Oncological emergencies faced in Pediatric Hematology & Oncology department of BSMMU

1. Presenters:
DR. RENESHA ISLAM
DR. MD IMRAN HABIB
YEAR-3 RESIDENT (PHASE-B)
PAEDIATRIC HAEMATOLOGY & ONCOLOGY
WELCO
ME TO
SEMINA
R

2. ONCOLOGIC EMERGENCIES

3. ONCOLOGIC EMERGENCY
Any acute, potentially life threatening event, either
directly or indirectly related to a patient’s cancer or
its treatment, which if not anticipated, quickly
recognized & effectively treated, may rapidly result
in permanent morbidity or death of the patient.
Importance:-
o Need to be addressed before therapy can begin or
continue.
o To avoid end-organ injury.

4. Pediatric Malignancies
Adapted from: American Cancer Society Cancer Facts & Figures, 2007. Atlanta, American Cancer Society, 2007.
Leukemia, 30%
CNS, 22.3%
Other, 17.1%
Neuroblastoma, 7.3%
Wilms, 5.6%
Rhabdo, 3.1%
HL, 3.5%
NHL, 4.5%
Osteo, 2.4%
Rb, 2.8%
Ewing’s, 1.4%

5. • To facilitate recognition and management,
emergencies are categorized in following way-
o Metabolic
o Haematologic
o Cardiothoracic
o Abdominal
o Genitourinary
o Neurological
o Endocrine
o Treatment related emergencies &
o Miscellaneous.

6. METABOLIC EMERGENCIES
• Tumor lysis syndrome (TLS) and associated
electrolyte derangements.
• Hypercalcaemia
• Syndrome of inappropriate anti diuretic
hormone secretion (SIADH)
• Shock.

7. TUMOR LYSIS SYNDROME
TLS arises due to the rapid release of intracellular
metabolites (such as phosphorous, potassium & uric
acid) from dying tumor cells in quantities that exceed
the excretory capacity of the kidneys.
• Although it can occur prior to any cytotoxic therapy,
its manifestations usually appear 12 to 72 hours from
the initiation of therapy.
More common in:
Lymphoproliferative tumors with abdominal
involvement (e.g. B cell/ T cell Iymphoma, leukaemias
and Burkitt's Iymphoma)

8. pathophysiology

9. Complication of Tumor Lysis Syndrome

10. Risk Factors for the Tumor Lysis Syndrome
CATEGORIES OF RISK FACTORS
1.CANCER MASS:-
Bulky tumor or extensive metastasis
Organ infiltration by cancer cells
Bone marrow involvement
Renal infiltration or outflow-tract
obstruction
2. CELL LYSIS POTENTIAL:-
High rate of proliferation of
cancer cells
Cancer-cell sensitivity to
anticancer therapy
Intensity of initial anticancer
therapy
3. FEATURES ON PATIENT PRESENTATION
Nephropathy before diagnosis of
cancer
Dehydration or volume depletion
Acidic urine
Hypotension
Exposure to nephrotoxins
4. SUPPORTIVE CARE
Inadequate hydration
Exogenous potassium
Exogenous phosphate
Delayed uric acid removal

11. Risk Factors for the Tumor Lysis Syndrome
Risk Factor Comment
Bulky tumor or
extensive metastasis
The larger the cancer mass or the higher the number of
cells that will lyse with treatment, the higher the risk of
clinical tumor lysis syndrome.
Organ infiltration by
cancer cells
Hepatomegaly, splenomegaly, and nephromegaly generally
represent tumor infiltration into these organs, and
therefore a larger tumor burden than that of patients
without these findings.
Bone marrow
involvement
Healthy adults have 1.4 kg of bone marrow.
A marrow that has been replaced by leukemic cells
contains a cancer mass greater than 1 kg and therefore
represents bulky disease.
Renal infiltration or
outflow-tract
obstruction
Decreased urine flow predispose to nephropathy from
other causes, such as the tumor lysis syndrome.
1. Cancer mass:-

12. Risk Factors for the Tumor Lysis Syndrome.
Risk Factor Comment
High rate of
proliferation of
cancer cells
Lactate dehydrogenase level is a surrogate for tumor
proliferation.
The higher the level, the greater the risk of the tumor lysis
syndrome.
Cancer-cell
sensitivity to
anticancer therapy
Cancers that are inherently more sensitive to therapy have
a higher rate of cell lysis and a greater risk of the tumor
lysis syndrome than the other cancers.
Intensity of initial
anticancer therapy
Preexisting nephropathy from hypertension, diabetes, gout,
or other causes has a greater risk for acute kidney injury
and the tumor lysis syndrome.
2. Cell lysis potential:-

