1) A 5-year-old child presented with fever, lethargy, and posturing for 3 days and was brought to the hospital in a comatose state.
2) The document discusses terminology related to altered states of consciousness, various etiologies of coma including infectious, structural, metabolic and toxic causes, and provides details on the pathophysiology of coma and consciousness.
3) It outlines the approach to managing a comatose patient, including rapid assessment, stabilization, detailed history and examination with focus on neurological assessment, appropriate investigations and treatment.
Pediatric Coma
Introduction
Disorders of Consciousness
Coma Mimics
Etiologies
Evaluation
Brainstem Reflexes
Pediatric Glasgow Coma Scale
Management
Coma Sequelae
Pediatric Coma
Introduction
Disorders of Consciousness
Coma Mimics
Etiologies
Evaluation
Brainstem Reflexes
Pediatric Glasgow Coma Scale
Management
Coma Sequelae
ABSTRACT:
Nocturnal enuresis or night time urinary incontinence, commonly called bedwetting or sleep wetting, is involuntary urination while asleep after the age at which bladder control usually occurs. Bedwetting is a common childhood urologic complaint and one of the most common pediatric health issues. Enuresis is notoriously difficult to treat and is frequently related to psychological factors. The emotional impact of enuresis on a child and family is considerable. Children with enuresis are commonly punished and are at risk for emotional and physical abuse. Numerous studies of children with enuresis report feelings of embarrassment and anxiety, loss of self-esteem, and effects on self-perception, interpersonal relationships, quality of life, and school performance. The condition can be successfully treated with homoeopathic medicines but require a long term follow – up. The present article focuses on management of this medical condition with our medicines.
Consciousness consists of awareness of one’s surrounding and responsiveness to external stimulation and inner need.
A normal level of consciousness (wakefulness) depends upon activation of the cerebral hemispheres and by neurons located in the brainstem reticular activating system (RAS).
Both components and the connections between them must be preserved for consciousness to be maintained
Unconsciousness implies that is a stage of depressed cerebral function that result impairment in response to sensory stimuli; abnormal loss of awareness of self & surroundings.
common problem faced by medical faternity .
It is a systemic effort made to assess a case and identify sinister signs of illness. draw an outline of management
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
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
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.
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.
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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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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!
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
2. • A 5 year old child was brought with history of
fever, progressive lethargy and posturing for 3
days . He had been vomiting several times
since morning. His temperature was 40
degree celsius.
• how will you manage this patient?
5. Impairment of consciousness
states
• Impairment of consciousness with activated
mental state
• Impairment of consciousness with reduced
mental state
• Impairment of consciousness along the
continuum of coma–vegetative state–
minimally conscious state.
6. Impairment of consciousness with
activated mental state
• Confusion: state of impaired ability to think
and reason clearly, resulting in difficulty with
orientation, simple cognitive processing, and
acquisition of new memory.
• Delirium is an activated mental state that may
include disorientation, irritability, fearful-
responses, and sensory misperception.
Patients may be hyperactive and have signs of
increased sympathetic tone.
7. Impairment of consciousness with
reduced mental state
• Drowsiness
• Obtundation arousal is present to stimuli
• Stupor
State Stimulus needed for arousal
Drowsiness Verbal and light touch
Obtundation Deep touch
Stupor Vigorous, painful, or noxious
stimulation
8. • Coma is a “state of deep, unarousable,
sustained pathologic unconsciousness with
the eyes closed that results from dysfunction
of the ascending reticular-activating system in
the brainstem or in both cerebral
hemispheres”
• Patients in coma lack both wakefulness and
awareness.
13. Etiology -cont
C. Nutritional
Thiamine deficiency
Niacin or nicotinic acid
deficiency
Pyridoxine dependency
Folate and B12 deficiency
D. Exogenous Toxins and
Poisons
Alcohol intoxication
Over-the-counter
medications
Prescription medications
(oral and ophthalmic)
Herbal treatments
Heavy-metal poisoning
Mushroom and plant
intoxication
Illegal drugs
Industrial agents
E. Hypertensive
Encephalopathy
F. Burn Encephalopathy
14. PATHOPHYSIOLOGY OF COMA
• Consciousness has two dimensions –
wakefulness and awareness.
