality22
1. Rengachary S et al Neurosurgery 1981: vol 8/3, 321-328
2. Wagner S et al. Journal of Neurosurgery, May 2001, vol./is. 94/5(693-6)
19. ResultsResults
Group (A) trauma patients:Group (A) trauma patients:
In the current study, using the inclusion criteria ; 65In the current study, using the inclusion criteria ; 65
patients had severe head injuries. The mean GCS ofpatients had severe head injuries. The mean GCS of
patients was 5.83± 1.76 with a range of 4-9 (9 casespatients was 5.83± 1.76 with a range of 4-9 (9 cases
were moderate head injury with GCS 9 while the restwere moderate head injury with GCS 9 while the rest
were severe head injury with GCS 8 or less).In ourwere severe head injury with GCS 8 or less).In our
study, 25 cases were managed within the first 12 hoursstudy, 25 cases were managed within the first 12 hours
of admission with a range from 2-8 hours. The timeof admission with a range from 2-8 hours. The time
interval from admission to initial management in hoursinterval from admission to initial management in hours
for the studied cases ranged between 2 to 8 hours withfor the studied cases ranged between 2 to 8 hours with
mean of 3.27 ± 0.98. According to GOS , the outcomemean of 3.27 ± 0.98. According to GOS , the outcome
was favorable in 54% , unfavorable in 38.4% , and deathwas favorable in 54% , unfavorable in 38.4% , and death
in 7.6% .in 7.6% .
20. ResultsResults
Group (B) post-ischemic:Group (B) post-ischemic:
This group included 15 patients with malignant MCA infarction , one ofThis group included 15 patients with malignant MCA infarction , one of
them with carotid artery dissection causing hemispheric infarction . Allthem with carotid artery dissection causing hemispheric infarction . All
underwent ipsilateral frontotemporal decompressive craniectomy . Largeunderwent ipsilateral frontotemporal decompressive craniectomy . Large
parenchymal hyperdensity more than 50% and within 48 hours of strokeparenchymal hyperdensity more than 50% and within 48 hours of stroke
onset . The outcome was favorable in 53.4% , unfavorable in 26.6% andonset . The outcome was favorable in 53.4% , unfavorable in 26.6% and
death in 20% .death in 20% .
Group (C) post-intra-axial temporal lobe tumorGroup (C) post-intra-axial temporal lobe tumor::
This group included only 4 patients who underwent elective craniectomyThis group included only 4 patients who underwent elective craniectomy
for excision of temporal intra-axial lesion (two patients with glioblastomafor excision of temporal intra-axial lesion (two patients with glioblastoma
multiformi and two patients with oligodendroglioma) where in the firstmultiformi and two patients with oligodendroglioma) where in the first
post-operative 24 hours the patients showed marked deteriorationpost-operative 24 hours the patients showed marked deterioration
together with signs of lateralization and an immediate CT scan wastogether with signs of lateralization and an immediate CT scan was
done which showed no residual lesion , no hematoma, yet extensivedone which showed no residual lesion , no hematoma, yet extensive
temporal lobe edema with subfalcine herniation for more than 2 cms.temporal lobe edema with subfalcine herniation for more than 2 cms.
These cases add a new indication for decompressive craniotomy as aThese cases add a new indication for decompressive craniotomy as a
lie saving procedure when all other conservative maneuvers fail. Thelie saving procedure when all other conservative maneuvers fail. The
outcome was favorable in 75% and unfavorable in 25% .outcome was favorable in 75% and unfavorable in 25% .
21. ResultsResults
Group (D) spontaneous intra-cerebral hematoma:Group (D) spontaneous intra-cerebral hematoma:
This group included 6 cases admitted to the ICUThis group included 6 cases admitted to the ICU
suffering from spontaneous intra-cerebral hematoma insuffering from spontaneous intra-cerebral hematoma in
the temporal lobe which caused disturbance in the levelthe temporal lobe which caused disturbance in the level
of conscious. All patients where operated upon forof conscious. All patients where operated upon for
primary evacuation of the hematoma and simultaneouslyprimary evacuation of the hematoma and simultaneously
for decompressive craniectomy to avoid the effect offor decompressive craniectomy to avoid the effect of
post-operative vasogenic edema and subsequentpost-operative vasogenic edema and subsequent
subfalcine shiftsubfalcine shift.. The outcome was favorable in 50 % ,The outcome was favorable in 50 % ,
unfavorable in 33% and death in 17% .unfavorable in 33% and death in 17% .