13. Risk Factors for the Tumor Lysis Syndrome.
Risk Factor Comment
Nephropathy before
diagnosis of cancer
Urine flow predispose to nephropathy from other causes,
such as the tumor lysis syndrome.
Dehydration or
volume depletion
Dehydration decreases the rate of urine flow through renal
tubules and increases the level of solutes
Acidic urine Uric acid has a lower solubility in acidic urine and therefore
crystallizes more rapidly
Hypotension Hypotension decreases urine flow and increases the level of
solutes that can crystallize. Hypotension can also
independently cause acute kidney injury.
Exposure to
nephrotoxins
Vancomycin, aminoglycosides, contrast agents for diagnostic
imaging, and other potential nephrotoxins increase the risk
of acute kidney injury from lysis of cancer cells.
3. Features on patient presentation:-

14. Risk Factors for the Tumor Lysis Syndrome.
Risk Factor Comment
Inadequate
hydration
Increases the risk of crystallization inside tubules
Exogenous
potassium
Unless the patient has severe hypokalemia or a
dysrhythmia from hypokalemia, potassium should not
be included in the intravenous fluids, and potassium
(from food or medications) should be minimized until
the risk period for the tumor lysis syndrome has
passed.
4. Supportive care:-

15. Risk Factors for the Tumor Lysis Syndrome.
Risk Factor Comment
Exogenous phosphate Restricting dietary phosphate and adding a phosphate
binder reduce the exogenous load of phosphate so that the
kidneys need only excrete the endogenous load of
phosphate released by cancer-cell lysis.
Delayed uric acid
removal
Allopurinol prevents formation of new uric acid by inhibiting
xanthine oxidase and preventing conversion of xanthine to
uric acid. It does not remove existing uric acid and does
increase urinary excretion of xanthine, which can crystallize
and cause nephropathy. Rasburicase is an enzyme that
rapidly removes uric acid by converting it to allantoin,
which is highly soluble and readily excreted in the urine.
The longer the uric acid level remains high, the greater the
risk of crystal formation and acute kidney injury.
4. Supportive care:-

16. Diagnostic Criteria for Laboratory & Clinical TLS
• Laboratory TLS (LTLS): The presence of two or more
abnormal serum values at presentation. Such as-
• Clinical TLS (CTLS): Presence of LTLS and one or more
of the following clinical complications: renal
insufficiency, cardiac arrhythmias, seizures or sudden
death.
MetabolicAbnormality Laboratory level
Hyperuricemia S. uric acid ≥8 mg/dl
Hyperphosphatemia S. Phosphate ≥6.5 mg/dl (2.1 mmol/L)
Hyperkalemia S. K+ ≥6.0 mmol/L
Hypocalcemia S. Ca+ ≤7.0 mg/dl (≤1.75 mmol/L)
S. Creatinine >normaL

17. Evaluation and Diagnosis
Close attention to symptoms of
electrolyte abnormalities
Laboratory investigation
– Abdominal pain, Fullness
– Back pain
– Vomiting
– Anorexia, Cramps
– Diarrhoea
– Signs of dehydration
– Muscle spasms
– Tetany, seizures
– Diminshed urine output
-CBC
-S. Electrolytes
-S. Ca
-S. Phosphate
-S. Uric acid
-LDH
-ECG

18. MANAGEMENT
• Hydration: 2–4 times maintenance fluid.
Maintain urine output >100 mL/m2/hr
Urine specific gravity <1.010
5% Dextrose in 0.25% Normal saline
No K+, Ca+, PO4.
• Alkalinization:
40-80 mEq/L to maintain urine pH 7.0–7.5
Increase NaHCO3 as needed
Stop NaHCO3 when cytotoxic therapy is initiated
or the urine pH >7.5 or S. TCO2 reaches 30mEq/L.

19. MANAGEMENT
• Diuresis: If U/O poor (< 60ml/m2/hr)
Avoid if hypovolemia present
Furosemide (0.5–1.0 mg/kg)
Mannitol (0.5 g/kg over 15 min) --if patient
has oliguria, unresponsive to increased hydration and
furosemide.
• Uric acid reduction:
Allopurinol 300 mg/m2/day or 10mg/kg/day PO
Rasburicase (recombinant urate oxidase)-
0.15-0.2mg/kg/day IV, for 1 or 2 days
The dose can be repeated.