• Integral Consciousness requires an intact -
1) RAS
2) Cerebral hemispheres,
3) Healthy projections between the two
systems.
15. ANATOMY AND PHYSIOLOGY - CONSCIOUSNESS
Function Site
Awake – RAS
(Reticular Activating
System)
•Rostral brainstem (midbrain
and upper pontine tegmentum)
to the lower thalamus .
•The hypothalamus.
Awareness
(a higher cognitive
function) =
cognition + affect
Cerebral
hemispheres.
17. • Coma with focal signs
Intracranial hemorrhage
Stroke: arterial ischemic or sinovenous thrombosis
Tumors
Focal infections: brain abscess
Post seizure state: Todd’ paralysis
Acute disseminated encephalomylelitis
18. • Coma without focal signs and with meningeal
irritation:
Meningitis
Encephalitis
Subarachnoid hemorrhage
• Coma without focal signs and without
meningial irritation:
Hypoxic-ischemia: cardiac or pulmonary failure,
shock, near drowning.
20. • Post infectious disorders:
ADEM
Hemorrhagic shock and encephalopathy syndrome
• Post immunisation encephalopathy
Whole cell pertusis vaccine
• Drugs and toxins
• Cerebral malaria
• Rickettsial : lyme disease, rocky mountain spotted
fever
• Hypertensive encephalopathy
• Post seizure states
• Non-convulsive status epilepticus
21. The goals of coma therapy
(a) Adhere to the principles of neuroresuscitation, the A,
B, and Cs
(b) Immediately identify signs of intracranial pathology:
herniation, increased intracranial pressure (ICP), or a
focal neurologic signs, head trauma.
(c) Identify and specifically treat the underlying cause.
(d) Determine prognosis.
(e) Plan appropriate long-term therapy.
22.
23. Rapid assessment and stabilization
• Establish and maintain airway: intubate if
GCS<= 8 ,impaired airway reflexes, abnormal
breathing pattern, signs of raised ICT, oxygen
saturation<92% despite high flow oxygen,
fluid refractory shock.
• Circulation: establish IV access, take samples
(serum electrolytes), fluid bolus if in
circulatory failure (20ml/kg NS), inotropes if
required
• Blood glucose : regent strip testing , if
<50mg/dl give 10% D 2ml/kg.
24. • Identify signs of cerebral herniation or raised
ICT: ( if GCS<8,abnormal pupil size and
reaction, absent dolls eye
movements,abnormal tone or posturing,
hypertension with brdycardia, abnormal
respiratory pattern) Must act immediately
(Elevate the Head end of bed 30 degrees,
short term Hyperventilation, 20% Mannitol
(0.5-1g/kg) or 3% NaCl(if in shock).
25. • If there are seizures: give IV lorazepam
0.1-0.2mg/kg , then phenytoin 20mg/kg
loading.
• Immobilisation of cervical spine in suspected
cases of traumatic coma.
• Manage hypo/hyperthermia accordingly.
26. History ,physical examination and
neurological assesment
• History: age
Infant Child Adolescent
CNS infection
(meningitis,encephalitis)
Ingestion Drug/Alcohol overdose
Systemic infection with shock CNS infection Intentional poisoning
Metabolic disorders Seizure Trauma, seizures
Abuse / Trauma, Abuse / Trauma CNS infection,
Inborn errors of
metabolism,seizures
DKA, Rey’s
syndrome
DKA, , Rey’s syndrome
Post immunisation
encephalopathy, hemorrhagic
shock and encephalopathy
syndrome ,
27. Approach: History
• Onset :
– Sudden onset: vascular catastrophy or a
convulsion
– Acute onset in normal child: ingestion of drug,
toxin, poison.