The total outcome for all groups was favorable outcomeThe total outcome for all groups was favorable outcome
in 54.4 % [49 patients] . unfavorable in 35.6 % [ 32in 54.4 % [49 patients] . unfavorable in 35.6 % [ 32
patients ] , death in 10 % [9 patients ]patients ] , death in 10 % [9 patients ]
22. Literature SearchLiterature Search
Ovid Medline, Embase, Cochrane & finallyOvid Medline, Embase, Cochrane & finally
handsearchhandsearch
keywords “stroke, middle cerebral arterykeywords “stroke, middle cerebral artery
infarction, brain oedema, decompressiveinfarction, brain oedema, decompressive
hemicraniectomy and decompressivehemicraniectomy and decompressive
surgery” from Januarysurgery” from January 1998 to July 20091998 to July 2009
Medline – 165, Embase 465, CochraneMedline – 165, Embase 465, Cochrane
1717
3 RCTs, one meta-analysis, 3 SR, 503 RCTs, one meta-analysis, 3 SR, 50
observational studiesobservational studies
23. Scoring systemScoring system
NIHSSNIHSS
National Institute Health Stroke ScaleNational Institute Health Stroke Scale
Motor / sensory / speech / visionMotor / sensory / speech / vision
11 parts, scores -4011 parts, scores -40
>25 severe stroke>25 severe stroke
Barthel Index (BI)Barthel Index (BI)
Assess disability in regards to activity ofAssess disability in regards to activity of
daily livingdaily living
Total score 0-100Total score 0-100
Dependency - Score < 60Dependency - Score < 60
24. Scoring systemScoring system
Modified Rankins ScoreModified Rankins Score
0 No symptoms at all
1 No significant disability despite symptoms; able to carry out all usual
duties and activities
2 Slight disability; unable to carry out all previous activities, but able to
look after own affairs without assistance
3 Moderate disability; requiring some help, but able to walk without
assistance
4 Moderately severe disability; unable to walk without assistance and
unable to attend to own bodily needs without assistance
5 Severe disability; bedridden, incontinent and requiring constant
nursing care and attention
6 Dead
25. Scoring systemScoring system
Glasgow Outcome ScoreGlasgow Outcome Score
1 Dead
2 Persistent vegetative state
Patient exhibits no obvious cortical function.
3 Severe Disability
(Conscious but disabled). Patient depends upon others for daily
support due to mental or physical disability or both
4 Moderate Disability
(Disabled but independent). Patient is independent as far as daily
life is concerned. The disabilities found include varying degrees of
dysphasia, hemiparesis, or ataxia, as well as intellectual and
memory deficits and personality changes.
5 Good Recovery
Resumption of normal activities even though there may be minor
neurological or psychological deficits.
26. Case seriesCase series
30 case series (4 prospective)30 case series (4 prospective)
Early mortality : mean 23% (range 7% to 60%) [18Early mortality : mean 23% (range 7% to 60%) [18
studies]studies]
Long termLong term mortality, ≥6 months to 3.4 yr : meanmortality, ≥6 months to 3.4 yr : mean
29.68% (15.7% to 49%)29.68% (15.7% to 49%) [19 studies][19 studies]
Barthel Index - mean 45 to 80 [9 studies]Barthel Index - mean 45 to 80 [9 studies]
mRS – no/ mild in 20%, moderate/severe in 50% (9mRS – no/ mild in 20%, moderate/severe in 50% (9
studies)studies)
GOS – similar to mRSGOS – similar to mRS
28. Comparative StudiesComparative Studies
Schwab et al – 63 pts, Early (<24 hr, b/4Schwab et al – 63 pts, Early (<24 hr, b/4
MLS) vs. Late (>24 h), early mortality wasMLS) vs. Late (>24 h), early mortality was
16%16%vs. 34.4% and BI 68.8 vs. 62vs. 34.4% and BI 68.8 vs. 62
Cho et al – 52 pts, (<6h vs. > 6 h vs.Cho et al – 52 pts, (<6h vs. > 6 h vs.
Medical), early mortality (Medical), early mortality (7.8%7.8% vs. 36.7%vs. 36.7%
vs. 80%), better BI (70)and GOS (4)vs. 80%), better BI (70)and GOS (4)
6 studies compared DH with medical Rx.6 studies compared DH with medical Rx.
