This document provides an overview of various types of leukemia, including acute myeloid leukemia (AML), chronic myeloid leukemia (CML), and infantile leukemia. It discusses the classification, signs and symptoms, diagnosis, and management of these leukemias. Specific hematologic emergencies that can occur in leukemia patients are also reviewed, such as leukostasis, tumor lysis syndrome, spinal cord compression, and respiratory distress syndrome.
chronic myeloid leukemia, CML, epidemiology, BCR ABL1 gene, philadelphia chromosome, t(9;22), CML incidence, etiology of CML, pathophysiology of CML, phases of CML, treatment of CML, Allogenic stem cell transplant, TKI therapy for CML, Sokal index for CML,
Chronic myelogenous leukemia ( CML )
Tests to be done in order to differentiate CML from other dieases with common clinical features.
It's pathogenesis, clinical presentation and features of diagnostic tests.
Methods of treatment. Prognosis of a disease according to "Sokal" score
chronic myeloid leukemia, CML, epidemiology, BCR ABL1 gene, philadelphia chromosome, t(9;22), CML incidence, etiology of CML, pathophysiology of CML, phases of CML, treatment of CML, Allogenic stem cell transplant, TKI therapy for CML, Sokal index for CML,
Chronic myelogenous leukemia ( CML )
Tests to be done in order to differentiate CML from other dieases with common clinical features.
It's pathogenesis, clinical presentation and features of diagnostic tests.
Methods of treatment. Prognosis of a disease according to "Sokal" score
BIBLIOGRAPHY:
Datta Parul, Textbook of Pediatric Nursing, edition 4, The medical sciences publishers, 4838/24 Ansari road, Daryaganj, New Delhi, 110002, India
INTRODUCTION
Leukemia is the most common type of childhood malignancy.
It is characterized by persistent and uncontrolled production immature and abnormal WBCs.
It is a disease of abnormal proliferation and maturation of bone marrow which interferes with the production of normal RBCs, WBCs and platelets.
Leukemia is defined as uncontrolled neoplastic proliferation of leukocyte precursors.
According to National Cancer Institute,
Leukemia is defined as a cancer that starts in blood-forming tissue, such as the bone marrow, and causes large number of abnormal cells to be produced and enter the bloodstream.
95-98% of childhood leukemia are acute type.
70-75% of acute lymphocytic leukemia.
common malignancy of children less than 15 years.
peak incidence is four years of age.
males are more affected than females.
twice more common in white then black in children.
The exact cause is unknown.
viruses like HPV ,Epstein Barr virus ,human T cell lymphoma leukemia virus (HTLV).
Radiations
exposure to chemicals and drugs like benzene and Dilantin
familial predisposition
chromosomal abnormalities like Down syndrome
Genetic like Fanconi's anemia ,bloom syndrome
ACUTE LYMPHOCYTIC LEUKEMIA
Primary disorder of bone marrow in which normal bone marrow elements are replaced by immature or undifferentiated blast cells.
develop when lymphoid cell line is affected.
characterized by anemia, thrombocytopenia, neutropenia, especially granulocytopenia.
the incidence rate is one in 2000 live birth.
the peak age of onset is 3 to 7 years and males are more affected than females
According to French American British classification on the basis of cell morphology it is classified as
L1
L2
L3
According to type of cell it is classified as
T cell
B cell
Pre-B cell
Null cell
T cell
10 to 15% ,high risk ,seen in older children especially males ,featured as mediastinal mass ,hepatosplenomegaly ,high WBC count ,CNS involvement and has poor prognosis.
B cell
1 to 2% children ,aggressive form ,poor prognosis and high-risk type.
Pre-B cell
Good prognosis and respond well to therapy.
Null cell
No cellular surface markers (80% ).
Great imitator, with vague and varied signs and symptoms, resembling almost any disease.