20. Urate Oxidase Metabolism
Hypoxanthine
Xanthine oxidase Allopurinol
Xanthine
Xanthine oxidase Allopurinol
Uric acid
Rasburicase
Allantoin
Purine Catabolism

21. TLS Management - Hyperkalemia
Mild (< 6 mEq/l) and asymptomatic:
Hydration and diuretics.
Kayexelate(1g/kg+ 50% sorbitol)
Moderate to severe:
-Rapid insulin (0.1 U/kg/h) plus
glucose (dextrose 0.5 g/kg/h)
- Life-threatening arrhythmias IV calcium gluconate
(100-200 mg/kg) or calcium chloride (10 mg/kg)
- NaHCO3 (1-2 mEq/kg IV)
- Dialysis
CAN BE FATAL
K+=

22. TLS Management - Hypocalcemia
• Only treat if symptomatic
– Fatigue, cramping, tetany, laryngospasm, weakness,
paresthesias, Seizure, ECG changes.
• Control Phos Level
– PO4 binders
• CaCl2
– 10 mg/kg IV
• Ca Gluconate
– 100 mg/kg IV
Hall and Todd, Postgrad Med J, 2006

23. • Hyperphosphatemia: Low phosphate diet & Hydration
Aluminum hydroxide (150 mg/kg/day)
• Transfusion: If indicated.
• Dialysis: Indicated in-
-Progressive renal failure with K+ > 6 mEq/l, PO4 > 10 mg/dl
-Persistent hyperkalemia with QRS interval widening
-Severe metabolic acidosis.
-Volume overload unresponsive to diuretic therapy.
-Anuria and overt uremic symptoms (i.e., encephalopathy).
-Severe symptomatic hypocalcemia.
-Hypertension (BP150/90) and inadequate U/O at 10 hr from
start of treatment.
-Congestive heart failure.
MANAGEMENT

24. Patients at high risk for the tumor lysis syndrome may also
receive low-intensity initial therapy.
– Slower lysis of the cancer cells allows renal homeostatic
mechanisms to clear metabolites before they
accumulate and cause organ damage.
– This strategy, in cases of advanced B-cell non-Hodgkin’s
lymphoma or Burkitt’s leukemia, has involved treatment
with low-dose cyclophosphamide, vincristine, and
– prednisone for a week before the start of intensive
chemotherapy. Similarly, many groups subscribe to a
week of prednisone monotherapy for childhood acute
lymphoblastic leukemia.
PREVENTION OF ACUTE
KIDNEY INJURY

25. Bedside TLS Monitoring
• Clinical assessment
– Hourly intake output & vital signs
• Laboratory
– Na, K, Glucose, iCa--
– BUN, S. Cr, Uric acid, iPo4--
– CBC / Diff / Platelet count --
– Coags, LFTs, Albumin--
– Imaging --
4-6 hourly
4-6 hourly
6-8 hourly
24 hourly
as indicated
• Respiratory, CNS, and cardiac monitoring if
hyperkalemia or hypocalcemia are present.

26. Haematologic Emergencies
1. Hyperleucocytosis
& Leukostasis
2. Bleeding tendency
3. Bone Marrow
Depression.

27. Hyperleukocytosis & Leukostasis
• Peripheral leukocyte count >100 000/ml
• Clinically significant if- > 200,000/mL in AML,
> 300,000/mL in ALL & CML
• May be asymptomatic or may present with-
Mental status change, headache, blurred vision,
dyspnoea, cyanosis, dactilytis seizure, stroke, coma.
• May lead to death by-
-CNS Hemorrage
-Pulmonary Leukostasis
-Metabolic derangements that accompany tumor lysis.

28. CNS and Pulmonary Leukostasis

29. Mechanism:
• High number of blasts in microcirculation ⇒ sludging ⇒
interferes with oxygenation of local tissue ⇒ Tissue
Ischemia
• Adhesive reaction between abnormal vascular
endothelium & the circulating blasts worsening
leukostasis, thrombosis ⇒ secondary hemorrhage.
•Higher metabolic rate of blasts & local production of
cytokines ⇒ Tissue hypoxia.
•Thrombi in the circulation ⇒ vascular damage &
parenchymal ischemia ⇒ pulmonary or cerebrovascular
hemorrhage & edema.

30. Management of Hyperleukocytosis
 Hydration
•To facilitate excretion of toxic metabolites
•To reduce blood viscosity
 Alkalinization
 Allopurinol/Urate oxidase
 Avoid ↑ blood viscosity
•Cautious use of blood transfusion and diuretics.
 Exchange transfusions/ leukopheresis.
 Ultimate Rx- Systemic anti-cancer chemotherapy
initiated soonest possible.