Early mortality wasEarly mortality was 4.8%4.8% - 21% in DH- 21% in DH
whereas 42-83% in Medical groupswhereas 42-83% in Medical groups
29. Different outcomes in non-Different outcomes in non-
randomised studiesrandomised studies
AgeAge
Timing of surgery – before or after signsTiming of surgery – before or after signs
of brain herniationof brain herniation
Additional vascular territory involvementAdditional vascular territory involvement
30. Can we predict brain oedema?Can we predict brain oedema?
Kasner S et al, 2001Kasner S et al, 2001
Hypertension, heart failure, ↑ WBCHypertension, heart failure, ↑ WBC
CT - > 50% hypodensity and additionalCT - > 50% hypodensity and additional
vascular involvementvascular involvement
Hofmeijer J et al 2008Hofmeijer J et al 2008
Infarct size > 66%Infarct size > 66%
additional vascular involvementadditional vascular involvement
Thormalla G et al 2003Thormalla G et al 2003
Quantitative analysis of early DWI & PWIQuantitative analysis of early DWI & PWI
can predict MMCAIcan predict MMCAI
31. Systematic ReviewsSystematic Reviews
Cochrane (Morley N et al, 2002) – noCochrane (Morley N et al, 2002) – no
RCT evidence to support DH (reviewedRCT evidence to support DH (reviewed
non-randomised studies from 1971-2001)non-randomised studies from 1971-2001)
Hofmeijer J et al (CCM 2003; 31/2: 617-Hofmeijer J et al (CCM 2003; 31/2: 617-
25) - 2 large non-randomised studies25) - 2 large non-randomised studies
showed promising results in terms ofshowed promising results in terms of
reduction in mortality and functionalreduction in mortality and functional
outcomeoutcome
32. Juttler E et al (DESTINY) 2007,Juttler E et al (DESTINY) 2007,
Germany (RCT)Germany (RCT)
Age 18 to 60 years withAge 18 to 60 years with
clinical signs of MCA territoryclinical signs of MCA territory
infarctioninfarction
Severity - NIHSS >18 for (D)Severity - NIHSS >18 for (D)
and ≥ 20 for (ND) lesions,and ≥ 20 for (ND) lesions,
CT - ≥ 2/3 of MCA territory,CT - ≥ 2/3 of MCA territory,
Concious level - score ≥ 1 onConcious level - score ≥ 1 on
item 1a of NIHSSitem 1a of NIHSS
Timing -Timing - onset >12 hr and <onset >12 hr and <
36hr36hr, possibility to start, possibility to start
within 6 hr afterwithin 6 hr after
randomizationrandomization
Surgery (n=17) vs.Surgery (n=17) vs.
medical (n=15)medical (n=15)
Mean age: 43.2±9.7 vsMean age: 43.2±9.7 vs
46.1±8.446.1±8.4
Dominant side 53% vs.Dominant side 53% vs.
73%73%
Median NIHSS 21 vs.24Median NIHSS 21 vs.24
Time to surgery 24.4±6.9Time to surgery 24.4±6.9
hh
30 day survial : 88% vs.30 day survial : 88% vs.
47%47%
mRS 0-3: 47% vs. 27%mRS 0-3: 47% vs. 27%
33. Vahedi et al 2007 (DECIMAL),Vahedi et al 2007 (DECIMAL),
FranceFrance
Onset within 24 hrOnset within 24 hr
of malignant MCAof malignant MCA
infarct defined by –infarct defined by –
3 criteria:3 criteria:
NIHSS ≥ 16NIHSS ≥ 16
(including score ≥ 1(including score ≥ 1
on item 1a),on item 1a),
CT ischaemic signsCT ischaemic signs
> 50% of MCA> 50% of MCA
territory,territory,
Surgery (n=20) vs.Surgery (n=20) vs.
medical (n=18)medical (n=18)
Mean interval toMean interval to
surgery20.5 ± 8.3 (7-43)surgery20.5 ± 8.3 (7-43)
hrhr
Mean age 43.5 ± 9.7 vs.Mean age 43.5 ± 9.7 vs.
43.3 ± 7.1 yr43.3 ± 7.1 yr
28 day mortality: (25%)28 day mortality: (25%)
vs. (77.7%), p<0.0001vs. (77.7%), p<0.0001
mRS ≤ 3 at 12 months:mRS ≤ 3 at 12 months:
50% vs. 22.2% (NS)50% vs. 22.2% (NS)
mRS ≤ 4 at 12 months:mRS ≤ 4 at 12 months:
34. Hofmeijer et al 2009 [HAMLET] –Hofmeijer et al 2009 [HAMLET] –
NetherlandNetherland
Age 18 to 60 years withAge 18 to 60 years with
clinical signs of MCA territoryclinical signs of MCA territory
infactioninfaction
Severity - NIHSS >16 forSeverity - NIHSS >16 for
(ND) and ≥ 21 for (D)(ND) and ≥ 21 for (D)
lesions,lesions,
CT - ≥ 2/3 of MCA territory +CT - ≥ 2/3 of MCA territory +
formation of spaceformation of space
occupying oedemaoccupying oedema
Concious level - GCS ≤ 13Concious level - GCS ≤ 13
for (R) or ≤ 9 for (L)for (R) or ≤ 9 for (L)
Timing -Timing - onset < 96hronset < 96hr,,
possibility to start within 3 hrpossibility to start within 3 hr
after randomizationafter randomization
64 (DH vs.64 (DH vs.
