1. The patient presented with headache and right-sided hemiplegia, consistent with an acute stroke.
2. Strokes in sickle cell disease are most commonly ischemic and occur bimodally, peaking in younger children and those over 30 years old. Hemorrhagic strokes are rarer and peak during the second decade.
3. Diagnostic workup includes blood tests and neuroimaging to determine if the stroke is ischemic or hemorrhagic, as management differs between the two.
Aplastic anemia is one of the stem cell disorder which leads to pancytopenia in the peripheral blood and decrease production of all cell line in bone marrow. it require bone marrow transplantation to cure the patient.
A presentation made about Sickle cell disease by Yara Mostafa, Yasser Osama, Yaser Mostafa ,Ain shams university, Medicine faculty, first year students.
Aplastic anemia is one of the stem cell disorder which leads to pancytopenia in the peripheral blood and decrease production of all cell line in bone marrow. it require bone marrow transplantation to cure the patient.
A presentation made about Sickle cell disease by Yara Mostafa, Yasser Osama, Yaser Mostafa ,Ain shams university, Medicine faculty, first year students.
Haemolysis indicates that there is shortening of the normal red cell lifespan of 120 days. There are many causes.
To compensate, the bone marrow may increase its output of red cells six- to eightfold by increasing the proportion of red cells produced, expanding the volume of active marrow, and releasing reticulocytes prematurely. Anaemia occurs only if the rate of destruction exceeds this increased production rate.
hemolytic disease of new born is an aquire alla immune hemolytic anemia characterize by production extravascular destruction of RBC within the spleen of new born baby resulting anemia, positive coomb,s test
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration.
causes of macrocytic anemia pathopysiology, sign and symptoms and the difference between macrocytic anemia megaloblastIc anemia. causes of hypersegmented neutrophils and its association between them. investigation and medical management plus pictures illustration.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Haemolysis indicates that there is shortening of the normal red cell lifespan of 120 days. There are many causes.
To compensate, the bone marrow may increase its output of red cells six- to eightfold by increasing the proportion of red cells produced, expanding the volume of active marrow, and releasing reticulocytes prematurely. Anaemia occurs only if the rate of destruction exceeds this increased production rate.
hemolytic disease of new born is an aquire alla immune hemolytic anemia characterize by production extravascular destruction of RBC within the spleen of new born baby resulting anemia, positive coomb,s test
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration.
causes of macrocytic anemia pathopysiology, sign and symptoms and the difference between macrocytic anemia megaloblastIc anemia. causes of hypersegmented neutrophils and its association between them. investigation and medical management plus pictures illustration.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Interactive talk on common hematological and oncological emergencies - which if not noticed early can lead to irreversible complications and death .
Intended to be used for educational purposes for the fertile minds in medicine .
case presentation on diagnosis of beta thalassemia majorDrShinyKajal
case history of 9 month old infant
Paediatric Clinical Approach to this case
examination
workup at blood centre
HPLC screening
laboratory findings
screening of father mother
prominent facial features
PBF and bone marrow findings
usg abdomen
xray skull
prbc transfusion therapy in thalassemia major
classification of thalassemia
national burden in india
pathogenesis- anemia skull bone iron overload
world thalassemia day
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.
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
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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.
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.
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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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
2. Sickle cell anemia
• Autosomal recessive disorders occur by point mutation in beta globin
gene results in the production of sickle hemoglobin.
Pathophysiology
Point mutation in chromosome 11 in the beta-chain gene lead to change glutamate to valine in
position 6 of the Hb beta chain.
3. Classification
Sickle cell trait Hb AS :
• Mutation only in one allele of
beta-chain gene (heterozygous
state).
• Usually no serious clinical
consequences.
Sickle cell disease:
• Occur as mutation in two allele of
beta-chain gene (homozygous
state) as Hb SS.
• Or occur as mutation in two
different location of beta chain
but one of them should be in
sickle mutation include :
- Hb S/Bthal
- Hb SC
- Hb SO
- Hb SE
6. Diagnosis
The goals and methods of diagnosis of sickle cell disease (SCD) vary with the age
of the patient and need at least two confirmatory test to diagnose.