31. BLEEDING IN THE CANCER PATIENT
Third most common cause of death after organ failure
due to tumor invasion and infection.
 Thombocytopenia
 Coagulation abnormality
 Effect of other drugs-mucositis caused by cytotoxic
drugs or corticosteroids.
 Acute GIT Bleeding-hematemesis & melena.
 Massive Hemoptysis
 Oral Bleeding
 Epistaxis.

32. DIC
• Microthrombi &
bleeding
– Platelet & clotting
factor consumption
– Microangiopathy
– Hyperfibrinolysis.
• Etiologies
– Gram -ve sepsis
– Leukemia (AML M3,M5;
ALL with high WBC)
– Metastatic solid tumors.
Semin Thromb Hemost. 2007 33(4):408-15
www.medscape.com
Sepsis/
Malignancy
Systemic
activationof
coagulation
Widespread
intravascular
fibrin
deposition
Consumption
of plts,
clotting
factors
Severe
Bleeding
Thrombosis,
organ
failure

33. DIC -Management
• Anticipation, frequent lab/clinical monitoring.
• Replace consumed factors
– Platelets: Transfuse to keep > 50K initially
– Fibrinogen: FFP or Cryo to keep > 150 mg/dL
– No routine use of heparin or antifibrinolytics.
• Treat underlying cause
– AML: Start chemo
– APML: Start ATRA as soon
as suspected
– Sepsis: Antibiotics.

34. Depression Of Bone Marrow Activity
 Depression of normal bone marrow activity
results in –
-Anaemia
-Thrombocytopenia and
-Neutropenia.
 Treated with supportive care, regardless of their
etiology.
 Supportive care often includes transfusion of
individual blood components.

35. Cardiothoracic Emergencies
o Superior vena cava syndrome & superior
mediastinal syndrome
o Pleural & pericardial effusion
o Cardiac Temponade
o Pneumothorax & pneumomediastinum
o Massive Hemoptysis
o ATRA syndrome.

36. CVCS & SMS
• consists of the S/S of superior vena
cava (SVC) obstruction due to
compression or thrombosis.
• Pathophysiology:
– Compression, obstruction of SVC
– Thin wall, low intraluminal
pressure
– Impaired venous return.
Superior mediastinal syndrome(SMS)
consists of SVCS with tracheal
compression.
-Airways more compliant and
compressible in children.

37. Clinical Picture – SVCS/SMS
Airway Compromise
• Hoarseness (17%)
• Cough (54%)
• Dyspnea (54%)
• Stridor (4%)
• Tachypnea
• Orthopnea
• Wheezing
• Anxiety
CNS
• Syncope (10%)
• Headache (9%)
• Confusion (4%)
• Lethargy (2%)
• Blurry vision (2%)
• Papilledema
• Ear fullness
Venous Obstruction
• Facial
swelling,
edema (82%)
• Engorged chest
wall vessels
(53%)
• Arm edema (42%)
• Cyanosis of
face, neck, &
upper
extremities
• Petechiae of head,
neck, arms, &
trunk
• Pleural effusion
• Pulsus paradoxsus
Seth & Bhat, Ind J Pediatr, 2011
Wilson et al., NEJM, 2007

38. Chee et al., Nature Clinical Practice
Cardiovascular Medicine, 2007

39. Diagnosis should be made quickly by least invasive
procedure.
1. Chest radiography
2. CT Scan
3. CBC, Serum LDH, Uric acid, α-fetoprotein, β-HCG
4. ECG
5. If possible, a tissue specimen for diagnosis
Several reports suggest a stepwise approach to
diagnosis.
If tolerated

40. SVCS/SMS CXR MASS
Non diagnostic Diagnostic
Generate D/Ds
Assess risk
Anesthesia Low
risk
Anesthesia High
risk
Biopsy Treat
Re-assess
Treat
Treat
Low risk Biopsy Treat
High risk Treat
CBC, other studies

41. o Establishing a tissue diagnosis may not be possible &
patients may need empiric Rx as a life-saving measure.
1st-line treatment in emergent situations is high-dose
steroids (Prednisolone or Methylprednisolone).
Patient should undergo biopsy as soon as the mass
shrinks & the patient is stable.
o If poor response to steroids
chemotherapy such as vincristine, cyclophosphamide
with or without an anthracycline can be added.
Therapy

42.  If a solid tumor not responsive to steroids or
chemotherapy
Emergent radiation can be performed.
 For symptomatic venous thrombosis with no
evidence of hemorrhage
• Anticoagulation can be initiated using systemic or
low-molecular-weight heparin (LMWH)