Medical)Medical)
Age 50 vs. 47 yrAge 50 vs. 47 yr
Mean interval ofMean interval of
randomisation – 31randomisation – 31
hrhr
Mortality 21 vs.Mortality 21 vs.
59% (ARR 38%, p59% (ARR 38%, p
0.002)0.002)
mRS 4-6 - no diff
35. Pooled analysis of 3 RCTsPooled analysis of 3 RCTs
At 12 month Surgery Medical ARR
mRS > 3 35/58 – 60.3% 39/51 – 76% 16.3% (- 0.1- 33.1)
mRS > 4 19/58 – 32.7% 38/51 –
74.5%
41.9% (25.2 to 58.6)
Death 12/58 – 20.6% 36/51 –
70.5%
49.9% (33.9 to 65.9)
109 patients included (DESTINY+DECIMAL+ HAMLET)
Inclusion – within 45 hr (DH < 48 hr)
NNT
To prevent mRS > 3 at one year is 6
To prevent mRS > 4 at one year is 2
To prevent death at one year is 2
36.
37.
38.
39. Summary of EvidenceSummary of Evidence
Decompressive Hemicraniectomy ifDecompressive Hemicraniectomy if
performed early (< 48 hr) improve survivalperformed early (< 48 hr) improve survival
and functional outcome in patients (< 60and functional outcome in patients (< 60
yr) with malignant MCA infarction [RCTyr) with malignant MCA infarction [RCT
confirms the results of observationalconfirms the results of observational
study)study)
Level of evidence 1Level of evidence 1++
, Grade B, Grade B
Recommended by National ClinicalRecommended by National Clinical
Guideline for Stroke, 4.6.1.k, 3Guideline for Stroke, 4.6.1.k, 3rdrd
editionedition
July 2008July 2008
40. FutureFuture
Quality of life by SF36 and SIS, andQuality of life by SF36 and SIS, and
Aphasia by Aachen aphasia test at 2-3Aphasia by Aachen aphasia test at 2-3
year from DESTINY trial are stillyear from DESTINY trial are still
awaitedawaited
4 Ongoing trials4 Ongoing trials
HeaDDFIRSTHeaDDFIRST
HeMMIHeMMI
DEMITURDEMITUR
DESTINY 2DESTINY 2
Economic AssessmentEconomic Assessment
41. ConclusionConclusion
Malignant MCA syndrome should beMalignant MCA syndrome should be
consideredconsidered
For ICU oncall - If indicated,For ICU oncall - If indicated,
mechanical ventilation should bemechanical ventilation should be
offered in appropriate patients (age <offered in appropriate patients (age <
60 y, no significant comorbidity)60 y, no significant comorbidity)
Decompressive surgery is aggressiveDecompressive surgery is aggressive
but life saving and should be discussedbut life saving and should be discussed
with patient/ familywith patient/ family
Need s a hospital guideline agreed byNeed s a hospital guideline agreed by
42.
43. 1. Japanese guidelines for the management of severe
head injury (1st ed., 2000; 2nd ed. 2006)
“ DC may be done after the evacuation of intracranial
hematoma such as acute subdural hematoma and so
on (level III evidence).”
2. Japanese guidelines for the management of stroke
(2004)
① “DC in cerebellar infarction with brain stem
compression is recommended as level III evidence.”
② “DC in hemispheric infarction involved in MCA
territory is recommended as level IIa and III evidence.”
Operative Indications for DC
based on the guidelines in Japan
44. Early DC should be performed before the onset
of brain herniation to achieve satisfactory outcome
in patients with large infarction (Mori K, et al., 2004)
Early DC Delayed DC
Operative timing for DC
45. Surgical Technique for DC (4)
・ The autologous bone flap is sealed in a
sterilized
vinyl bag and stored in a deep freezer at -70℃.
