1. CANCER IN CHILDREN SOLID
MODIFY STILL THE SLIDE
By: Cecilia Galan- Fernandez, DPPS, DPSHBT, DPSPO Place: 5th floor ASMPH Date : January 11,2011 1

2. Cancer Pathogenesis
Normally, your body forms new cells as you need them, replacing old cells that die
All kinds of cancer, including childhood cancer, have a common disease process
cells grow out of control,
develop abnormal sizes and
shapes
ignore their typical boundaries
inside the body
destroy their neighbor cells
spread (or metastasize) to other
organs & tissues
As cancer cells grow, they demand
more nutrition from the body
Cell cycle

3. Epidemiology Incidence 14/100,000 Among all age groups, the most
common childhood cancers are leukemia, lymphoma, and brain cancer.
As children enter their teen years, there is an increase in the incidence of osteosarcoma (bone cancer).
The sites of cancer are different for each type

4. Risk Factors Pediatric vs. Adult Cancers
Lifestyle factors that contribute to the development of cancer in adults:
smoking
diet
obesity
occupation
prolonged exposure to carcinogenic agents

5. For the 0-14 yrs old
Acute leukemias (ALL-most common)
Central nervous system tumors
Neuroblastoma
Wilms’ tumor
Non Hodgkin’s Lymphoma
Rhabdomyosarcoma, soft tissue tumors,germ cell tumors, retinoblastoma and bone tumors
For 15 – 19 yrs old
Hodgkin’s disease
Germ cell tumors
Osteosarcoma, Ewing’s sarcoma

6. Risk Factors Pediatric vs. Adult Cancers
Lifestyle factors are not associated with cancer in children
Genetic condition- anomalies
Family history
Environmental- ionizing radiation, chemicals
Infections – EBV
Chemotherapy
Precise cause – unknown

7. Signs of Childhood Cancer
Continued, unexplained weight loss Headaches, often with early morning vomiting Increased swelling or persistent pain in bones, joints, back, or legs Lump or mass, esp. in the abdomen, neck, chest, pelvis, or armpits Development of excessive bruising, bleeding, or rash
Constant/recurrent infections A whitish color behind the pupil Nausea which persists or vomiting with or w/o seizure
Constant tiredness or noticeable paleness Eye or vision changes which occur suddenly and persists Recurrent or persistent fevers of unknown origin

8. WHY DIFFICULT TO DIAGNOSE CHILDHOOD CANCER?
Vague manifestations
Childhood malignancies are rare
Doctor’s reluctance to consider cancer diagnosis

9. Important Factors to Cure
EARLY DETECTION
PROPER TREATMENT
GOOD SUPPORTIVE CARE

10. RETINOBLASTOMA

11. RETINOBLASTOMA Most common intraocular malignancy of childhood
2nd most freq solid malignancy
80% are diagnosed before 3-4 years old
Median age at diagnosis: 2 years old
Beyond 6 years old is rare!!!
Incidence:
1. 60% --non-heriditary & unilateral
2. 25% --hereditary & bilateral
3. 15% --hereditary & unilateral

12. CLASSIFICATION 1.Laterality ---unilateral or bilateral
2.Focality ---Unifocal or multifocal
3.Genetics --- hereditary or nonheriditary

13. LATERALITY UNILATERAL -Knudson’s two hit phenomenon
-15% carry constitutional mutation
BILATERAL
-asstd. with advanced parental age
-present earlier than unilateral
-hereditary form
-worse prognosis
-autosomal dominant

14. Retinoblastoma RB gene on Chromosome 13, “two-hit theory”
Round blue cell tumor arising in any of the nucleated layers of the retina
Hematogenous, lymphatic spread, direct extension thru the optic nerve
Only 10% detected by ophthalmologic screening 14