Prenatal testing :
• using specific
molecular methods
for detecting the
HbS gene by taking
fetal DNA samples
obtained by
chorionic villus
sampling at 8 to 10
weeks gestation.
Older children and adult:
• Sickledex
• HPLC
• Hb electrophoresis
• Molecular testing
Newborn :
• in the fetal and newborn
periods can be difficult to
detect HbS because of the
predominance of hemoglobin F
(HbF), which confounds
detection of hemoglobin S
(HbS) by solubility testing.
• Use newborn screening
including :
- Hb Electrophoresis
- HPLC
- Molecular testing
7. Diagnostic approach :
Detailed history taking and physical examination.
Laboratory test including :
• CBC with finding of :
- Low Hb
- Finding of chronic hemolysis including high or normal MCV, high retics.
• Peripheral blood smear :
- Sickled red cells.
- Polychromasia indicative of reticulocytosis.
- Howell-Jolly bodies reflecting hyposplenia.
8. Confirmatory tests:
• Sickledex :
- By taking blood sample and putting under stress lead to polymerize and precipitate.
- Detect the presence of HbS but doesn’t differentiate between sickle cell disease or
trait.
• Hb eletrophoresis :
- Analyze different type of Hb based on charge and size.
- In SCD the HbSS or other type will be predominate.
• HPLC ( high performance liquid chromatography) :
- Give the percentage of Hb types.
• Molecular test based on genetic sequences.
Sickledex test
12. General management
General measure :
• Educate the patient and family
about SCD.
• Obtaining steady state laboratory
value as baseline for comparison
during exacerbation.
• Infection prevention by :
- Immunization for all patient (PCV,
Hib, influenza, meningococcal)
- Prophylactic penicillin for all young
children (<5 yrs old).
• Nutrition :
- Folic acid 1 mg oral supplement
daily and multi-vitamin.
- Screening of iron for those non-
tranfused.
• Routine evaluation for any
complication
Cure of SCD :
• Bone marrow
transplantation.
Management of
complication:
• Depend on present of
complication (as
explain next pages).
14. Hydroxyurea
The mechanism of hydroxyurea
• Inhibition of
ribonucleotide reductase
to inhibit DNA synthesis.
• As affect cell devision,
cause global
myelosuppression
including neutropenia,
anemia and
thrombocytopenia.
Other mechanism include :
- Increase production of
NO by endothelial cell.
- Reduce WBC count
and/or neutrophil
adhesivity to the
vascular endothelium.
• Increased HbF production
which lead to :
- Reduce sickling by reduce
Hb polymerization.
- RBC lifespan increased
- Improved RBC hydration
- Reduce hemolysis
- Reduce the adhesion of
cell to vascular
endothelium.
Which in general :
• Reduce frequency/quality of pain
• Reduce recurrence of ACS
• Reduce hospitalization and need to transfusion
• Reduce hemolysis
15. Indication and contra-indication
Indication :
• 4 or more severe episodes of
painful crisis.
• ACS
• Stroke
• Priapism
• Renal disease
• Severe anemia
Contra-indication:
• Pregnancy
• Breastfeeding
• Severe anemia
• Severe decreased WBC
• Severe decreased Plt
• Reduction in kidney function
Prediction for response and compliance :
• Higher HbF
• High MCV
• Reduce WBC, Plt and retics
18. Vaso-occlusive crisis (VOC)
• A 24 yrs old lady from Nizwa known case of SCD, presented with two days history of increasing
pain involving the right leg and both arms which not relieved by oral analegsia. She gave history
of repeated admission to peripheral hospital with painful episodes. On examination, she was
mildly pale and afebrile. Chest was clear. Liver was palpable at 2 cm below the right costal margin
and spleen was palpable at 3cm below the left costal margin.
According from case, patient present with
painful crisis in different sites which
caused by VOC
CSSCD defined painful episodes (painful crisis) as pain related to SCD
in the extremities, back, abdomen, chest, or head lasting at least two
hours and leading to a clinic visit or hospitalization. But this
underestimates the true degree of pain because many individuals
have pain that is treated at home. The painful crisis precipitate by :
• Exposure to cold.
• Dehydration
• Excessive exercise or stress
• Hypoxia or infection
Quick HIT :
• the patient had
splenomegaly and
hepatomegaly which
might associated with
spleen sequestration.