・ Cranioplasty is performed 2 to 3 months after
DC. On the morning of cranioplasty, the bone
flap is allowed to remain at room temperature
and gently rinsed in sterile saline containing
antibiotics.
Autoclaving the bone flap has shown to denature
bone protein and impair vascularization and resorption
and therefore is not routinely performed.
46. Hydrocephalus with shunt valve
adjusted at 200 mmH2O
After bed-up 30°
Complications of DC
“sinking skin flap syndrome” and
paradoxical transtentorial herniation
Sinking skin flap syndrome
Midline shift & herniation
After bed rest
47. Surgical Technique for DC (5)
Recently, a variety of custom-made alloimplants,
(including polymerized polymethylmethacrylate
(PMM),
titanium mesh, ceramics and hydroxyapatite) are used
as a bone graft material, if the autologous bone
flap is out of use.
Custom-made polymerized PMM Custom-made titanium mesh
48. CT scans obtained before and after DC
Cerebral
infarction
SAH with
vasospasm
Acute subdural
hematoma
with internal
decompression
Intracerebral
hematoma
Preope
Postope
49. SummarySummary
DC improves ICP and brain tissueDC improves ICP and brain tissue
oxygenationoxygenation
DC likely to be more effective in youngDC likely to be more effective in young
and when done earlyand when done early
Lack of Class I evidence at presentLack of Class I evidence at present
Two big RCT’s on the wayTwo big RCT’s on the way
50. Study designStudy design
We retrospectively reviewed a series of 90We retrospectively reviewed a series of 90
patients who were operated upon forpatients who were operated upon for
Decompressive craniotomy with augmentedDecompressive craniotomy with augmented
duroplasty over a period of 3 year startingduroplasty over a period of 3 year starting
from June 2005 to June 2009. All patientsfrom June 2005 to June 2009. All patients
were admitted to the neurosurgerywere admitted to the neurosurgery
department, Alexandria University sufferingdepartment, Alexandria University suffering
from severe intracranial hypertension thatfrom severe intracranial hypertension that
was refractory to the all conventional anti-was refractory to the all conventional anti-
edema measures done at the intensive careedema measures done at the intensive care
unit.unit.
51. classificationclassification
Group (A) : resulting from traumatic brain injury .Group (A) : resulting from traumatic brain injury .
Group (B) : ischemic resulting from middleGroup (B) : ischemic resulting from middle
cerebral artery occlusion causing malignantcerebral artery occlusion causing malignant
infarction .infarction .
Group (C) : postoperative after excision of anGroup (C) : postoperative after excision of an
intra-axial temporal lobe tumor .intra-axial temporal lobe tumor .
Group (D) : suffering from spontaneousGroup (D) : suffering from spontaneous
intracerebral haematoma with surroundingintracerebral haematoma with surrounding
vasogenic edema..vasogenic edema..
52. ResultsResults
The study included 90 patients 57 of them were malesThe study included 90 patients 57 of them were males
while 33 were females, with a mean age of 47 yearswhile 33 were females, with a mean age of 47 years
(range, 18-66 years), underwent DC. Mean preoperative(range, 18-66 years), underwent DC. Mean preoperative
GCS score was 7/15 (range, 3-8/15),GCS score was 7/15 (range, 3-8/15),
Unilateral dilated un-reactive pupil was seen in 18 casesUnilateral dilated un-reactive pupil was seen in 18 cases
and bilateral variants in 6 cases. All patients received aand bilateral variants in 6 cases. All patients received a
wide DC with duroplasty. Median preoperative time waswide DC with duroplasty. Median preoperative time was
8 hours from the time of trauma. The patients’ outcome8 hours from the time of trauma. The patients’ outcome
was evaluated by using the GOS. Furthermore, thewas evaluated by using the GOS. Furthermore, the
results were analyzed toward the time of surgicalresults were analyzed toward the time of surgical
intervention (early or late), the patient’s age, and theintervention (early or late), the patient’s age, and the
preoperative GCS using a multivariate analysis.preoperative GCS using a multivariate analysis.
53. ConclusionsConclusions
The encouraging results of our study asThe encouraging results of our study as
well as those of recent published reportswell as those of recent published reports
emphasize the importance of thisemphasize the importance of this
procedure in changing and improving theprocedure in changing and improving the
Glasgow coma score of the patients. ItGlasgow coma score of the patients. It
was observed that the early the surgicalwas observed that the early the surgical
intervention was the better the outcome ofintervention was the better the outcome of
patients. Decompressive craniotomypatients. Decompressive craniotomy
showed minor complications in unilateralshowed minor complications in unilateral
temporal lobe edema.temporal lobe edema.