Peripheral blood examination which shows decrease hemoglobin, RBC, hematocrit and platelet count
bone marrow analysis in which large number of lymphoblasts and lymphocytes with hypercellular visible.
chest X-ray
CSF
Chemotherapy
radiation therapy
bone marrow transplantation
supportive and symptomatic management
Chemotherapy
Remission induction chemotherapy
Vincristine, Prednisolone, Asparaginase and Adriamycin are given for 4-6 weeks.
maintenance therapy or systemic continuation
6 MP (Mercaptopurine) and MTX (Methotrexate) are given for 2.5-3 years.
late intensification or THERAPY
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
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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
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
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
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.
4. Acute Myeloid Leukemia
- Clonal expansion of myeloid precursor cells
with reduced capacity to differentiate
- As opposed to ALL/CLL, it is limited to the
myeloid cell line
– differentiated from ALL based on morphology,
cytogenetics, cytochemical analysis, cell surface
markers
6. Hereditary Disorders Associated With
an Increased Risk of AML
• Down syndrome
• Ataxia telangiectasia
• Li-Fraumeni syndrome
• Klinefelter’s syndrome
• Fanconi’s anemia
• Wiskott-Aldrich syndrome
• Bloom syndrome
• NF-1
• Shwachman-Diamond syndrome
• Kostmann syndrome.
6
7. Epidemiology
• M > F
• 11% of childhood leukemia
• ALL which predominantly affects younger
individuals
• AML – adults and the elderly
• Median age group-65yr
7
10. WHO Classification
• AML with certain genetic abnormalities
– t(8;21), t(16), inv(16), chromosome 11 changes
– t(15;17) as usually seen with AML M3
• AML with multilineage dysplasia (more than one abnormal myeloid cell type is involved)
• AML related to previous chemotherapy or radiation
• AML not otherwise specified
– undifferentiated AML (M0)
– AML with minimal maturation (M1)
– AML with maturation (M2)
– acute myelomonocytic leukemia (M4)
– acute monocytic leukemia (M5)
– acute erythroid leukemia (M6)
– acute megakaryoblastic leukemia (M7)
– acute basophilic leukemia
– acute panmyelosis with fibrosis
– myeloid sarcoma (also known as granulocytic sarcoma or chloroma)
• Undifferentiated or biphenotypic acute leukemias (leukemias that have both lymphocytic
and myeloid features. Sometimes called ALL with myeloid markers, AML with lymphoid
markers, or mixed lineage leukemias.)
11. Clinical symptoms
• Due to the excessive proliferation of myeloid
precursor cells in bone marrow, followed by
marrow replacement and failure certain
symptoms/lab findings are expected (e.g. as
a result of pancytopenia)
1. Functional neutropenia – fever, chills
(INFECTION)
2. Thrombocytopenia – bleeding, bruising
3. Anemia – weakness, fatigue
12. Specific
• Chloroma:-presents as a mass lesion ‘tumor of
leukemic cells’
• DIC indicative of APL.
• Infiltration of soft tissues, gum infiltration, skin
deposits ,Meningeal involvement-headache,
vomiting, eye symptoms
• Subcutaneous nodules or blue berry muffin
lesions in skin
• CNS involvement is more common in AML then
ALL
12
13. Diagnosis
• Blood count : WBC usually elevated (50,000- 1,00,000 / cmm
); may be normal or low; often anemia & thrombocytopenia
• Bone marrow: Bone marrow aspirate & trephine:
Hypercellular,
–blast cells ( > 20%),
–presence of Auer rods - AML type
• Cytochemistry : Special stains to differentiate AML from ALL
Positivity with Sudan black & Myeloperoxidase (MPO) in AML
13
17. MANAGEMENT
• SPECIFIC THERAPHY:
–Chemotherapy : Aggressive multiagent
chemotherapy is successful in approx 85-90%.
– Survival has increased from 15% in 1970 to 60-
70% with modern therapy.
