This document discusses neurological disorders, specifically focusing on convulsions disorders/seizure disorders/epilepsy. It defines epilepsy as recurrent episodes of cerebral origin involving disturbances of movement, sensation, behavior and consciousness. Various causes of epilepsy are described, including perinatal conditions, infections, metabolic conditions, poisoning, and genetic/hereditary syndromes. The document then classifies epilepsy and outlines the clinical features, diagnostic evaluation, and management including drug therapy, diet therapy, and surgery. Meningitis is also discussed, describing the causes, risk factors, pathophysiology, types (bacterial, viral, tuberculosis), clinical features, diagnostic evaluation, and treatment of various forms of meningitis.
Hydrocephalus
introduction
Hydrocephalus, also known years ago as “water on the brain”, is a condition where the circulation system of the body’s cerebrospinal fluid (CSF) is not functioning properly. The CSF accumulates in the brain and causes intracranial pressure. A shunt is usually placed to equalize the flow of CSF, which requires surgery. The diagnosis and surgery can be very frightening for the parents as well as the child
definition
Hydrocephalus is a condition characterized by an excess of cerebrospinal fluid (CSF) within the ventricular and subarachnoid spaces of the cranial cavity
INCIDENCE
It is found in 1-3 of every 1000 born children in world wide
Classification
Non communicating. In the non communicating type of congenital hydrocephalus, an obstruction occurs in the free circulation of CSF.
Communicating. In the communicating type of hydrocephalus, no obstruction of the free flow of the CSF exists between the ventricles and the spinal theca; rather, the condition is caused by defective absorption of CSF, thus causing increased pressure on the brain or spinal cord.
CAUSES
Obstruction. The most common problem is a partial obstruction of the normal flow of CSF, either from one ventricle to another or from the ventricles to other spaces around the brain.
Poor absorption. Less common is a problem with the mechanisms that enable the blood vessels to absorb CSF; this is often related to inflammation of brain tissues from disease or injury.
Overproduction. Rarely, the mechanisms for producing CSF create more than normal and more quickly than it can be absorbed.
PATHOPHYSIOLOGY
CLINICAL MANIFESTATION
Poor feeding. The infant with hydrocephalus has trouble in feeding due to the difficulty of his condition.
Large head. An excessively large head at birth is suggestive of hydrocephalus.
Bulging of the anterior fontanelles. The anterior fontanelle becomes tense and bulging, the skull enlarges in all diameters, and the scalp becomes shiny and its veins dilate.
Setting sun sign. If pressure continues to increase without intervention, the eyes appear to be pushed downward slightly with the sclera visible above the iris- the so-called setting sun sign.
High-pitched cry. The intracranial pressure may increase and the infant’s cry could become high-pitched.
Irritability. Irritability is also caused by an increase in the intracranial pressure.
Projectile vomiting. An increase in the intracranial pressure can cause projectile vomiting
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conclusions
Hydrocephalus
introduction
Hydrocephalus, also known years ago as “water on the brain”, is a condition where the circulation system of the body’s cerebrospinal fluid (CSF) is not functioning properly. The CSF accumulates in the brain and causes intracranial pressure. A shunt is usually placed to equalize the flow of CSF, which requires surgery. The diagnosis and surgery can be very frightening for the parents as well as the child
definition
Hydrocephalus is a condition characterized by an excess of cerebrospinal fluid (CSF) within the ventricular and subarachnoid spaces of the cranial cavity
INCIDENCE
It is found in 1-3 of every 1000 born children in world wide
Classification
Non communicating. In the non communicating type of congenital hydrocephalus, an obstruction occurs in the free circulation of CSF.
Communicating. In the communicating type of hydrocephalus, no obstruction of the free flow of the CSF exists between the ventricles and the spinal theca; rather, the condition is caused by defective absorption of CSF, thus causing increased pressure on the brain or spinal cord.
CAUSES
Obstruction. The most common problem is a partial obstruction of the normal flow of CSF, either from one ventricle to another or from the ventricles to other spaces around the brain.
Poor absorption. Less common is a problem with the mechanisms that enable the blood vessels to absorb CSF; this is often related to inflammation of brain tissues from disease or injury.
Overproduction. Rarely, the mechanisms for producing CSF create more than normal and more quickly than it can be absorbed.
PATHOPHYSIOLOGY
CLINICAL MANIFESTATION
Poor feeding. The infant with hydrocephalus has trouble in feeding due to the difficulty of his condition.