15. COMMON SIGNS & SYMPTOMS
Leukokoria --most common
Strabismus --2nd most common
Decreased visual acuity
Inflammatory changes
Glaucoma
Vitreous hemorrhage resulting in black pupil
Rubeosis iridis –(neovascularization of surface of iris)
*in 50% with advanced dsespontaneous bleed---hyphema

17. Investigations for Diagnosis of Retinoblastoma
1.Examinations
-done under anesthesia by pedia ophtha
-done by pedia oncologist
-Audiology evaluation if chemo with carbplatin
2. Imaging studies
-CT scan of brain and orbits
3. Laboratory evaluations
-CBC,Bld chem,electrolytes
-Creatinine clearance if chemo with carboplatin

18. Investigations for Diagnosis of Retinoblastoma
4. Diagnostic Studies
-Lumbar puncture ---only if with radiographic or clinical suspicion of CNS disease
-Bone scan --- only if with bone pain or other extra-
ocular disease
-Bone marrow biopsy –only with abnormal CBC(without alternative explanation) or other extraocular disease
5.Pathologic evaluation---if enucleation is performed

19. Histology: The only human tumor that is radically treated without tissue biopsy confirmation
Flexner-Wintersteiner rosettes: lined by tall cuboidal cells that circumbscribe and an apical lumen

20. Patterns of Spread Intraocular: 1
Patterns of Spread Intraocular: 1. With endophytic growth, there is a white hazy mass. 2. With exophytic growth, there is retinal detachment. 3. Most tumors have combined growth. 4. Retinal cells frequently break off from the main mass and seed the vitreous or new locations on the retina.

21. Extraocular:
Retinoblastoma spreads first to surrounding structures and then by hematogenous or lymphatic extension.
Retinoblastoma invades the optic nerve. From there it can spread directly along the axons to the brain or may cross into the subarachnoid space and spread via the CSF to the brain.
Hematogenous spread leads to metastatic disease, most commonly to brain, bone marrow, or bone.
Lymphatic spread is rare because there is minimal lymphatic drainage of the orbit. Occasionally, retinoblastoma spreads lymphatically to the preauricular and submandibular nodes.

22. PARTS OF THE EYE

24. retinoblastoma

26. SITES OF METASTASIS
BRAIN
BONE
BONE MARROW
LUNGS

27. RISKS FOR METASTATIC SPREAD
1. If optic nerve stump is <5mm—bad
>5mm---better
2. Tumor invasion into the anterior chamber
3. Large tumor with vitreous seeding
4. Rubeosis iridis
5. Glaucoma

28. Retinoblastoma Primary Goal: Cure!!!!
GOAL OF TREATMENT:
Primary Goal: Cure!!!!
Secondary Goal: Preservation of vision 28

29. TREATMENT Surgery Enucleation—if no hope for salvage of useful vision
II. Radiotherapy
III. Chemotherapy

30. Neuroblastoma Most common extracranial solid tumor in infancy
8-10% of all childhood malignancies
Affects infants & preschool
50% younger than 2 year old
30% younger than 1 year old

31. NEONATAL NEUROBLASTOMA
Subcutaneous nodules. If massaged, a zone of pallor develops around the nodule due to catecholamine discharge
Extensive metastasis to the liver
Bone marrow involvement
Massive adrenal hemorrhage into tumor
Hydrops fetalis and/or signs of erythroblastosis fetalis
Stage 4S
Diagnosis: prenatal ULTZ
In many cases, a mass is not palpable
Only 50% have elevated urinary catecholamines
Prognosis: favorable course (if with + favorable factors)
Treatment: Curative by surgery
Course: Others regress

32. NEUROBLASTOMA
Originates from primordial neural crest cells that normally give rise to adrenal & sympathetic ganglia
Are tumors of the sympathetic nerve tissue
Can occur anywhere along the sympathetic neural pathway