– Targeting therapy to genetic markers may be
benefecial.
– Upto 5% of patients die of either infection or
bleeding before remission can be achieved.
17
18. TREATMENT
• Matched-sibling bone marrow or stem cell
transplantation after remission achieves long
term disease free survival in 2/3rd .
• Continued chemo for those who don’t have
matched donor is less effective than
transplant, but curative in half patients.
• Matched unrelated stem cell transplant may
be effective but there is risk of GVHD
19. TREATMENT CONTINUED
• Acute promyelocytic leukemia APL
charaterized by gene rearrangement involving
retinoic acid receptor is very responsive to
retinoic acid with anthracycline.
• Increased supportive care :
Anemia correction, filgrastim(GMCSF), platelets
transfusion, antibiotics, antifungal
prophylactic.
19
20. DOWN SYNDROME AND ACUTE
LEUKEMIA/TRANSIENT
MYELOPROLIFERATIVE DISORDERS.
• 15-20 times higher than in general population.
• AML:ALL Ratio is the same.
• Outcome of ALL to treatment is inferior.
• Higher sensitivity to MTX and antimetabolite
so higher risk of toxicity
• Better outcome than non down syndrome
>80% long term survival.
21. Transient leukemia
• Develops in 10 % neonates with Down
syndrome
• High TLC, Blast cells on P.Film, anemia,
thrombocytopenia and hepatosplenomegaly.
• Resolve within 1st 3 months of life.
• Require temporary transfusion support and no
chemotherapy.
• Require close follow-up 20-30 % will develop
typical leukemia by 3 yr of life
22. Chronic myeloid leukemia (CML)
• Clonal disorder of hematopoeitic tissue
accounting for 2-3 % of all cases of childhood
leukemia.
• 99% cases are characterized by translocation
of specific chromosome t(9;22)(q34:q11)
known as Philadelphia chromosome resulting
in BCR-ABL fusion protein.
23. (CML) SIGNS SYMPTOMS
• Nonspecific: fever, fatigue, weight loss, and
anorexia
• Splenomegaly with pain in right upper
quadrant.
• CNS menifistation from hyperleukocytosis
resulting in increased blood viscosity and
decreased CNS perfusion.
24. (CML) DIAGNOSIS
• CBC: High WBC count, anemia, and
thrombocytosis
• High myeloid cells at all stages of
differentiation in peripheral blood and bone
marrow
• Confirmed by cytogenetic and and molecular
studies that demonstrate Philadelphia
chromosome and BCR-ABL gene
rearrangement
25. (CML) TREATMENT
• Imatinib (Gleevec), an agent which inhibit
BCR-ABL tyrosine kinase, produce major
cytogenetic response in > 70% of patients
• 2nd generation tyrosine kinase inhibitor
dasatinib have improved remission rate in
adults and now being studied in children.
• HLA matched family donor allogenic stem cell
transplant produces cure in upto 80 % of
children.
26. Juvenile myelomonocytic leukemia
(JMML)
• Previously called juvenile CML is clonal
proliferation of stem cell affects children <2 yr
• JMML< 1% of all childhood leukemia.
• Present with rash, lymphadenopahy,
splenomegaly, and hemorrhagic
menifestation.
• Patient with Noonan syndrome, NF-1 have a
predilection for this leukemia.
27. JMML Diagnosis Treatment
• CBC: shows leukocytosis esp monocytosis,
thrombocytopenia, and anemia with presnece
of blasts.
• BM shows myelodysplastic pattern, with
blasts accounting for < 20%.
• Stem cell transplantation offer the best
opportunity of cure but much less than for
classic CML.
28. Infantile leukemia
• 2% of childhood leukemia occures in children
<1 year of age.
• Ratio of ALL:AML is 2:1
• Leukemic cells have been noted in cord blood
at birth
• Chromosomal translocaton can also occur in
utero during fetal hematopoiesis.