43. Intubation
Airway obstruction occurs distally
ET tube stops here

44.  Characterised by:
fever, respiratory distress,
respiratory failure, oedema,
pleural/pericardial, effusion,
hypotension.
Pathophysiology:
 Respiratory distress due to
leukocytosis associated with ATRA
induced multiplication and
differentiation of leukaemic
promyelocytes.
Treatment:
 Dexamethasone 0.5 – 1mg/kg/dose
BD.
ATRA (all-trans retinoic acid) syndrome

45. ABDOMINAL EMERGENCIES
 Hemorrhage – Oesophageal varcies
 Upper GIT bleeding (hematemesis/melena)
 Bowel Obstruction
 Perforation
 Infection & Inflammation
 Perirectal Abscess
 Cholecystitis & Biliary Obstruction
 Acute Massive Hepatic Enlargement
 Pancreatitis.

46. Evaluation & Diagnosis
• Pain is the principal symptom : detail history regarding
Location, quality & timing,
Relation to status of cancer
Recent medication
Surgical history
• Observation and a gentle examination-
Whether the child lies still
Winces with cough, movement or motion
Distension, asymmetry, surgical scar
Rectal examination.

47. Investigations
 Serial CBC
 Blood Culture
 Serum Electrolytes
 Abdominal X-ray ( supine, erect and left
lateral decubitus)
 Chest X-ray
 Endoscopic and Colonoscopic examination
 Imaging Studies : Abdominal US, CT, MRI

48. Typhlytis/ Neutropenic Enterocolitis
 Necrotizing colitis typically localised to terminal ileum
and caecum. May progress from inflammation to full
thickness infraction and perforation.
 Caused by : Pseudomonas species, E. coli &
other Gram (-)ve bacteria, Staphylococcus, alpha-
hemolytic Streptococcus, Clostridium, Candida and
Aspergillus.
 Occurs in : 6% of Acute leukaemia cases common in
AML, but also in ALL, HSCT recipient.

49. Diagnosis

51. Neutropenic Colitis
• Thickened cecum
• Peri-intestinal soft-tissue stranding
• Free Fluid
• Pneumatosis Intestinalis
Van de Wetering, Supp Care Can, 2003
www.meddean.luc.edu
radiology.rsna.org

52. Treatment
In the past mortality was 20% to almost 100%
But now, 70% - 80% pt can be managed medically.
 Nothing per oral
 N-G suction
 Broad spectrum Antibiotic to cover gram (-)ve,
Clindamycin or Metronidazole for anaerobes, and anti-
fungal
 IV fluid and Electrolytes
 Tranfusion of PRBC & platelet
 Vasopressin (as needed)

53. Proposed criteria for surgical intervention
 Persistent gastro-intestinal bleeding despite resolution
of thrombocytopenia and coagulation abnormalities.
 Evidence of free air.
 Need for vasopressor support or large volumes of
fluid.(Suggestive of uncontrolled sepsis from intestinal
infraction)
 Development of symptom of an intra-abdominal
process that would normally require an operation.

54. Genito-urinary Emergencies

55. Oliguria/Anuria
• Differential Diagnoses
• Prerenal: septic shock, dehydration, emesis,
diarrhea, decreased oral intake, metabolic
abnormalities from tumor lysis.
• Postrenal: bulky abdominopelvic tumors with
obstruction, hemorrhagic cystitis.
• Renal insufficiency: chemotherapy agents, contrast
dyes, anti-infectives.

56. .
• Evaluation
• BUN, creatinine, electrolytes.
• Close monitoring of all intake and output.
• CT or ultrasound (US) of abdomen/pelvis.

57. Treatment
Vigorous hydration for prerenal etiologies including BK
viremia.
• Decompression of obstructed kidney with stenting or
catheter placement.
• Treatment of underlying tumor with chemotherapy,
surgery, or radiation to decrease outflow obstruction.
• Avoidance of nephrotoxic agents.
• With significant electrolyte abnormalities, fluid
overload or true anuria, consideration of dialysis may be
indicated.

58. .
Definition
• Systolic or diastolic blood pressure outside the
95th percentile for age, gender, and height.
Etiology
• Secondary to pain or anxiety, and often transient.
• Secondary to tumor compression of renal
parenchyma leading to increased renin production
(secondary hyperaldosteronism).
• Secondary increased renin production from tumors
(e.g., pheochromocytoma, Wilms’ tumor,
neuroblastoma)
Hypertension

59. ..
• Secondary to medications: steroids, anti-infectives,
calcineurin inhibitors.
• Renal vein thrombosis.
• Increased intracranial pressure (ICP).
• Symptoms
• Symptoms may include headache, irritability,
lethargy, confusion, and, if untreated, seizures, posterior
reversible encephalopathy syndrome (PRES).
• Treatment
• Acute hypertension:
• Hydralazine (0.20.6 mg/kg/dose IV).