54. ConclusionsConclusions
Decompressive craniectomy (DC) is
an effective treatment, able to reduce
mortality
improve neurological outcome in
patients with massive brain swelling.
However, there is still a lack of
randomized trials showing the effects
of DC.
55. ii)) Do you do bifrontal craniectomy or bifrontoDo you do bifrontal craniectomy or bifronto--temporaltemporal
craniectomycraniectomy
We perform decompressive craniectomy (DC) accordingWe perform decompressive craniectomy (DC) according
with the morphology of the brain edema.Bifrontotemporalwith the morphology of the brain edema.Bifrontotemporal
ii) do you divide the sagittal sinus anteriorly? You youii) do you divide the sagittal sinus anteriorly? You you
divide the falx? how do you divide the falx? YES , it givesdivide the falx? how do you divide the falx? YES , it gives
adequated decomptression of the frontal lobes bur avoidadequated decomptression of the frontal lobes bur avoid
venous injury as it leads to hemorrhagic lesion .venous injury as it leads to hemorrhagic lesion .
iii) do you open the frontal sinus and remove theiii) do you open the frontal sinus and remove the
posterior wall of the frontal sinus?posterior wall of the frontal sinus?
If the anatomy of frontal sinus is wide, YES. And weIf the anatomy of frontal sinus is wide, YES. And we
taponade the nasal ostium with temporal muscletaponade the nasal ostium with temporal muscle
56. iviv)) do you leave the bone over the sagittal sinus intact?do you leave the bone over the sagittal sinus intact?
NO . i remove all the boneNO . i remove all the bone
A special consideration is taken with the borders of theA special consideration is taken with the borders of the
craniectomy, that must be drilled to become angledcraniectomy, that must be drilled to become angled
(app.45º ), to impede a cutting pressure over the draining(app.45º ), to impede a cutting pressure over the draining
veins.And when we go to the media fossa, we reach theveins.And when we go to the media fossa, we reach the
skull base.skull base.
v) do you monitor ICP in patients who had craniectomy?v) do you monitor ICP in patients who had craniectomy?
if so do you use a parenchymal probe or subduralif so do you use a parenchymal probe or subdural
catéter. YES. i suse parenchymal sensor ..catéter. YES. i suse parenchymal sensor ..
vi) do you do duroplasty-YES. With artificial duravi) do you do duroplasty-YES. With artificial dura
vii) do you leave a silastic sheet between the brain andvii) do you leave a silastic sheet between the brain and
the scalp/temporalis muscle.NO.the scalp/temporalis muscle.NO.
57. ii)) Do you do bifrontal craniectomy or bifrontoDo you do bifrontal craniectomy or bifronto--temporaltemporal
craniectomycraniectomy
ii) do you divide the sagittal sinus anteriorly? You youii) do you divide the sagittal sinus anteriorly? You you
divide the falx? how do you divide the falx?divide the falx? how do you divide the falx?
iii) do you open the frontal sinus and remove theiii) do you open the frontal sinus and remove the
posterior wall of the frontal sinus?posterior wall of the frontal sinus?
iv) do you leave the bone over the sagittal sinus intact?iv) do you leave the bone over the sagittal sinus intact?
58. vv)) do you monitor ICP in patients who haddo you monitor ICP in patients who had
craniectomy? if so do you use acraniectomy? if so do you use a
parenchymal probe or subdural catheterparenchymal probe or subdural catheter
vi) do you do duroplastyvi) do you do duroplasty
vii) do you leave a sialastic sheet betweenvii) do you leave a sialastic sheet between
the brain and the scalp/temporalis musclethe brain and the scalp/temporalis muscle
59. Comparison of the effect ofComparison of the effect of
decompressive craniectomy on differentdecompressive craniectomy on different
neurosurgical diseasesneurosurgical diseases
60. However, there are no reports in the literature thatHowever, there are no reports in the literature that
compare the effect of decompressive craniectomy oncompare the effect of decompressive craniectomy on
different neurosurgical diseases.different neurosurgical diseases.
Therefore, the authors performed decompressiveTherefore, the authors performed decompressive
craniectomy with dural expansions in severe traumaticcraniectomy with dural expansions in severe traumatic
bran injury (TBI), massive intracerebral haemorrhagebran injury (TBI), massive intracerebral haemorrhage
(ICH) and major infarction (MI) patients following the(ICH) and major infarction (MI) patients following the
same indications for the surgery. The patient outcomessame indications for the surgery. The patient outcomes
in terms of mortality andin terms of mortality and
Glasgow Outcome Scale (GOS) as well as the ventricularGlasgow Outcome Scale (GOS) as well as the ventricular
pressure changes during the decompressive craniectomypressure changes during the decompressive craniectomy
were compared between the different disease groupswere compared between the different disease groups..