33. Neuroblastoma – Clinical Features
Arise from the sympathetic outflow
Primary sites
70% abdominal primary
(50% adrenal medulla, 50% extra-adrenal tissue)
Thoracic tumours, posterior mediastinum (20%)
Head & neck tumours (10%)
Epidural (dumbbell or hourglass shaped) tumors – cord compression/paraplegia
Bone
Lymph nodes are enlarged
Lungs—rarely involved(0.7%), involvement should be proven by bx
Pelvis---constipation,urinary retention,presacral

34. MANIFESTIONS Excessive catecholamine (VMA/HVA)
intermittent attacks of sweating,pallor
Headaches,palpitation
Hypertension—renin induced due to renovascular compromise & seen in 1-5%

35. MANIFESTATIONS
2. Signs & symptoms of Vasoactive Intestinal Peptide (VIP)
Intractable watery diarrhea resulting to failure to thrive
Abdominal distention
hypokalemia

36. MANIFESTATIONS 3. Acute myoclonic encephalopathy
Bursts of rapid involuntary random eye movements in all directions of gaze (OPSOCLONUS)
Motor incoordination due to frequent,irregular jerking of muscles of the limbs and trunk (MYOCLONIC JERKING)
Note:
1.May or may not resolve after the tumor is removed or symptoms may resolve only after several months. Some , it may be permanent
2. Prognosis is good

37. PATHOPHYSIOLOGY OF OM
NOT DUE due to direct involvement of the CNS by tumor or due to the production of catecholamines
It is associated by well-defined IgG & IgM autoantibodies that bind to the cytoplasm of cerebellar Purkinje cells & to some axons in the white matter
Diffuse & extensive lymphocytic infiltration with lymphoid follicles is a characteristic histologic feature of OM
This suggests an IMMUNE-MEDIATED MECHANISM OF THIS RARE SYNDROME

38. Recommended Criteria at INSS Conference for a Diagnosis of Neuroblastoma
Established if:
(1) Unequivocal pathologic diagnosisa is made from tumor tissue by light microscopy
(with or without immunohistology, electron microscopy), and/or increased urine or
serum catecholamines or metabolites.b OR
(2) Bone marrow aspirate or trephine biopsy contains unequivocal tumor cellsa (e.g.,syncytia or immunocytologically positive clumps of cells) and increased urine or
serum catecholamines or metabolites
Source: Manual of Pediatric Hematology & Oncology (4th ed) p534

39. Recommended Studies for Assessment of Extent of Disease
Tumor site Recommended tests
Primary site CT and/or MRI scana with 3-D measurements; MIBG scan.b
Metastatic sites
Bone marrow Bilateral posterior iliac crest marrow aspirates and trephine core bone marrow biopsies required to exclude marrow involvement.
A single positive site documents marrow involvement. Core
biopsies must contain at least 1 cm of marrow (excluding
cartilage) to be considered adequate.
Bone MIBG scan; 99Tc scan required if MIBG scan negative or
unavailable. Plain radiographs of positive lesions.
Lymph nodes Clinical examination (palpable nodes confirmedhistologically.
CT scan for nonpalpable nodes (3-D measurements).
Abdomen/liver CT and/or MRI scana with 3-D measurements.
Chest AP and lateral chest radiographs. CT/MRI necessary if chest
radiograph positive, or if abdominal mass/nodes extend
into chest

40. NB – Clinical features Metastases Bone marrow- anaemia Bone (Pain)
Orbit (Peri-orbital
Skin (blue-berry muffin)

41. NB – Therapy Surgery –laminectomy to decompression
Chemotherapy-responsive in 80-85%;advantageous in making surgery safer by reduction of tumor size
Transplant (Stage 4, Nmyc amplification
HD Chemo with Autologous Bone Marrow Transplant