60. ‘
• Nicardipine (0.51 μg/kg/min infusion to be titrated to
desired blood pressure).
• Labetalol (0.21 mg/kg/dose IV, to be avoided in
patients with bronchospasm or diabetes).
• Sublingual nifedipine (510 mg/dose for children
weighing .10 kg).
• Oral clonidine (0.050.1 mg/dose).
Chronic hypertension:
• Amlodipine (0.1 mg/kg per dose, or 2.55 mg/day).
• Consider ACE inhibitors or beta-blockers.
Hypertension from fluid overload:
• Furosemide (0.51 mg/kg)

61. .
Signs and symptoms of hemorrhagic cystitis are
hematuria caused by bleeding and inflammation of
the bladder, leading to dysuria, urgency, and
frequency. Substantial blood loss and urinary
obstruction can result.
• Therapy with CPM and IFOS are the most common
causes of hemorrhagic cystitis.
• The early phases of hemorrhagic cystitis are mucosal
edema, ulceration, epithelial necrosis, and submucosal
fibrosis. Long-term complications include bladder
fibrosis and contraction, urinary reflux, renal failure,
and transitional cell bladder tumors..
Hemorrhagic Cystitis

62. .
The diagnosis is made by
• History and urinalysis.
• Ultrasonography
Treatment:
Chemotherapy-induced cystitis is best prevented by
vigorous hydration and brisk diuresis.
Concurrent use of the uroprotective agent sodium-2-
mercaptoethanesulfonate (MESNA)
Antiviral.

63. Neurological Emergencies

64. CNS EMERGENCIES: Acute alterations
in consciousness
• Tumor
– Primary
– Metastatic
– Hyperleukocytosis
• Stroke
• Seizure
• Leukoencephalopathy
• Post-XRT somnolence
• Chemotherapy
• Drugs
• Metabolic
• Infection
• Hypo/hypertension
• Dehydration
• Hypoxia
• Liver failure
• Depression

65. Chemotherapy causing acute
alterations in consciousness
• Corticosteroids:
Mood swings, hallucinations, psychosis
• Cytosine arabinoside:
Cerebellar dysfunction, seizures, coma
• Methotrexate: Encephalopathy, seizures
• Ifosfamide: Somnolence
• Retinoic acid: Pseudotumor.

66. SPINAL CORD COMPRESSION
EWING SARCOMA 30/168 (17.9%)
NEUROBLASTOMA 32/402 ( 7.9%)
OSTEOSARCOMA 16/243 ( 6.5%)
RHABDOMYOSARCOMA 14/287 ( 4.9%)
SOFT TISSUE SARCOMA 4/102 ( 3.9%)
GERM CELL TUMOR 5/130 ( 3.8%)
HODGKIN DISEASE 8/404 ( 2.0%)
HEPATOMA 1/69 ( 1.4%)
WILMS TUMOR 2/290 ( 0.7%)
OTHER 0/164 -
TOTAL 113/2259 ( 5.0%)
KLEIN JNs 74:70, 1991

67. Spinal Cord Compression
3-5% of children with cancer develop acute spinal cord or
cauda equina compression. Sarcomas account for about half
of the cases of spinal cord involvement in childhood.
Pathophysiology
 The most common scenario for cord compression is the
direct extension of a metastatic lesion from the vertebrae
into the epidural space
 The most common site of compression is the thoracic
spine (70%). The lumbar spine 20%, cervical spine10%.
Clinical Presentation
 Back pain with localized tenderness occurs in 80% of
patients.
 Incontinence, urinary retention, and other abnormalities
of bowel or bladder function.

68. .
• Loss of strength and sensory deficits with a sensory level
may occur.
Evaluation
A thorough history and neurologic examination.
Spinal radiographs, MRI
Cerebrospinal fluid analysis
Treatment:
It is crucial to initiate treatment immediately.
Dexamethasone is initiated to decrease local edema,
prior to diagnostic studies.
If an epidural mass is identified, treatment is aimed at
rapid decompression. Chemotherapy, radiation therapy,
or surgical decompression may be used.