– Gradual onset : infectious process, metabolic
derangement.
35. Clues to etiology of coma in general examination
Look for if present ,think of
Pallor Cerebral malaria, intracranial bleed, hemolytic uremic
syndrome
Icterus Hepatic encephalopathy, leptospirosis, complicated malaria
Rashes Meningococcemia, dengue , measles, rickettsial diseases,
arboviral diseases
Petechiae Dengue, meningococcemia , hemorrhagic fevers
Head and scalp
hematomas
Traumatic/ non accidental injury
Dysmorphism,
neurocutaneusmarkers
Possibility of seizures
Abnormal odour DKA, hepatic coma
36. Rapid neurogical assesment
• The goal of neurologic examination are:
To determine depth of coma.
To localise the process leading to coma.
• Includes
Level of consciousness
Pupillary responses
Eye movements(spontaneous or induced)
Motor response
Respiratory pattern
37. A.Level of conciousness
• The level of conciousness must be recorded
in the form of an objective scale.
• The Glasgow coma scale is a useful tool for the
grading of the degree of altered consciousness
and the severity of CNS insult.
• Glasgow coma scale is used for adults and
older children and its modification is used in
infants and young children.
38. Glasgow coma scale
ACTIVITY
BEST RESPONSE
Adults/Older Children Infants ( modified GCS ) Score
Eye Opening
( E )
1. Spontaneous
2. To speech
3. To pain
4. None
1. Spontaneous
2. To speech
3. To pain
4. None
4
3
2
1
Verbal
( V )
1. Appropriate speech
2. Confused speech
3. Inappropriate words
4. Incomprehensible or
none specific sounds
5. None
1. Coos, babbles
2. Irritable, cries but
consolable
3. Cries, inconsolable
4. Moans to pain
5. None
5
4
3
2
1
Motor
( M )
1.Obeys commands
2.Localizes pain
3.Withdraws to pain
4.Decorticate to pain
5.Decerebrate to pain
1. Normal spontaneous
movement
2. Withdraws to touch
3. Withdraws to pain
4. Decorticate to pain
5. Decerebrate to pain
6
5
4
3
2
39. Significance of Glasgow coma scores:
• Diagnosis of different grades of altered
consciousness.
• Coma is defined as: No eye opening (1), No
recognizable words uttered (2 ), Not obeying
commands (5), ie, score = 8 or less.
• Fall of GCS of 2 or more – Indicates deterioration and
need of active intervention
• Prediction of prognosis of comatose child:
– GCS >8: Good chances of recovery
– GCS 3-5: Fatal brain damage
40. B. Size and reactivity of pupils
Pupils Lesion/Dysfunction
Pinpoint Pons, opiates, cholinergic intoxication
Mid position –
fixed or irregular
Midbrain lesion
Unilateral , dilated
and fixed
Uncal herniation
Bilateral , dilated
and fixed
Diffuse damage, central herniation, global
hypoxia ischemia, barbiturates, atropine
41.
42. C. Eye movements
• Oculocephalic or Doll’s eye response: Shows Intact
Brainstem.
• Oculovestibular response: Lost in pontine lesions,
labyrinthitis, Sedatives, Phenytoin induced coma
• Both lost but intact pupillary reflexes present in
metabolic encephalopathy
• Stimulation of cortical centre for gaze e.g. seizure focus
→ conjugate deviation of eye to contralateral side
• Destructive lesion at gaze centre → conjugate deviation
of eye to same side .
• Neuropthalmolgic examination is incomplete without
fundus examination.
43. D. Motor response
• Single best indicator of the depth and severity
of coma
1. Spontaneous movements.
2. Tone and reflexes
3. Induced movements.
44. Motor responses to noxious stimuli. A, Localization of pain
as patient attempts to remove stimulus. B, Decorticate posturing. C,
Decerebrate posturing. D, Flaccid patient with no response.