42. Evaluation of a Lymph Node
A diagnosis of lymphoma or any malignancy must always be considered when evaluating a child with an enlarged peripheral lymph node
It must be emphasized that not all palpable nodes are pathologically enlarged and that most pathologically enlarged nodes are benign.
Points to consider in evaluating a lymph node:
I. LOCATION OF THE NODE
a. Nodes of the axilla, neck and groin are often palpable in normal children
b. Palpable supraclavicular nodes -- always considered abnormal
* if with left-sided (Virchow’s) – metastases from intra-abdominal CA
* if with right-sided nodes intrathoracic disease

43. II When size matters a.Cervical and axillary nodes --- > 1 cm
b. Inguinal node >1.5 cm
c. Epitrochlear node ----> 0.5 cm

44. IV.INDICATIONS
III. GENERALIZED OR LOCALIZED?
a. Generalized involvement of more than two (2) noncontiguous areas
caused by many different disease process
b. Localized enlarged lymph nodes within contiguous anatomic regions and usually due to one of two ( infection or malignancy)
III. CHARACTER
Malignant nodes ---- non-tender, firm, rubbery and rapidly enlarging becoming cnonfluent and located in the supraclavicular region

45. INDICATIONS FOR LYMPH NODE BIOPSY
Chronic,persistent,progressive adenopathy
If an infectious etiology has not been uncovered, a dominant node that persists for 6 weeks should be biopsied
Node > 2.5 cm in diameter in the absence of signs of infection that warrant a trial of antibiotic
Supraclavicular adenopathy
Sytemic symptoms

46. Non-Hodgkin Lymphoma 5-7% malignant disease of childhood
3rd most common childhood malignancy
60% of childhood lymphomas
M>F
Peak age: years old
Etiology: unknown
Risk factors:
Genetic-- SCID, WAS
Posttransplantation immunosuppression
Drugs ex. Phenytoin (cause pseudolymphoma that regress with cessation of treatment)
Radiation – treatment with radiotherapy (4-5% develop NHL within 10 years
Virus---EBV and HIV

47. APPROACH TO THE DIAGNOSIS OF NON
HODGKIN’S LYMPHOMA
History and PE
childhood lymphoma more often extranodal rapid tumor growth
frequently involved site: Intra-abdominal ( B-cell)
Intrathoracic (precursor T-cell)
Sites:
Abdomen --- primary site (35%)
Head and neck %
Mediastinum %
CNS and BM --- CNS involvement and epidural tumor uncommon at presentation but more common in the presence of BM involvement.
/3 with BM disease have simultaneous CNS involvement
--- Intracranial tumor more likely epidural although it can occur within brain parencyma

48. B SYMPTOMS OF HODGKIN LYMPHOMA
1. Unexplained fever with temp above 38.0ْ C orally
2. Drenching night sweats
3. Unexplained weight loss of 10% within 6 months preceding diagnosis
Source: Principles & Practice of Pediatric Oncology 5th ed p.701

49. IMPORTANT INVESTIGATIONS FOR NHL
Histologic analysis- Primary mode of definitive diagnosis
CBC and APC
Chemistries and Serum electrolytes
Liver and renal function tests
SLDH- measures tumor volume
Uric acid
Imaging studies
Chest X-ray
Chest CT
Abdominal CT/ Ultrasound
BMA with biopsy ( bilateral)
CSF examination -- essential

50. ST. JUDE CHILDREN’S STAGING SYSTEM
STAGE I
A single tumor (extranodal) or single anatomic area (nodal) with the exclusion of mediastinum or abdomen
STAGE II
A single tumor (extranodal) with regional node involvement
Two or more nodal areas on the same side of the diaphragm
Two single (extranodal) tumors with or without regional node involvement on the same side of the diaghragm
A primary gastrointestinal tract tumor, usually in the ileocecalarea, with or without involvement of associated mesenteric nodes only
STAGE III
Two single tumors (extranodal) on opposite sides of the diaphragm
Two or more nodal areas above and below the diaphragm
All the primary intrathoracic tumors (mediastinal, pleural and thymic)
All extensive primary intraabdominal disease
All paraspinal or epidural tumors, regardless of other tumor site(s)
STAGE IV
Any of the above with initial CNS and/or bone marrow involvement