But that can’t be
confirmed as we don’t
have the baseline of
spleen and liver.
Investigation :
CBC , Blood smear, LFT and RFT
21. Acute chest syndrome
• Khalid 19 yrs old known case of SCD, came to the A&E with SOB, productive cough and fever. He
looked sick. Physical examination revealed T 38.8C, HR 112, BP 100/50 mmHg and RR 28 with
oxygen saturation of 88% on room air. Chest examination revealed bilateral basal crackles.
ACS Defined as a NEW radio-density on chest radiograph (consolidation or infiltration) accompanied by
fever and/or respiratory symptoms including chest pain, SOB and cough, wheeze desaturation caused by :
Bone marrow fragment and/or fat
emboli :
• More common in adult compared to
children.
• Could associated with lipemia retinalis,
petechiae and neurological symptoms
(but less common).
• Test to confirm (not performed
routinely):
- need bronchoalveolar lavage for the
presence of fat-containing alveolar
macrophages.
- Bone marrow aspiration and biopsy show
necrosis and infraction of bone marrow.
Other causes :
• Pulmonary infection.
• Pulmonary thrombosis.
VOC and lung
sequestration :
• More common in
children.
23. Investigation :
• CBC, blood smear, ECG, AP and lateral X-ray, blood and
sputum culture.
• Other test in some cases including chest CT scan for
pulmonary emboli, serum troponin for myocardial
damage, bone marrow aspiration and biopsy,
Bronchoscopy with bronchoalveolar lavage for fat
embloi.
Quick HIT :
• the differential diagnosis of ACS
are pulmonary embolus, acute
coronary syndrome and
pneumonia.
• But even the patient present with
one of previous differential, still
consider ACS otherwise excluded
as different management require
for ACS.
Management :
• Adequate and immediate pain control as same guideline of VOC.
• Supplemental oxygen.
• Hydration to prevent hypovolemia by typical regimen is 1.5 times maintenance fluids of D5 in one-
half normal saline for the first 24 to 48 hours.
• Exchange transfusion :
- if the Hb >8 g/dL to reduce hemoglobin S percentage <30 percent
- if Hb < 8g/dL give first simple transfusion to achieve Hb >8 g/dL and then apply exchange transfusion.
• Bronchodilator.
• Antibiotic with a third generation cephalosporin along with a macrolide, or a fourth generation
fluoroquinolone are typical regimens including :
- cefotaxime 1 to 2 grams IV every eight hours plus azithromycin 500 mg orally or IV once daily for seven
days
- moxifloxacin 400 mg orally or IV for seven days.
- ceftriaxone should be used with caution as drug-induced immune hemolysis
24. • Incentive spirometry : to prevent ACS episodes in children with SCD who were admitted to the hospital
for a painful crisis by Performing incentive spirometry using 10 maximal breaths every two hours while
awake was associated with a significantly reduced rate of developing ACS.
•
Prevention :
• Consider hydroxuria if not started before.
• Chronic transfusion therapy might use in some cases.
• Bone marrow transplantation.
Quick HIT :
• type of antibiotic given depend
on presence of spleen or its
function :
- In case of splenectomized patient
will give antibiotic for
encapsulated bacterial including
tazocin and azithromycin
- If not splenectomized will give
cefuroxime and azithromycin.
25. Acute stroke
• Khalid 19 yrs old known case of SCD, came to the A&E with headache and right sided hemiplegia
started recently. He had some episodes of seizure.
ACS Defined as a NEW onset of neurological defect including hemiparesis, aphasia, seizure, sensory
deficit, altered consciousness, intellectual decline and other depend on site of lesion:
27. Investigation :
important to differentiate between ischemic and hemorrhagic stroke as different management
• CBC, cross-match for transfusion, coagulation profile, electrolyte, RFT and blood glucose.
• Neuroimaging :
- Head CT scan done first which might detect hemorrhagic stroke but less sensitivity for ischemic stroke.
- If head CT not clear, do head MRI which more sensitive for ischemic stroke.
• EEG might done in some cases for seizure.
Management :
Immediate management for all patient with ischemic or hemorrhagic stroke include:
• Stabilize the patient with ABC.