Large head. An excessively large head at birth is suggestive of hydrocephalus.
Bulging of the anterior fontanelles. The anterior fontanelle becomes tense and bulging, the skull enlarges in all diameters, and the scalp becomes shiny and its veins dilate.
Setting sun sign. If pressure continues to increase without intervention, the eyes appear to be pushed downward slightly with the sclera visible above the iris- the so-called setting sun sign.
High-pitched cry. The intracranial pressure may increase and the infant’s cry could become high-pitched.
Irritability. Irritability is also caused by an increase in the intracranial pressure.
Projectile vomiting. An increase in the intracranial pressure can cause projectile vomiting
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conclusions
An immersive workshop at General Assembly, SF. I typically teach this workshop at General Assembly, San Francisco. To see a list of my upcoming classes, visit https://generalassemb.ly/instructors/seth-familian/4813
I also teach this workshop as a private lunch-and-learn or half-day immersive session for corporate clients. To learn more about pricing and availability, please contact me at http://familian1.com
complete information for the management and care of patient suffering from epilepsy definition ,classification, types, pathophysiology ,clinical manifestation, diagnostic evaluation, medical management, nursing management, care provided to the patient suffering from epilepsy .
Learn about coma/lethergy/stupor/lockdown syndrome
Unconscious.
In psychiatry, it is always difficult to distinguish the different reduce level of conscious states from catatonia.
This presentation shows more light about coma and how we differentiate it from other forms
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
Follow us on: Pinterest
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
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
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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Neurological disorders
1. NEUROLOGICAL DISORDERS
Convulsions Disorders (or) Seizure Disorders or Epilepsy
It is a condition of recurrent episodes, primary of cerebral origin in
which there is disturbance of movement, sensation, behaviour and consciousness.
Causes:
Perinatal Condition:
Cerebral malformation
Intrauterine infection
Hypoxic- ischemic state
Trauma and haemorrhage
Infection-Encephalitis:
Meningitis
Brain abscess
Metabolic Condition:
Hypoglycemia, hypocalcemia, hypomag nesemia, hyponatremia,
hypernatremia, storage diseases, reye syndrome, porphyria.
Poisoning:
Lead, cocaine drug toxicity,
Drug with drawal
Neurocutaneous Syndromes:
Tuberous sclerosis
Neurofibromatosis
Sturge-weber syndrome
Klippel-trenaumay-weber syndrome
2. Systemic Disorders:
Vasculitis (CNS or systemic)
SLE
Hypertensive encephalopathy
Renal failure
Hepatic encephalopathy
Other:
Trauma
Tumor
Febrile
Idiopathic
Familial
Classification of Epilepsy:
Clinically epilepsy can be broadly classified in two groups i.e. generalized or
partial
1.Generalized Seizures:
2. Tonic — &No seizures (Grand ma])
3. Absence seizures:- i) Typical (petit ma]) ii) Atypical
4. Atopic seizures (Dropattacks) Myoclonic seizures
2. Partial Seizures:
a) Simple partial seizures: (with elementary symptoms and or impaired
consciousness)
I. With motor signs (Jacksonians or Focal motor).
II. With somato-sensory or special sensory i.c visual or auditory
3. III. With autonomic manifestations (Abdominal epilepsy)
b) Complex partial seizures: manifested with impaired consciousness and with
Automatism it include psychomotor or temporal lobe seizures.
Clinical Features:
Generalized tonic-clonic seizures (grand ma! type)
The classical form has five phases, i.e an aura, tonic spasm, cionio phase and
postectal phase.
Aura-dizziness tonic spasm phase-body becomes stiff, face, may become
pale and distorted, eyes fixed in one position, back may be arched.
Head turned to backward in one side,
Arms are equally flexed and hands are clenched.
Due to spasm of respiratory muscles, there is ineffective breathing and cyanosis.
The clonic phase- the child may pass stool and urine involuntarily in the
postectal patient become confused or exhassted or perform automatic actions
Headache
3. Absence Seizures (Petitmal):
The child may loss contact with the environment for a few seconds.
Day dreaming
The child may discontinues the activity suddenly (e.g. reading, writing)and
may resume the same activity when the seizures occur.
A typical absence seizure may present as redding of the eyes, nodding of the
head, slight hand movements and smacking of lips.