51. Lymphomas – 3rd most common
Hodgkin Lymphoma
Childhood form < 14yo, young adult form 15-34yo, older adult form 55-74yo
EBV implicated, <10 yrs, male, with preexisting immunodeficiency
Reed-Sternberg cell hallmark of disease
Painless lymphadenopathy, anterior mediastinal mass and systemic symptoms like fever, night sweats and weight loss
Ann Arbor Staging System
Same + neck CT, ESR, serum copper and ferritin
Non- Hodgkin Lymphoma
Classified as B or non-B types (previously classified as lymphoblastic, SNCCL, LCL)
Intrathoracic, abdominal skin , bone, soft tissues, CNS
St Jude Staging system
CBC, electrolytes, uric acid, sldh, creatinine, sgpt,chest Xray or scan, abdominal scan or MRI, bone scan, BMA or biopsy, CSF cytology 51

52. WILMS’ TUMOR Most common primary malignant tumor of childhood
EPIDEMIOLOGY:
– 7.6 Cases per million children
younger than 15 y/o
6% of childhood cancer
higher for blacks, low in Asians
F>M

53. A CHILD WITH ANIRIDIA Wilms’ tumor associated syndrome (WAGR)
2.Hemihypertrophy
3.Genitourinary abnormalities
4. Mental retardation

54. Wilm’s Tumor (Nephroblastoma)
Clinical Features:
1.Abdominal mass
-Synchronous (4.4-7%)
-Metachronous(1-1.9%)
2.Abdominal pain
3. Hematuria (10%)
4.Hypertension (25%)

55. PHYSICAL EXAMINATION Location Size of the mass Note:
WT is usually a large flank mass that does not particularly move with respiration.

56. WORKUP CBC Liver tests Renal function tests (urinalysis,creatinine)
Serum calcium (elev.in rhabdoid or cmn)
Coagulation assays
Imaging studies:
CT (abdomen)
Doppler ULTZ –to assess the IVC
CXR/ CT (chest)
Bone scan or skeletal survey
Brain imaging (MRI)

57. STAGING (NWTS-5)
Stage I ---confined to the kidney & completelyresected.
no renal capsule penetration
or involvement of renal sinus vessel
Stage II --- tumor extends beyond the kidney but completely resected (neg.margins & LN)
At least 1 of the ff:
a. Penetration of the renal capsule
b. Invasion of renal sinus vessels
c. biopsy of tumor prior to removal

58. STAGING (NWHTS-5) (lung,liver,bone,brain)
STAGE III --- Gross or microscopic residual tumor remains postop,including inoperable tumor
spillage of tumor preop or intraop regional LN metastasis or transected tumor thrombus
STAGE IV Hematogenous or LN mets outside the abdomen
(lung,liver,bone,brain)
STAGE V Bilateral Wilms’ tumor

59. Predictive factors (recurrence/progression
1.size
2.age of patient
3.histology
a .blastemal– hi stage/invasive
b. stromal
c. epithelial –low stage/ less invasive and resistant to chemotx

60. PROGNOSIS 4. LN metastasis 5. local features of tumor – capsular or
vascular invasion
IMPORTANT:
The histologic finding of ANAPLASIA is the most important determinant prognosis

61. BILATERAL WILMS’ TUMOR
Histology: favorable
Prognostic factors:
1. Age
diagnosis at early age (<2 y/o) –better
survival rate:
<2 y/o %
>2 y/o %
2. Stage
Stage 1 & II ---85%
Stage III & IV --- 0%

62. POSITIVE PROGNOSTIC FACTORS
Stage I an II
2. Neg. Para-oartic nodes
3. Absence of anaplasia/sarcomatous
4. Absence of tumor rupture
5. Time of relapse (later better than early)
(> 15 months from diagnosis)
6. Site of metastases at relapse
(Lung better than liver)