29. INFANTILE LEUKEMIA
• Presentation is usually with hyperleukocytosis
and extensive tissue infiltration with
organomegaly.
• Subcutanous nodules , leukemia cutis and
tachypnoea caused by leukemic cells
pulmonary infiltration
• leukemic cell morphology shows irregular
lymphoblasts with phenotype negative for
CD10
30. INFANTILE LEUKEMIA
• TREATMENT:
• Intensive chemotheray.
• Stem cell transplantation
• None of them satisfactory.
• Meticulous supportive care is necessary
because of the young age and aggressive
therapy needed in these patients.
32. Leukostasis
• Leukostasis – predominantly in those with WBC
counts > 100,000 (10% of patients); can also be seen
in patients with WBC > 50,000
– Most common in those with M4 or M5 leukemia
– Function of the blast cells being less deformable than
mature myeloid cells. As a result, intravascular plugs
develop.
– High metabolic activity of blast cells and local production
of various cytokines contribute to underlying hypoxia
35. Leukostasis
• Transfuse platelets to keep count above 20,000/μL.
• Avoid (RBC) transfusions because they will raise viscosity
(keep Hb ≤10 g/dL). If RBCs are required, consider partial
exchange transfusion.
• Hydration, alkalinization, and allopurinol should be initiated .
• Administer fresh frozen plasma (FFP) and vitamin K for
coagulopathy.
• Before cytotoxic therapy, consider leukapheresis or exchange
transfusion to lower WBC count if CNS or pulmonary
symptoms exist.
• Start disease treatment as soon as patient is clinically stable.
36. Leukostasis
• Leukapheresis
– Limited affect on established vascular plugs
– Limited benefit in those with underlying pulmonary
symptoms following chemotherapy. Symptoms in this case
related to leukocyte lysis and subsequent inflammatory
response
– Should not be used as a single modality agent in patients
with leukostasis.
– May consider as adjunct to chemoterapy in patients with
WBC >100,000 and symptoms suggestive of leukostasis
37. Tumor Lysis Syndrome
• Characterized by metabolic derangements
caused by massive release of cellular
components following lysis of malignant cells
• Commonly seen in malignancies with high
rates of cell proliferation (esp. ALL, Burkitt’s
lymphoma); also can be seen with AML
38. Tumor Lysis Syndrome
• Hyperuricemia, hypocalcemia, hyperkalemia,
hyperphosphatemia.
• Can lead to acute kidney injury due to precipitation
of uric acid crystals and/or calcium phosphate
crystals in renal tubules and micovasculature,
respectively.
39. Tumor Lysis Syndrome
• Release of intracellular proteins →catobilized to hypoxanthine
→ xanthine → uric acid → Crystalization of uric acid and in
renal tubules → impaired renal function
• Release of phosphate from malignant cells → calcium
phosphate precipitation and further renal impairment along
with hypocalcemia and resultant symptoms from ↓Ca
– Hyperphosphatemia: nausea, vomiting, diarrhea, seizures, lethargy
– Hypocalcemia: arrhythmia, hypotension, tetany, cramps
– Hyperkalemia: arrhythmia, cramps, paresthesia
40. Tumor Lysis Syndrome
• Hydration: Dextrose 5% (D5) 1/4 normal saline (NS) ± 40 mEq/L
NaHCO3 (without K) at double maintenance. Keep urine
specificgravity <1.010 and urine output >100mL/m2/hr.
• Hyperuricemia: Allopurinol inhibits formation of uric acid and can
be given (PO) or (IV) Rasburicase converts uric acid to the more
soluble allantoin. Use in higher-risk patients, especially those with
uric acid >7.5 mg/dL.
• Monitor K+, Ca2+, phosphate, uric acid, and urinalysis closely (up to
Q2 hr for high-risk patients). There is an increased risk of calcium
phosphate precipitation when Ca × Phos > 60
• Consider stopping alkalinization after uric acid levels return to
normal to facilitate calcium phosphate excretion.