4. Status Epilepticus:
Cerebral damage may occur due to prolonged cerebra] hypoxia or
4. hypoglycemia
In postectal state the child may have cardio respiratory arrest or aspiration
of vomitus.
5. Partial Seizures:
Motor, sensory, psych], or autonomic abnormalities, but consciousness
is preserved
6. Myoclonic Seizures (Infantile spasms):
Cerebral abnormalities
Mental retardation
The child presents with sudden forceful myoclonic contractions
involving the muscles of trunk, neck and extremities
7. Neonatal Seizures:
Eye blinking
Flutering and buccolingual movements
Diagnostic Evaluation:
Careful history taking
Physical and neurological examination
Laboratory tests.
EEG:- It may confirm type of abnormality and may detect facility, extent of
affection
C.T scan of head
Blood studies:-Blood glucose, calcium and lead and amino acid in serum,
5. to exclude metabolic causes.
Cranial imaging like x-ray of skull, PET or SPECT scan and MRI are also
very useful,
Parital seizure
Tonic clonis
simple
Complex
Involves both
Hemispheres
seizure activity Epilepsy
(idiopathic/secondary) Migrane,
uremia, allergies
Hypoglycemic disorders,
Brain damage congenital
anarnalies
P henylketonuri a, retarded
Psychomotor development
Recurrent seizure activity
Pathophysiology:
Non recurrent
Febrile episode
tumor or edema, toxins
intra cranial
Infection/hemorrhage,
metabolic disorders
Spontaneous paroxysmal electrical
discharge from cortical centers
Neuronal exitation in
s t e m
Centre cephalic (or) focal
Area of the brain
Spread of neuronal excitation to brain
Generalized seizure
Infantile spasms Absence
6. Jack nife
Posture eyes
Roll up ward
Brief loss of
contact with
environment
may have loss
of
consciousness
Flaush, pallor
or cyanosis
Un conscious
Involve one
tonic Heriphere
contractive
Of muscle
local motor
rigidity
movement
related falls to
To involved
area of grocind
Brain
incontinent
Sensory muscle
craving
r e l axat i o n
Related to
involved deep
respiration
Area of brain
deep sleeps.
(Numbness, haggling,
Crawling sensation focal
Taste in mouth)
autonomic
Manifestation
(tachycardia
Diaphoresis, blood pressure
( o r )
Papillary changes),
Unfamiliarity with
Events (or) environment
Loss of
conscious
Hallucination
auto matism
Unusually
sensation
Blank start
Unresponsive
change in
postural tone
Lip smacking
Drowsiness
or sleep
High ling
7. Management of epilepsy/convulsive disorders:
Managements of convulsive disorders depend upon the identified course. The
management mainly done with drug therapy diet therapy and surgery if indicated
Emotional support, psychosocial rehabilitation and vocational guidance are
also important aspect of management.
Drug therapy:-the selection of anti epileptic drugs depends upon age type of
seizure and economic status.
1. Phenobarbital-3-50 mg/kg/day in 1 or 2 divided doses and indicated in
tonic-clonic partial, allmetic and febrile convulsion.
2. Diphanghy dantion -5 to 8mg/kg/day in 2 dicided doses indicated in tonic-
clonic atomic, alanetic and partial seizures
3. Carbamazepine -10 to 20mg/kg/days-in 2 to 3 divided doses and indicated in
tonicclonic, atonic, almetic, and partial seizures.
4. Diazepam -0.2 mg/kg/dose IV or per rectal is indicated in status eoilepsies
5. Sodium valproate -15 to 20mg/kg/day 3 to 4 divided doses in indicated has
braod spectrum anticonvuisive agent.
6. Ethosuximide -10 to 20 mg/kg/day in 2 devided doses in indicated in absence
seizures.
Diet Therapy:
Ketogenic diet may be given to raise the seizures threshold with
calculated amount of proteins and fats without carbohydrates
The child should not be given 11/ fluid with dextrose and strict fluid
restriction to be maintained
Dose observation and frequent monitorining of child's conditions for vital
signs airways breathing patterns preseizures events persevere of aura
8. etc.
Administering prescribed medications IV/IM or per rectal or oral as indicated
Following special instruction about diet and activities.
Preventing Respiratory Arrest and Aspiration:
Loosen the clothing around neck and placing the child flat.
Avoid restraining the child and not to give anything in between teeth or in
the mouth when the teeth are clenched during convulsions
Clear airways, remove secreations turn on, turn head one side during
seizures.