45. • Decorticate posturing with flexion of the
upper extremities and extension of the lower
extremities suggests involvement of the
cerebral cortex and preservation of brainstem
function.
• Decerebrate posturing with rigid extension of
the arms and legs is indicative of cortical and
brainstem damage.
• The flaccid patient with no response to
painful stimuli has the gravest prognosis with
injury sustained to deep brainstem lesions.
46. E. Respiratory pattern
• Patient breathing pattern is also helpful in
localising area of CNS dysfunction. They are :
• Cheyne-Stokes respiration.
• Central neurogenic hyperventilation.
• Apneustic breathing.
• Cluster breathing.
• Ataxic breathing.
48. Herniation syndromes
• Brain tissue deforms intracranially and moves from
higher to low pressure when there is asymmetric,
unilateral or generalised increase in intracranial
pressure.
• Signs of cerebral herniation
1. Glasgow coma score <8
2. Abnormal pupil size and reaction (unilateral or bilateral)
3. Absent doll’s eye movements
4. Abnormal tone (decerebrate/decorticate posturing,
flaccidity)
5. Hypertension with bradycardia
6. Respiratory abnormalities (hyperventilation, Cheyne-
Stokes breathing, apnea, respiratory arrest)
7. Papilledema
49.
50. • In transtentorial or central herniation, the
diencephalon is displaced through the notch
of the tentorium cerebelli into the posterior
fossa, with progressive rostral - caudal
compression and ischemia of the brainstem.
• In Uncal herniation, medial displacement of
the uncus compresses upon the oculomotor
nerve leading to unilateral dilated fixed pupil
with ptosis.
51. Central vs uncal herniation
Central uncal
•Arousal
•Breathing
•Pupils
•Oculocephalic
responses
•Motor signs
•Impaired early, before other signs
•Sighs , yawns, sometimes
Cheyne-Stokes respirations
•First , small reactive (hypothalamus),
then one or both approach midposition
•Initially sluggish, later tonic conjugate
Early hemiparesis opposite to hemispheric
lesion followed late by ipsilateral motor
paresis and extensor plantar response
•Impaired late, usually with
other signs
•No early change
•Ipsilateral pupil dilates,
followed by somatic third
nerve paralysis
•Unilateral third nerve
paralysis
•Motor signs late, sometimes
ipsilateral to lesion
52. Metabolic vs structural coma
METABOLIC, TOXIC,
INFECTIOUS CAUSES
• Confusion or stupor
precede motor signs
• Pupillary reactions
preserved
• Symmetrical motor
responses
• Asterixis, myoclonus
• Hyper or hypoventilation
STRUCTURAL
• Supratentorial destructive
or mass lesions:
Initial focal signs
Rostral to caudal progression
• Infratentorial destructive or
mass lesions:
Preceding brainstem dysfunction
Sudden onset of coma
Cranial nerve palsies
Early respiratory disturbances
53. Investigations
1. neuroimaging:
• CT scan:Any comatose child or infant in whom
the neurological findings suggest a structural
lesion or in whom the clinical diagnosis is evasive,
done after stabilistion of a patient.
• Magnetic Resonance Imaging (MRI) of brain is
valuable in identifying evidence of herpes simplex
encephalitis or an acute demyelinating process,
such as acute disseminated encephalomyelitis.
62. SPECIFIC THERAPY
• Acute febrile encephalopathy:
In sick children with Acute febrile
encephalopathy, empirical therapy with
antibiotics, acyclovir, antimalarials should be
considered while awaiting for reports.
63. Specific therapy-Acute febrile encephalopathy:
• Empiric antibiotic therapy: IV ceftriaxone+
amikacin
• Acyclovir - in sporadic meningo-encephalitis
with or without: focal neurological
findings,behaviour changes, aphasia, suggestive
CT(frontotemporal changes), hemorrhagic CSF.
• Antimalarials: (quinine/artesunate)- smear
positive, rapid tests positive , empiric treatment if
short history(<48 hours),P.falciparum endemic
area, absent meningial signs,anemia,
hypoglycemia,retinal hemorrhages.