70. Causes:
 brain tumours e.g. astrocytoma, disseminated
subarachnoid tumor, Pseudotumor cerebri, APL
treated with ATRA, and with Abscesses, massive
cerebrovascular accidents , CNS hemorrhage, and
extensive meningeal tumor.
 Signs and symptoms vary according to age/site.
 Infant: vomiting, lethargy, regression of milestones,
seizures, symptoms of obstructive hydrocephalus.
 Older: early morning recurrent headaches with or
without vomiting.
 Cerebellar: Ipsilateral hypotonia and ataxia
 Herniation of cerebellar tonsil – head tilt and neck
stiffness.
Increased ICP and brain herniation

71. .
 Tumors near 3rd ventricle – visual loss, ICP and
hydrocephalus - obstruction of aqueduct of Sylvius due
to pineal tumour – ICP & Parinaud’s syndrome.
 Evaluation and Treatment
Emergent CT scan is the radiologic study of choice than
MRI.
 ICP should receive dexamethasone (1st dose, 1 to 2
mg/kg, then 0.25 to 0.5 mg/kg every 6 hours)
 Acute manifestations of herniation (altered
consciousness and respiratory or circulatory collapse)
from increased ICP require mannitol (0.5 to 1 g/kg IV
over 30-60 minutes).
 Removal of the mass lesion is the definitive therapy for
increased ICP.

72. .
Tumor
Primary central nervous system
tumor
Metastatic tumor
Leukemic meningitis
Hyperleukocytosis
Central nervous system
infection
Viral
Bacterial
Fungal
Protozoal
Cerebrovascular accident
Etiology of Seizures in Children with Cancer
Treatment
Intrathecal methotrexate
Intrathecal cytosine arabinoside
L-Asparaginase. Others, hypoxia.

73. Cerebrovascular accident
 Direct or metastatic spread of tumour,
antineoplastic agent, haematologic abnormality.
 L-Asparaginase associated with venous or lateral and
sagittal sinus thrombosis caused by rebound
hypercoagulable state
 AML especially APML associated with CVA. Due
to release of procoagulant.
• Management
 Suportive
 Use of anticoagulant potentially
detrimental
 In L-Aspa induced, recommended FFP

74. Endocrine Emergencies

75. .
Etiology
1. Involves continuous pituitary release of antidiuretic
hormone (ADH)
2. Results from physiologic stress, pain, surgery,
mechanical ventilation, infections, CNS and pulmonary
lesions, lymphomas, and leukemias.
4. Occurs as a side effect of vincristine, vinblastine,
cyclophosphamide, ifosfamide, cisplatin, and melphalan.
5. Occurs in overhydration with hypotonic fluids,
diabetes insipidus with free water replacement, and
cerebral salt wasting.
Syndrome of Inappropriate Antidiuretic
Hormone Secretion (SIADH)

76. .
Clinical Features
• Oliguria,Weight gain,fatigue, headache, and nausea.
• Late manifestations include lethargy, confusion,
hallucinations, seizures, and coma.
Laboratory Features of SIADH
• Low serum osmolality (,280 mOsm/l).
• High urine osmolality (.500 mOsm/l).
• Urine to serum osmolality ratio >1.
• Hyponatremia (sodium, ,130 mEq/l).
• Increased urine specific gravity.

77. .
Treatment
1.Fluid restriction.
2. Furosemide 1 mg/kg should be administered.
3. Hydration with normal saline limited to insensible
losses (500 ml/m2/24 h) plus ongoing losses.
4. severe neurologic involvement (seizures or coma),
hydrate carefully with hypertonic saline 3%

78. Associated with Non Hodgkin & Hodgkin Lymphoma.
Rare in children.
Ca+ > 12mg/dl – Affect multiple organ system.
> 20mg/dl- Fatal.
• S/S: Nausea, constipation, polyuria, profound muscle
weakness, bradyarrhythmias, renal insufficiency, coma.
• Treatment:
- Excretion: Hydration, Forced diuresis
- Mobilization: Prednisone (acts slowly)
Calcitonin
Biphosphonates
-Treatment of the malignancy.
Hypercalcaemia

79. Adrenal Insufficiency
• Etiology
1.Secondary to significant prior
corticosteroid exposure.
2. During periods of critical
illness, trauma, surgery, or
infection.
3. Tissue resistance to steroids.
4. Adrenal gland failure.
Clinical Features
1. Fatigue, dizziness,
weakness, myalgia,
nausea/vomiting.
2. Severe hypotension,
shock.
3. Hyponatremia,
hyperkalemia, metabolic
acidosis with normal anion
gap