63. NEPHROGENIC RESTS

64. TREATMENT 2. Tumor removal by partial nephrectomy OBJECTIVE:
1. Maximum preservation of renal tissue
2. Tumor removal by partial nephrectomy

65. TREATMENT Laparotomy and bx of both kidneys (stage and histology)
LN should be bx & each side is staged separately.
Excision of the tumor(s) is performed at the initial operation only if all of the tumor can be removed with preservation of sufficient renal parenchyma for normal renal function on at least one side
Chemotherapy
Babies < 12 mo.– half the dose
Babies > 12 mo.– full dose

66. CHEMOTHERAPY DOSE: A- Dactinomycin (45ug/kg,IV)
D* Doxorubicin (1.0mg/kg, IV)
D # Doxorubicin (1.5mg/kg,IV)
V – Vincristine(0.05mg/kg,IV)
V* Vincristine(0.67mg/kg,IV)
XRT – Radiation therapy
** for StageIII and IV, FH or StageII-IV,UH

67. TREATMENT Evaluation and Abdominal CT – at week 5
at wk 6 – if the imaging showed persistent
but resectable tumor or tumor responded completely
do second look surgery and biopsy
at 2nd look surgery ---complete excision of the tumor frm.the least involved kidney shld. be carried out.
If the procedure leaves a viable & functioning kidney on 1 side & the other kidney, if extensively involved with tumor, should be removed.

68. TREATMENT
Postoperative chemo shld. be adapted to renal function abnormalities:
a.If 2nd look surgery showed no gross or pathologic evidence of persistent tumor, chemo be given accordingly
b. If 2nd look surgery showed gross or pathologic evidence of persistence that can’t be resected, do radiotx and change chemo
(ICE)

69. Abdominal Tumors Neuroblastoma Wilms’ tumor – 2nd
Peripheral sympathetic nervous system malignancy
<5 yrs old, median 2 years old, male predominance
Most common abdominal malignancy
Shimada classification, MYC gene
Retroperitoneal, palpable causing abdominal discomfort, opsomyoclonus, diarrhea
(+) calcification and hemorrhage on CT
Bone, marrow liver, nodes skin mets
Wilms’ tumor – 2nd
Nephroblastoma or mixed embryonal neoplasm of the kidney with three elements: blastema, epithelia and stroma
2-5 years of age
WT1 gene (11p13) Denys-Drash syndrome, WT2 gene Beckwith-Wiedenman syndrome, GUT abn
Smooth and firm, pain, vomiting and hematuria, hypertension
(-) calcification
Pulmonary metastasis, nodes 69

70. Abdominal Tumors Neuroblastoma Wilms’ tumor – 2nd
CT or MRI, BMA, bone scan, urine VMA and HVA (95% +)
Prognostic factors: age at diagnosis, stage, MYCN status, Shimada histology and ploidy in infants
Stage IV-S: <1year old, with dissemination to the skin, liver, bone marrow without bone involvement plus a primary tumor
Wilms’ tumor – 2nd
CT or MRI and chest XRay
Prognosis affected by stage and type of histology, unfavoprable in the presence of large nuclei, hyperchromatism, multiple mitotic figures
Stage V – bilateral tumors 70

71. HEPATOBLASTOMA

72. Liver Tumours Hepatomegaly ± jaundice
Raised AFP (age-specific normogram)
2 types:
Hepatoblastoma
most common
infants & young children
Hepatocellular carcinoma
Rare, older
HBV, HCV

73. Rhabdomyosarcoma Most common soft tissue sarcoma
Found in any anatomic site: head/neck (40%), GUT (20%), trunk (10%)
Associated with Li Fraumeni syndrome and Neurofibromatosis
Arise from the same embryonic mesenchyme as striated muscle
Types: embryonal (60%) intermediate prognosis
boytryoid, alveolar, pleomorphic, undifferentiated 73