Promoting Socialization:
Some restricted activities like, not to climb high place, or to avoid smoking
and recreational activities.
Strengthening Self Esteem:
Promoting independence in self care and family counseling.
Surgical Management:
Neurosurgery is indicated in some cases of convulsive disorders
Possible surgical interventions include corpus colostomy, focal resection of
parts of cerebral cortex such as temporal lobe, extra-temporal regions
involved as epileptogenic foci.
Nursing Management:
Nursing assessment involve subjective and objective data to be collected.
9. Nursing Interventions are as Follows:
1. Ensuring safety during seizures
Providepreventive measures to protect the child from injury by removal of
hand objects sharp things or toys from the child.
Side rails of the bed or crib to be padded.
Removing of pharyngeal secreations by suctioning and turning head to one
side
Oxygen therapy to be given and all emergency
Providing Health Teaching:
Continuation of medications
Care during convulsion
Diet therapy, restricted activities, misconception regarding the
disease and follow up.
2. Meningitis
Infection of the central nervous system is fairly common in paediatric
period.
Acute bacterial meningitis, a major cause of morbidity and mortality in
young children, occurs both in epidemic and sporadic pattern.
Meningitis is an acute or chronic inflammation of the meningeal membrane and
Cerebrospinal fluid.
Incidence:
Acute bacterial meningitis is common in neonate and infants than the older
children.
10. Causes:
The common organisms implicated in the neonatal Period are:
Escherichia coli
Streptococcus pneumonia
Salmonella species
Staphylococcus auras
From the age of three months onwards i2-3 years the infection is due to:-
Hemophilic influenza
Streptococcus pneumonia
Meningococcal (Neisseria meningitides)
Others Causes:
Septicemia
Brain and spinal cord surgeries
Pilonidal sinus
Fracture in base of skull
Inresidual with compromised immune system.
Risk Factors:
Prematurity
Low birth weight
Complicated labour
Prolonged rupture of membranes
Maternal sepsis
Babies given artificial respiration
11. Pathogenesis:
The infection casually haematogenously to meninges from the distant foci
of sepsis such as pneumonia, purulent meningitis may follow head injury.
Recurrent meningitis may be associated with pilonidal sinus, traumatic
lesions, besides immune deficiency disorder.
Classification:
1. A septic-it is due to virus
2. Septic-it is due to bacteria
3. Tuberculosis-It is caused by mycobacterium tuberculi meningitis
Pathophysiology:
MENINGITIS
Haemophilus influenza
Neissaeria meningitis
(meningococcal)
Streptococcus Pneumonia
Over 1 month of age
Nasopharyngeal
Nasopharyngeal
Enters cerebral
blood stream from
ruptured vessels
From wounds, skull
fracture procedure
Spina bifida
Inflammation of brain parenchyma
Escheriachia coli
Streptococcus group B
Neonate
12. Nuchal
Pia mater
Arachnoid
Subarachnoid space
Behavioral changes
Aggressiveness poor
feeding
Fever
Head ache
Neurological
changes
Vomiting
Petechial rash
Exudate thrombophlebitis
Veins and venous sinuses
High-pitched cry
Bulging fontanellae
Photophobia
Confusion
Seizures
Stupor
Nuchal rigidity
Opisthotonos
Coma
Congestion and infarction
of surrounding tissue
Formation of adhesion
Cranial nerve palsy
Visual of auditory
Impairment
HydrocephalusAntibiotic therapy
Maintain hydration
Maintain ventilation
Control seizures
Resolution with or
without impairment
Death depending
onset, type,
severity, and
response to therapy
13. 1. Bacterial Meningitis:
Acute bacterial meningitis is a major cause of morbidity and mortality in
children.
Causes:
Neisseria meningitides
Streptococcus pneumonia
Haemophilus influenza
Prolong hospital stay
Immunocompromised hosts
Post lumbar puncture or post trauma patients.
Clinical Features:
Irritability, excessive crying, vomiting, head acheineck pain or stiffness in older
children
Alteration in sensorium
Altered repudiation
A full anterior fontanellae
Optic disc congestion or papillederna
Seizure
Cranial nerve palsy
Focal deficit
Apanea
Cyanosis
Fever
Photophobia
Drowsiness
14. Stupor
Coma
Kernigis Sign
Brudzinski sign
Clinical features of meningitis may remain masked in certain situations
Like severe protein energy malnutrition, immune compromised states
malignancies,
Prolonged corticosteroid therapy etc.