80. .
• 1. Glucocorticoid replacement therapy
(hydrocortisone): a. Hydrocortisone
b. Strict monitoring for hyperglycemia
• 2. Treatment includes interventions for sepsis and
hypotension .
• 3. Consider checking cortisol levels as patient may
need physiologic replacement once stress dosing is
complete
Treatment

81. TREATMENT-ASSOCIATED EMERGENCIES
• Anaphylaxis and
Hypersensitivity to
Chemotherapeutic Agents
Etiology
1. Asparaginase.
2. Platinum agents.
3. Etoposide.
4. Monoclonal antibodies.
• Presentation
1. Bronchospasm.
2. Dyspnea.
3. Wheezing.
4. Angioedema.
5. Flushing.
6. urticarial
7. Rhinitis

82. .
1. Discontinue inciting agent.
2. Maintain vascular access & Assess respiratory status.
3. If bronchospasm or hypotension: a. IM epinephrine
(0.01 mg/kg of 1:1000 dilution b. IV fluid boluses with
normal saline are recommended. c. Persistent wheezing,
consider albuterol and prepare for intubation.
4. H1 blockers
5. H2 antagonists (ranitidine).
6. Parenteral steroids, typically methylprednisolone or
hydrocortisone, are recommended to dampen the late
allergic symptoms.
Treatment

83. Miscellaneous:
1.Infections
2. shock
3. Veno occlusive disease

84. Why are cancer pts at risk for life-
threatening infection?
• Chemotherapy
– Decreased number and
function of immune cells
• Radiation
• Surgeries
• Breakdown of
mucocutaneous barriers
• Foreign bodies (CVL,
grafts, etc.)
Meckler, Lindemulder. Emerg
Med Clin N Am, 2009.

85. .

86. Common Pathogens
GP
Bacteria
Staph spp
Strep spp
Enterococcus spp
Corynebacterium
spp
Bacillus spp
Clostridium spp
GN
Bacteria
E. Coli
Pseudomonas
aeruginosa
Klebsiella spp.
Enterobacter
Anaerobes
HSV, VZV
RSV, Influenza,
Parainfluenza
Adenovirus
Rotavirus,
enterovirus
CMV, EBV, HHV6
BK, JC
Candida spp
Aspergillus spp
Zygomycetes
Fusarium
Scedosporium
Cryptococcus
Viral Fungal Other
Pneumocystis
jiroveci
Protozoa
Meckler, Lindemulder. Emerg Med Clin N Am, 2009.

87. Risk group Assessment
High Risk
-Any malignancy
not controlled
-ANC <100/cumm
-Duration>7 days
-Toxic appearance
- Evidence of
infections.
Low risk
Dx: ALL, NHL in remission
ANC >100/cumm
Duration< 7 days
Non toxic appearance.

88. .
 CBC with Differential
 Blood culture from each CVC lumen
 Culture from each suspicious lumen
 Urine R/E, Culture
 Stool R/E & culture
 S. Electrolyte, S. Creatinine
 CXR
 For CNS symptoms CSF study &
CT Scan brain
Lab. Assessment

89. .
Supportive management
 Empirical antibiotic therapy by broad spectrum with
antipseudomonal coverage
Monotherapy: cefepime, ceftazidime, imipenem,
meropenem, tazobactum/ piperacillin.
Dual Therapy: with monotherapy antibiotics Amikacin
or Gentamicin added.
Add gram positive coverage vancomycin and
clindamycin according to situation.
 Change antibiotic according to culture report.
 Empirical Antifungal
Management of Febrile Neutropenia

90. Shock
Common causes of shock in child with cancer
Management:
Ascertain cause and treat accordingly.

91. .
Also referred to as hepatic sinusoidal obstruction
syndrome.
 Characterized by rapid and often massive hepatic
enlargement with resultant right-upper-quadrant pain,
liver tenderness, jaundice, weight gain, and ascites.
 Ultrasonography shows ascites and reversal of flow in
hepatic vessels.
Etiology Preexisting hepatic disease, radiation,
allogeneic transplant, vincristine, actinomycin-D, and 6-
thiguanine, busulfan with or without
cyclophosphamide, and younger age.
Veno-Occlusive Disease

92. .
1. Primarily supportive in the nontransplant
setting including discontinuation of the
offending agent.
2. Studies evaluating defibrotide as a treatment
option are ongoing in the transplant setting.
Treatment

93. Summary
• Oncologic emergencies are common in the
pediatric population.
• The majority of these can be anticipated with
awareness of the clinical situation.
• Teamwork and communication among health
care professionals is essential for good
outcomes.