74. Clinical
Non-tender mass with no unusual hue to the overlying skin or subcutaneous tissue
Growth of a nontender mass esp. without a clearcut history of trauma, should always alert the MD to consider biopsy, esp. if expansion is confirmed by repeated observations over 1-2 weeks
Mass within a body cavity producing obstruction or discharge,mandates a biopsy

75. Rhabdomyosarcoma Diagnosis: disseminates early
CT/MRI, BMA, bone scans, lymph node biopsy
The most essential element of the work-up is examination of the tumor tissue w/c include the use of special stains(desmin, muscle specific actin, MyoD).
Completely excised tumors have the best prognosis. Favorable site: orbit
older children and disseminated diseases have poorer prognosis 75

76. Rhabdomyosarcoma
Sites
Head & neck
Orbit, nasopharyngeal & middle ear tumours
Genitourinary tract
Bladder & prostate, vaginal & uterine
Extremity
Prognosis
Orbit - excellent
GU tract - good
Extremity, retroperitoneal, metastatic - poor

77. Bone Tumours

78. Malignant Bone Tumors Osteosarcoma Ewing’s Sarcoma
Most common primary malignant bone tumors in children
Second decade of life, growth spurt, long bones, metaphysis
Pleomorphic, spindle shaped cells with malignant osteoid
Bone pain and swelling
“Sunburst pattern” xray
Primary site: FEMUR (metaphyseal portion)
Long bones
Ewing’s Sarcoma
More common in the first 10 years of life
Small round undifferentiated tumors of neural crest origin, flat bones, diaphysis
Askin tumor –if tumors arise in the chest wall
S100 and NSE (+)
Pain and swelling, (+) fever and weight loss
“onion-skinning” pattern xray (flat & diaphyses)
Primary: pelvic,LE,bones of chest wall 78

79. Radiological difference
Sunburst of Osteosarcoma
Onion skin of Ewings sarcoma

80. Malignant Bone tumors Diagnosis: MRI or CT of tumor SLDH bone scan
Alkaline phosphatase
chest ct scan
bone biopsy/BMA in Ewing’s Sarcoma
Both with 75% cure rate if non-metastatic on presentation.
Treatment: Multi-agent chemotherapy and surgery.
Radiotherapy also needed in Ewing’s Sarcoma 80

81. Brain Tumours Special problems Blood-brain barrier limits chemotherapy
Developing brain is vulnerable to toxicity of therapy
Proximity of tumours to vital structures precludes extensive surgery
Tendency to spread within neuraxis

82. Brain Tumours - Classification
Location
2/3 above & 1/3
below tentorium

83. Site and symptoms Posterior fossa – limited space, disrupt CSF flow
Vomiting, Increased ICP
Motor tract involvement – cranial n, long tracts
Supratentorial
Seizures – focal seizures
Deterioration in school performance
Hormonal defects – central precocity, diabetes insipidus

84. (L) parieto-occipital low grade astrocytoma

85. Brain Tumours - Therapy
Surgery
Resectability
Radiotherapy
Toxicity
IQ drop
Endocrinopathy
Growth failure
Chemotherapy
Prolong survival
Increase cure rates
Prognosis depends on:
Resectability
Age
Metastases
Chemosensitivity
Prognosis depends on
Resectability
Age
Metastases
Chemosensitivity 85

86. Oncologic emergencies
Tumour lysis syndrome

87. Tumour lysis syndrome
Metabolic derangement resulting from rapid death of malignant cells
Must have 2 important factors :
high tumour burden,
highly sensitive tumour – ALL, AML, NHL
Hyperkalaemia - hydration, no K supplements, K binders
Hyperuricaemia – hydration, alkalinisation, allopurinol, uricozyme to convert to allantoin
Hyperphosphataemia – Phosphate binders
Hypocalcaemia – if symptomatic, partial correction

88. Thank You!!! 88