61. Indications for surgeryIndications for surgery
The indications for decompressive craniectomyThe indications for decompressive craniectomy
with dural expansion werewith dural expansion were
(1) the appearance of definite unilateral or(1) the appearance of definite unilateral or
bilateral brain swelling on the CT scan e.g.bilateral brain swelling on the CT scan e.g.
midline shift of more than 6 mm and/ormidline shift of more than 6 mm and/or
obliteration of the cisternal structures on theobliteration of the cisternal structures on the
CT scan and/or aCT scan and/or a
(2) patients with an initial Glasgow Coma(2) patients with an initial Glasgow Coma
Scale (GCS) score of less than 8 or worseningScale (GCS) score of less than 8 or worsening
of the neurological status (GCS score less thanof the neurological status (GCS score less than
8).8).
62. Patients with primary fatal brainstem failure, asPatients with primary fatal brainstem failure, as
indicated by a GCS score of 3 and had noindicated by a GCS score of 3 and had no
spontaneous respiration did not undergospontaneous respiration did not undergo
surgical intervention. Thesurgical intervention. The
differential indication for either adifferential indication for either a
hemicraniectomy or bilateral decompressionhemicraniectomy or bilateral decompression
where decided. Unilateral oedema/swelling andwhere decided. Unilateral oedema/swelling and
opening ventricular pressure less than 25opening ventricular pressure less than 25
mmHg were treated by hemicraniectomy overmmHg were treated by hemicraniectomy over
the swollen hemisphere, whereas bilateralthe swollen hemisphere, whereas bilateral
diffuse oedema/swelling or opening ventriculardiffuse oedema/swelling or opening ventricular
63. . If the neurological status was were. If the neurological status was were
better than our surgical indications, otherbetter than our surgical indications, other
medical treatments such as intravenous ormedical treatments such as intravenous or
intraarterial thrombolysis wereintraarterial thrombolysis were
administered before consideringadministered before considering
decompression surgery.decompression surgery.
64. bilateral decompression was performed using largebilateral decompression was performed using large
bicoronal skin flaps. The skin flaps were placed justbicoronal skin flaps. The skin flaps were placed just
behind the parietal eminence, extending inferiorly tobehind the parietal eminence, extending inferiorly to
the zygoma on both sides and curving anteriorlythe zygoma on both sides and curving anteriorly
towards the midline. This was reflected subperiosteallytowards the midline. This was reflected subperiosteally
to the level of the supraorbital ridges.to the level of the supraorbital ridges.
The reference points used for the bone flaps were atThe reference points used for the bone flaps were at
the pterion of frontal bone, the parietal eminence andthe pterion of frontal bone, the parietal eminence and
in the temporal squamous areas.in the temporal squamous areas.
A frontal median segment of the bone, measuringA frontal median segment of the bone, measuring
about 3 to 4 cm in width along the sagittal sinus, wasabout 3 to 4 cm in width along the sagittal sinus, was
saved to avoid damage to the sagittal sinus and tosaved to avoid damage to the sagittal sinus and to
serve as a framework for later cranioplasty. Additionalserve as a framework for later cranioplasty. Additional
bone was removed at the temporal region to the floorbone was removed at the temporal region to the floor
65. Ten or fifteen minutes after completion ofTen or fifteen minutes after completion of
the craniectomy, the ventricular pressurethe craniectomy, the ventricular pressure
became stabilised. The dura was thenbecame stabilised. The dura was then
opened with a large cruciated or curved Z-opened with a large cruciated or curved Z-
shaped incision, in the areas involving theshaped incision, in the areas involving the
frontal, temporal and parietal lobes. Whenfrontal, temporal and parietal lobes. When
the dura was opened, the underlying brainthe dura was opened, the underlying brain
orhaematoma typically herniatedorhaematoma typically herniated
outwards..outwards..
66. In MI patients, cortical resection was notIn MI patients, cortical resection was not
performed. In TBI patients, the epidural orperformed. In TBI patients, the epidural or
subdural haematoma was removed butsubdural haematoma was removed but
haematoma mixed with contused brainhaematoma mixed with contused brain
parenchyma was not evacuated. In allparenchyma was not evacuated. In all
patients, artificial durapatients, artificial dura was placedwas placed
underneath the incised dura, and securedunderneath the incised dura, and secured
with several sutures to allow the brain towith several sutures to allow the brain to
herniated outward in a more controlledherniated outward in a more controlled
manner, and to prevent cortical adhesion.manner, and to prevent cortical adhesion.