Diagnostic Evaluation:
History collection
Physical or neurological examination
Lumbar puncture
Cerebrospinal fluid examination
Protein
Sugar
Polymorphonucleas cells
CST pressure
CT Scan —To exclude the pressure of subdural effusion, brain
abscess, hydrocephalus,
Exudates and vascular complications.
Polymerase chain reaction —To diagnose the infection with herpes simplex,
entero viruses,
Meningococci and tuberculosis
Blood culture
BUN
15. Serum and urine electrolyte level
Treatment of Bacterial Meningitis
Initial therapy should begin with third generation cephalosporin’s such as
ceftriaxone or cefotxime. A combination of Ampicillin (200 mg/ kg) and
chloramphenicol (100 mg/kg/24 hours) for 10-14 days.Specific Antimicrobial
therapy
2. Meningococcal or Pneumococcal Meningitis:
Pencillin — 4-5 lac units /kg/day 4 hourly
Cefotaxime — 150-200 mg/kg/day 8 hourly
Cefriaxone - 100-150 mg/kg/day 12 hourly
3. H. Influenza Meningitis:
Ceftriaxone or cefotaxime —IV
Alternatively, combination of ampioillin (300mg /kg/day 6 hourly)and
chloramphenical (100 mg / kg/day)
4. Staphylococcal Meningitis:
Vancomycin
5. Pyogenic Meningitis:
Dexamethazone- 0.15 mg/kg 16 hourly for 4 days
6. Viral Meningitis:
Acute Aseptic meningitis is a relatively common illness caused by a large
variety factors
16. Clinical Features:
Fever of variable degree
Irritability
Head ache
Vomiting
Pain in neck and back
Photophobia
Sensorial loss
Nuchal rigidity
Seizures
Raised iCP
Focal deficit
Diagnostic Evaluation:
Lumbar puncture:
CST analysis
Blood culture
Complete blood count
Serological examination
MRT
CT scan
EEG
Treatment:
It include management of symptoms, fluid therapy and control of ICP
Non specific therapy is available trials with
17. 7. Tubercular Meningitis:
Meningitis is a serious complication of childhood tuberculosis it is most
common 4 between 6 to 12 months of age.
Clinical Features:
It include 3 stages
1. Predromal stage or stage of invasion
2. Stage of meningitis
3. Stage of coma
1. Predromal stage or stage of invasion:
Low grade fever loss of appetite and disturbed sleep
irritable and restless
Vomiting
Head ache
Photophobia
Constipation
2. Stage of meningitis:
Neck rigidity and kerning’s sign
Elevated temperature (390c)
Pulse slow and disturbed breathing
Increased Muscle tone
Convulsion and drowsiness
Neurological deficit like monoplegia, hemiplegia
18. 3. Stage of coma:
Loss of consciousness and increased temperature
Altered respiration cheyne stroke respiration
Pupils are dilated and nystagmus, squint, ptosis opthalmoplegia
Bradycardia
Diagnostic Evaluation:
Lumbar puncture
CSF analysis
CT scan
Serological test
X ray
Complications:
Emphysema, Brain abscess, hydrocephalus
Deafness, learning difficulties, cranial nerve disorders.
Long term neurological deficits
Seizure
Increased intra craneal pressure (fCP).
Treatment:
a. Anti-tubercular therapy
Isoniazid -5 mg/kg/day
Rifampicin -10mg/kg/orally
Ethambutal -15-20 mg/kg/day
Pyracinamide -30mg/kg/day
19. b. Steroids:
Parenteral corticosteroids (Dexamethasone for 1-2 weeks)
c. Symptomatic Therapy:
Nursing Management
Isolation
Proper hand washing
Vital signs monitored frequently
Administer medications
Bright light should be avoided
The child level of consciousness and neurologic signs are monitor
Elevate the head end.
Monitor the head circumference
When moving holding the infant and the neck should be supported
Maintain intake and out put chart and weigh the patient
Parents and their child need ongoing support during the course of illness.
Bed sore should be prevented
Prognosis
Prognosis related to the age of the patient. Stage at which diagnosis is made
Early diagnosis and adequate and prolonged therapy improves prognosis
3 Encephalitis
Encephalitis is defined as an inflammatory process of the central nervous System
with dysfunction of brain.lt is an acute inflammation that is caused by viral
Infection.