64. Specific therapy
• Treat dyselectrolytemia and acid-base imbalance
• Space occupying lesions require prompt
neurosurgical management.
• Antihypertensives for hypertensive
encephalopathy.
• Hepatic encephalopathy – Lactulose, systemic
antibiotics, vitamins, protein restriction
• Medical management and Dialysis for ARF, CRF
• Poisoning – Gastric lavage, Antidotes
65. prognosis
• The prognosis for recovery from coma depends
primarily on the cause, rather than on the depth
of coma.
• Coma from drug intoxication and metabolic
causes carry the best prognosis.
• Prolonged coma after a global hypoxic ischemic
insult carries a poor prognosis.
• Infectious encephalopathies have a good
outcome with mild or moderate difficulties only.
• Children who survive traumatic injury have a
better prognosis than children who suffer a global
hypoxic-ischemic injury
66. appropriate long-term therapy
• Early rehabilitation, by a team comprising
doctors, teachers, physiotherapist, occupational
and speech therapist and a psychologist is often
very much rewarding.
• It is essential to test hearing early, particularly
after meningitis.
• Many children, who had seizures acutely, do not
develop epilepsy at follow up and may be
weaned off from their anticonvulsants after three
to six months.
71. Alert: Fully conscious
Lethargic: appear somnolent, but may be able to maintain
arousal
Obtunded: requires touch or voice to maintain arousal
Stuporous: unresponsiveness from which the individual can
be aroused only by painful stimulus
Comatose: State in which the patient is unable to arouse or
respond to noxious stimuli and is completely unaware of self
and surroundings
Levels of Consciousness:
72. • Minimally Conscious State
“a condition of severely altered consciousness
in which the person demonstrates minimal
but definite behavioral evidence of self or
environmental awareness”
73. • Vegetative State
“condition of complete unawareness of the
self and the environment, accompanied by
sleep–wake cycles with either complete or
partial preservation of hypothalamic and
brainstem autonomic functions”
74. Severe Disorders of Consciousness
Condition Self-
Awareness
Pain and
Suffering
Sleep–
Wake
Cycles
Motor Function Respiratory
Function
Coma Absent No Absent No purposeful
movement
Variably
depressed
Vegetative
state
Absent No Intact No purposeful
movement
Normal
Minimally
conscious
State
Very
limited
Yes Intact Severe limitation
of movement
Variably
depressed
75. Causes of Coma
• T Trauma, head injury Shaken baby syndrome: non-specific
history, retinal hemorrhages.
• I Intussusception Mental status changes may precede
abdominal finding
Insulin, Hypoglycemia
Inborn errors of metabolism
• P Psychogenic Common in adolescents
• S Seizures Postictal states, non-convulsive status may
masquerade as undifferentiated coma.
Shock, stroke Coma secondary to poor brain perfusion,
arterial and venous infarcts
Shunt Blocked or infected ventriculo-peritoneal
shunts
76. • A Alcohol ingestion, abuse
• E Electrolytes Disturbances of sodium, calcium,
magnesium
Encephalopathy Hypertensive, Reye syndrome, hepatic
failure, urea cycle defects, lead
encephalopathy
• I Infections Encephalitis, meningitis, malaria
• O Overdose, ingestion Consider with unexplained loss of
consciousness
• U Uremic encephalopathy
77.
78. Apneustic breathing:
• Lesion: Lower pons
• Characterized by inspiratory pause, lasting for 2-
3 sec, often alternating with end expiratory
pauses.
• Pontine infarctions
Anoxic encephalopathy
Central neurogenic hyperventliation:
• Lesion: Mid brain
79. Kussumaul’s breathing:
• Diabetic ketoacidosis
Uremia
• Characterized by rapid, deep respiration
Biot’s breathing:
• Fast & deep respirations with apnoea in between
Ataxic breathing:
• Lesion: Medulla
• Inco-ordination in breathing