After insertion of an ICP sensor at theAfter insertion of an ICP sensor at the
posterior temporal bone margin forposterior temporal bone margin for
67. Thin large gelfoam (less than 5 mmThin large gelfoam (less than 5 mm
thickness and 4×5 cm size) pieces werethickness and 4×5 cm size) pieces were
placed between the dura and muscle layerplaced between the dura and muscle layer
for postoperative bleeding control andfor postoperative bleeding control and
prevention of adherence between the duraprevention of adherence between the dura
and temporalis muscle. This gel-foamand temporalis muscle. This gel-foam
layer facilitated the dissection plane for thelayer facilitated the dissection plane for the
cranioplasty to be performed later.cranioplasty to be performed later.
68.
69. If the ventricular pressure exceeded 30If the ventricular pressure exceeded 30
mmHg more than 2 h, regardless ofmmHg more than 2 h, regardless of
previous mentioned medical therapy, mildprevious mentioned medical therapy, mild
hypothermia (rectal temperature, 32–hypothermia (rectal temperature, 32–
34°C) a cold blanket and/or barbiturate34°C) a cold blanket and/or barbiturate
coma therapy were initiated.coma therapy were initiated.
..
70. The bone flap was usually reimplanted 1–3The bone flap was usually reimplanted 1–3
monthsmonths
after the craniectomy, having been storedafter the craniectomy, having been stored
under sterile conditions at −70°C (Fig. 3).under sterile conditions at −70°C (Fig. 3).
A ventriculo-peritoneal shunt wasA ventriculo-peritoneal shunt was
performed if the diagnosis ofperformed if the diagnosis of
hydrocephalus was confirmedhydrocephalus was confirmed
71. Neurological outcomeNeurological outcome
The pre-operative clinical condition according toThe pre-operative clinical condition according to
GCS wasGCS was
similar in all study groups. The clinical outcomessimilar in all study groups. The clinical outcomes
werewere
evaluated at 6 months after the decompressiveevaluated at 6 months after the decompressive
surgery bysurgery by
other neurosurgeons who had no informationother neurosurgeons who had no information
about theabout the
patients. Mortality was 21.4% in TBI, 25% in ICHpatients. Mortality was 21.4% in TBI, 25% in ICH
andand
60.9% in the MI group. A favourable outcome of60.9% in the MI group. A favourable outcome of
GOS 4–5GOS 4–5
72. Decompressive craniectomy with duraDecompressive craniectomy with dura
expansion involves removing a definedexpansion involves removing a defined
portion of the skull with loose closure ofportion of the skull with loose closure of
the dura and skin layers. The surgery isthe dura and skin layers. The surgery is
intended to increase the volume of theintended to increase the volume of the
space available for expansion ofspace available for expansion of
oedematous brain tissue and therebyoedematous brain tissue and thereby
increase compliance which will result in aincrease compliance which will result in a
shift to the right of the pressure-volumeshift to the right of the pressure-volume
curve . This results in effective lowering ofcurve . This results in effective lowering of
73. Early reports of craniectomy, performed asEarly reports of craniectomy, performed as
a salvagea salvage
procedure for the relief of increased ICPprocedure for the relief of increased ICP
after TBI, were not promising [9, 27].after TBI, were not promising [9, 27].
According to the Traumatic Coma DataAccording to the Traumatic Coma Data
Bank (TCDB) study, patients with a GCSBank (TCDB) study, patients with a GCS
score of 8 or less on admission have anscore of 8 or less on admission have an
overall mortality of 33%, with 14% in theoverall mortality of 33%, with 14% in the
vegetative state, and only 7% achieving avegetative state, and only 7% achieving a
good outcome [10, 11, 16, 37].good outcome [10, 11, 16, 37].
74. Recent studies have reported an improvedRecent studies have reported an improved
outcome usingoutcome using
decompressive craniectomy after thedecompressive craniectomy after the
development of refractory intracranialdevelopment of refractory intracranial
hypertension. One to two thirds of the survivinghypertension. One to two thirds of the surviving
patients have been reported to have apatients have been reported to have a
favourable outcome and the mortality has beenfavourable outcome and the mortality has been
reported as less than 20% .reported as less than 20% .
In our study, decompressive craniectomy wasIn our study, decompressive craniectomy was
performed as the first treatment, if the patientsperformed as the first treatment, if the patients