20. Causes:
I. Viral
a. RNA virus
b. DNA virus
c. Arthropod borne
d. Rabies and lymphocytic choriomeningitis
e. Dengue fever
II. Non-viral
a. Richettsia
b. Fungi
c. Protozoa
d. Bacteria
III. Post infections
Typhoid, measles, mumps, Rubella, Pertusis
Pathophysiology:
Virus entering into the body
Enter into lymphatic system
Goes into blood
Enter into central nervous system
Antigen produce
Demyelination, vascular and perivascular destruction
Local vasculitic lesions with thrombus formation in brain tissue
21. Clinical Features:
High fever
Head ache —Vomitting
Mental confusion irritability
Apathy or loss of consciousness often associate with seizures
Sudden rise of intracranial pressure
Disturbance of speech
Neurological deficit such as ocular palsy,
hemiplegia and cerebellar syndromes ,coma
Papilledema with brain stem dysfunction
Pupillary abnormalities ,ptosis, sixth nerve palsy, opthalmoplegia
Cheyne-stoke breathing
Hyperventilation and bradycardia
Diagnostic Evaluation:
History collection
Neurological examination
Lumbar puncture
CSF analysis
Polymerase chain reaction (PCR) on CSF
Stool, blood examination
ELISA
Brain biopsy
MRI
CT scan
EEG
22. Complications:
Temporal lobe swelling which can result in compression of the brain stem.
Aphasia, major motor and sensory deficits
Mortality and morbidity rate depend on the infectious agents, host status and
other considerations.
Treatment:
Symptomatic and supportive therapy:
To reduce intra cranial pressure
Mannitol /IV -1g/kg as a 20 percent solution administration should be rapid.
Within 20 minutes, every 4-6 hours not beyond 24- 48hours
To reduce cerebral oedema eg: Acyclovir on suspicion of herpes
For treatment on suspicion of herpes eg: Acyclovir-10mg/kg/dose Iv every 8
hourly for 10 days.
Nursing Management:
Providing a quiet environment
Aspiration of nasopharyngeal secretions
Gavage or intravenous feeding
Oxygen administration
Oral hygiene
Provide skin care
catheterization and enemas
Administration of medications
Parents must be helped to understand the needed of children
Adequate nutrition provision
23. Control the convulsions.
4. Hydrocephalus:
The Greek term "hydrocephalus" literally meaning water logging of the head,
refers to the enlargement of the head as a result of abnormally high accumulation of
cerebrospinal fluid in the intracranial spaces.
Incidence:
Incidence of congenital hydrocephalus is not precisely known where as
acquired hydrocephalus occurs 1 in 1000 children.
Causes:
Excessive secretion of CSF
Abstraction of the path way of the CSF circulation
eg: Inflammatory adhesions
Interfere in absorption
Thrombosis
Space occupying lesions
Intracranial infection
Neoplasm's,
Hemorrhage
Pre-exiting developmental defects
Types:
1. Congenital hydrocephalus
Intracranial infection such as rubella, toxoplasmosis etc. It may cause
inflammation on the lining of ventricles and meninges. This will leads to
24. occlusion in the pathway of CSF.
Malformation at birth
a) Stenosis and mai development of the aqueduct
b) Mal development of arachnoids villi
c) Spinabifeda
2. Acquired hydrocephalus:
Inflammatory lesions:
Meningitis, Encephalitis.
Traumatic:
Birth trauma, head injury, intracranial hemorrhage
Neoplastic:
Space-occupying lesions like subdural hematoma or abscess.
Connective tissue disorders
Pathophysiology
Non communicating hydrocephalus
Due to any one cause, blockage between the
ventricular and subarachnoid systems
Interference with the circulation of CSF
Stenosis of the aqueduct of sylyius
Inflammation and compression of adequate
Lesions can occur in brain stem
Resulting in an
Aneurysm
Subdural hemorrhage
Atresia of the foramina
Obstructive hydrocephalus
Communicating hydrocephalus
Communication between the ventricular
subarachnoid space
Interference with absorption of CSF
Occlusion of the subarachnoid cisterns around
the brain stem
May due to
Subarachnoid haemorrhage
Meningitis
Toxoplasmosis
Cytomegalo virus infection
Communicating hydrocephalus
Atrophy & convulsions can occur
25. Clinical features:
Progressive pathological enlargement of head.