• Airway protection from aspiration
• Intravenous access and hydration with isotonic fluids, typically at 1.25 to 1.5 times the normal
maintenance rate
• Simple transfusion to raise the hemoglobin concentration to not more than 10 g/dL to prevent hyper-
viscosity.
• Attention to identification and treatment of concurrent infection; including antipyretics if needed.
• Management of seizures if present.
28. Ischemic stroke :
• For patients with SCD who have a
radiologically confirmed acute ischemic
stroke include :
- Urgent Exchange transfusion to reduce
sickle hemoglobin to ≤30 percent of total
hemoglobin.
- Thrombolytic/antithrombotic use only
for patients with a greater likelihood of
another cause of ischemic stroke such as
embolism.
Additional management depend on type
of stroke
Hemorrhagic stroke :
• for treat the bleeding :
- Discontinue all anticoagulants and antiplatelet
agents, unless their benefits are thought to
outweigh their risks for that patient.
- For patients with thrombocytopenia, administer
platelet transfusions as necessary to maintain the
platelet count over 100,000/microL
- Obtain neurosurgical consultation if an
intervention may be required (eg, to reduce
intracranial pressure or to treat a bleeding
aneurysm).
Prevent the recurrence:
• Consider hydroxuria if not started before.
• BMT if there is donor.
• Chronic exchange transfusion especially for those with higher risk.
29. Acute anemia
• 21 yrs old man with SCD was admitted with LUQ pain of 6 hrs duration. He had repeated admission in the past
with acute painful episodes and was on daily hydroxyuria and folic acid as well as mefenamic acid as needed.
He had one brother and two sisters with SCD. On examination, he was pale and jaundiced. His HR 110, BP
90/50, RR24, O 94% on room air, T 37.8C. Chest was clear. He had tender splenomegaly with being palpable at 8
cm below costal margin. CBC showed Hb 6g/dl, WBC 3.1 and Plt 110.
Sudden decline in Hb below than the baseline of patient which commonly caused by :
Splenic sequestration crisis :
• acute drop in hemoglobin
level caused by vaso-
occlusion within the spleen
and splenic pooling of RBCs.
• Present with :
- pallor.
- Rapidly enlarging spleen
which cause LUQ pain.
Hyperhemolytic crisis :
• sudden exacerbation of
hemolysis with worsening
anemia despite ongoing
reticulocyte production.
• Might associated by VOC,
infection or drug exposure.
• Present with :
- pallor.
- Jaundice
- Dark urine
Aplastic crisis :
• characterized by an acute drop
in hemoglobin level caused by
a transient arrest of
erythropoiesis, leading to
abrupt reductions in red cell
precursors in the bone
marrow commonly caused by
human parvovirus B19
infection.
• restoration of erythropoiesis
and reappearance of
reticulocytes in the peripheral
blood within 2 to 14 days.
30. Investigation :
Splenic sequestration crisis :
• CBC :
- Low Hb, might associated with
low plt or WBC.
- Normal or high retics.
• Blood smear show high retics
• Other test might be ordered
as LFT, U&E.
Hyperhemolytic crisis :
• CBC :
- Low Hb and might high
MCV.
- High retics
• Blood smear with high
retics.
• High unconjugated
hyperbilirubinemia.
• elevated serum lactate
dehydrogenase (LDH)
• low serum haptoglobin
Aplastic crisis :
• CBC :
- Low Hb.
- Low reticulocytes in the
peripheral blood (typically,
reticulocytes <1.0 percent,
absolute reticulocyte count
<10,000 per microL).
• Serology test for virus antigen.
• Blood smear show low retics
• Other test might be ordered as
LFT, U&E.• Give simple transfusion but
until return Hb to baseline or
being asymptomatic.
• Prevent to give high blood as
may worse the sequestration
and lead to rupture.
• Advise to splenectomy.
• Hydration
• Pain management if
associated with pain.
• Give simple transfusion but
until return Hb to baseline or
being asymptomatic.
• Hydration
• Pain management if
associated with pain.
• Give simple transfusion
but until return Hb to
baseline or being
asymptomatic.
• Hydration
• Pain management if
associated with pain.