41. SPINAL CORD COMPRESSION
• Etiology: Intrinsic or extrinsic compression of spinal
cord; occurs most commonly with brain tumors,
sarcomas, leukemia with lymphomatous
involvement, lymphoma, and neuroblastoma.
Presentation: Back pain (localized or radicular),
weakness, sensory loss, change in bowel or bladder
function.
Prognosis for recovery based on duration and level of
disability at presentation.
42. DIAGNOSIS
• Magnetic resonance imaging (MRI [preferred])
or computed tomography (CT) scan of spine.
• A plain film of spine has good specificity but
detects only two thirds of abnormalities
43. MANAGEMENT
• Management: (Steroids may prevent acurate diagnosis of
leukemia/lymphoma; plan diagnostic procedure as soon as
possible)
• Bolus dexamethasone 1–2mg/kg/day IV and obtain an
emergent MRI of the spine in case of severe symptoms
• In mild sign and symptoms lower dose of dexamethasone,
0.25–0.5 mg/kg/dayPO, divided Q6 hr. Perform MRI of
spine within 24 hours.
• If cause of tumor is known, emergent radiotherapy or
chemotherapy is indicated for sensitive tumors; otherwise,
emergent neurosurgery consultationis warranted.
• If cause of tumor is unknown or debulking may remove
most or all of tumor, surgery is indicated to decompress the
spine.
44. RESPIRATORY DISTRESS AND SV
SYNDROME
• Etiology: Mediastinal mass, edema, or
thrombosis; typically seen with Hodgkin
disease, non-Hodgkin lymphoma (e.g.,
lymphoblastic lymphoma), ALL (T-lineage),
germ cell tumors
• Presentation: Orthopnea, headaches, facial
swelling, dizziness, plethora, acute respiratory
distress or failure
45. DIAGNOSIS AND TREATMENT
Diagnosis: Chest radiograph. Consider CT or MRI to
assess airway.
• Attempt diagnosis of malignancy (if not known) by
least invasive method possible. Avoid sedation or
general anesthesia if unstable, high risk.
Management:
• a. Control airway
• b. Biopsy (e.g., bone marrow, pleurocentesis,
lymphnode biopsy) before therapy if patient can
tolerate sedation or general anesthesia
• Empiric therapy: radiotherapy, steroids, chemotherapy
46. NEUTROPENIC TYPHLITIS
Etiology: Inflammation of bowel wall, usually
localized to cecum. Occurs most often in
association with prolonged neutropenia.
Presentation: Right lower quadrant abdominal
pain, nausea, diarrhea, fever (fever may be
absent early in course
Neutropenic patient with abdominal pain
warrants evaluation for typhlitis .
47. DIAGNOSIS MNAGEMENT
Diagnosis:
• Careful serial abdominal examinations
• X-ray may show pneumatosis intestinalis, bowel wall
edema
• CT (IV and PO contrast) most sensitive imaging; may
reveal bowel walll thickening, pneumatosis intestinalis
Management:
• Keep(NPO), IV fluids; consider NG decompression.
• Broad anaerobic and gram-negative antibiotic
coverage (consider coverage for Clostridium difficile).
• Follow closely with surgery consult.
48. FEVER NEUTROPENIA
• Etiology: Presumed infection (bacterial, viral,
or fungal) in a neutropenic host. Bacterial
infection is the most common documented
infection.
• Occassionally, fevers may be due to
medications.
49. PRESNTATION AND DIGNOSIS
Presentation: Fever, fatigue, chills, rigors,
listlessness, lethargy, tachypnea,tachycardia,
localized pain.
Diagnosis: Fever (temperature [T] > 38.3°C or T
> 38.0°C for >1 hour) in the setting of
neutropenia (ANC < 500 cells/μL, or < 1000
cells but expected to drop to <500 in the next
48 hours).