Scalp becomes shiny and scalp veins will be dilated, fontanellae may be
evidenced
Precession of the skull reveals typical cracked-pot sound
Sun setting phenomenon of eyes,
Lethargy.
Poor feeding
High pitched cry
Hemiplegia with steady rise in intra cranial pressure.
Hydrocephalus children's are get normal intelligence in the period of late in
child hood dose not accompanying by big head.
Other feature will be presence such as
Papilloedema
Spasticity
Ataxia
Urinary incontinence
Seizures
Irritability
Headaches
Vomiting
In coordination
Confusion
Diagnostic Evaluation:
X ray of skull: shows sutural separation and enlarged cranium.
MRl scan: shows Arnold chiari malformation (down ward displacement of lower
26. brain stem, cerebellum and fourth ventricle in to foramen magnum.
Ventriculography
Pneumoencephalography
CT Scan : used in identifying
Site of blockage
Enlargement of ventricles
Chronic subdural effusion
Cerebral atrophy
Complications:
Infection
Obstruction or malfunction of shunt
Subdural hematoma
Infection or perforation of abdominal contents after placement
Death will occur if not diagnosed increased intracranial pressure.
Medical management:
Administer isosorbide pre operatively
postoperatively administer acetazolamicle, frusamide, antibiotics,
anticonvulsant
Surgical treatment:
1. Ventriculo-peritoneal shunt (VP shunt)
A ventricular catheter is inserted into the anterior portion of a lateral
ventricle through a burr hole in the skull. The valve unit is tested and attached to
the catheter. An incision is made in the abdomen and through the rectus muscle
into the peritoneum. The end of the catheter is slipped beneath the skin of the
27. anterior abdominal and chest wall of the neck. After the surgery CSF flow will be
normal and it is absorbed by abdominal tissues.
2. Ventriculo atrial shunt (V.A shunt)
A silicone catheter is passed from dilated ventricles through burr hole and down
through the internal jugular vein into the right atrium of the heart. The CSF
drains into the circulating blood.
Nursing management
Pre operative:
Be alert to sign and symptoms that indicates
Monitor for Sign of increasing intra cranial pressure.
Record the behavior of the infant.
The infant's position is changed frequently.
Prepare the child for operation
Post operative:
Monitor vital signs
Follow sterile aseptic technique
Monitor respiratory and neurostalus
Fluid restriction should be done for 24 hours
Maintain adequate hydration and nutrition
Measure intake and output carefully
Assess for signs indicating potential complication
Promote growth and development
Provide support to family and child
Observe for complication
28. 5. Spina Bifida:
Spina bifida is one of the most common congenital enamels, occurring in 1-2
/1000 live births, the defects involves spinal cord, meninges vertebra and
the brain, the cones auences of the problem can affect several functions.
Spina bifida is one of the most common structural congenital anomalies
and imply a failure of proper closures of neural tube and mesoderm and ectoderm.
Incidence:
This congital anomalies occurs in about 1.5 per 1000 live births and risk in
second sibling is 5 per 100 births the incidence in north India is as high 3.9-9
per 1000 live births.
Classification:
It is classified into meningocele and meningomyelocele.
i. Spina bifida occulta
Thire is no spinal cord and meninges involement. it is the mild type of spina
bifida.
Clinical Feature:
Tufts of hair will arise above the depressed area.
ii. Meningocele:
When the herniation from the vertebral column consist of meninges only and
forming a CSF filled sac, the condition is called meningocele.
Meningomylocele:
A congenital defect of central nervous system of infants in which membranesly
and the spinal cord protruded through an opening or defect in the vei/ibral
29. column.
Pathophysiology
Maternal folic acid deficiency is an environment-factor strongly
associated with neural tube defects. Serum from women with pregnancy
complicated receptors and block the cellular uptake of folate. Further study is
warranted to assess whether the observed association between maternal
antibodies against folate receptors and neural tube defects reflects a causal
relationship.
The ultimate cause of spinal dysraphism is unclear.
Dysraphic malformations probably occur when environmental agents affect
underlying hereditary risk factors.
Clinical Features:
The affected children usually have an anomaly of the brainstem an
Arnold-chiari malformation that may result in hydrocephalus and
sensory disturbances usually parallel motor dysfunction face below second
lumbar vertebrae.
Flaccid, facial paralysis of lower extremities
Varying degree of sensory deficit.
Outflow incontinence with constant dribbling of urine
Defect of bowel control
Skin depression or dimple
Some seens rectal prolapse
Progressive disturbances of gait Bladder and anal sphineter paralysis. Joint
deformity
Talipes vagus or yaws contrafuges Kyphosis
30. Lumbosacral scoliosis
Hip dislocation
Meningocele
The sac is covered only by skin and there is .np neurologic defect.
Lower body paralysis.
Bladder and bowel dysfunction
Learning disability
Causes:
Exact cause unknown
Drugs
Radiation
Maternal malnutrition
Chemicals
Genetic mutation
Maternal obesity
Previous NTD pregnancy
Diagnostic Evaluation:
MRI
Ultrasound
CT
Complete blood test are used primarily to determine causative organisms for the
major complications mylomeninancele-meningitis
31. Clinical Features:
Meningo myocele deficit includes varying degrees of flaccid, are flexic
paraparesis and sensory deficit in the trunk and legs correspond to the inolved
segments of the dysplastic cord.
Fecal and urine icontinence
Hydrocephalus may be present
impend tongue movement
Laryngeal stridor
Management:
Prenatal Diagnosis:-
Estimation of alpha-fetoprotien level in maternal blood between 14 and 16
weeks of gestation, or in the aminiotic fluid early pregnancy.
Ultra sound
Amniocentesis for alpha feta protein & acetyl choline esterale
Diagnostic Evaluation:
Ultrasound of head and sac
CRP and X-ray of spine
Culture from lesions and draning CSF Complete blood count
Serum electrolytes and blood for cross matching
Treatment
Management requires a firm approach with cooperation of paediatrician,
neurologist, neuro urologist and orthopedic surgeon with assistant,
physiotherapist, social worker and psychiatrits.
32. Surgery:
It include surgery of the defect and a associated with hydrocephalus
Early closure present neurological defects
Open lesion draining CSF should be closed within 24 hours.
Closed lesion should be operated
In case, the lesion is infected, the child begin anomalies, (90%) whould die in
the neonatal period.
Prevention:
Primary prevention folic acid supplementation to all mother including first
pregnancy. Food purfication is another possible approach Counselling of
family with a previous child with NTD is essential. Advise perceptional folate and
offer prenatal diagnosis in subsequent pregnancy.
Secondary prevention is imperative after an index care. Precaution of
supplementation is 2 month, before and 3 months after conception.
6. Cerebral patsy
A chronic impairment of motor control and muscle tone resulting from a non-
progressive abnormality in the pyramidal motor system. It is often associated with
perinatal brain ischemia, prematurity, low birth weight and birth trauma.
Incidence:
1-2/1000 population.
Causes:
1. From the onset of conception to the onset of labour 80 percent:
Disturbances of placental circulation,
33. Cord impairment.
Intrauterine infection.
Maternal drugs or alcohol abuse,
Rh incompatibility
Post maturity
Radiation
2. During labour and delivery
Premature separation of placenta
Maternal or fetal anoxia
Premature birth
Difficult or prolonged labour.
Arrested labour progress (CPD-Cephalo
pelvic disproportion) Intracranial bleeding
Anesthetic complication
Toxemia
Precipitous delivery Use of high forceps
3. Immediate post-partum:
Hypoglycemia
Jaundice
RDS (Resp: distress syndrome)
Bleeding diathesis
4. later in childhood (incidence rate is low)
Accidental head injury
Lead poisoning
34. Child abuse
Hydrocephalous
Meningitis
There are three major types:
1. Spastic
2. Athertoid
3. Ataxic
Clinical features:
Depend upon type
General findings includes delays and abnormalities in development especially
motor control and performance
Increased or decreased muscle tone
Persistent ADD
Mental retardation
Deficits in vision or hearing
Diagnostic evaluation:
Usually difficult to diagnose until child is 2-4 months or older when
neurological exam reveals abnormalities
Including impairment of voluntary muscle movement and posturing
Complications:
Delayed growth and development.
Skin break down.
Contractures.
35. Seizures.
Difficulty with vision.
Various degree of mental retardation.
Medical management:
Administer Anticonvulsant drugs and muscle relaxants eg. Diazepam,
dantrolene, baclofen.
Provide physiotherapy, braces, casts, corrective appliances, glasses,
hearing aids, technical aids (computer voice synthesizer)
Surgery:
May necessary to correction of spastioity and contraction, tenotomy of
Achilles tendon.