ONCCOLOGIC EMERGENCIES
 Emeregencies in patients with cancer may be
classified into 3 groups: Pressure or obstruction
caused by a space occupying lesion metabolic or
hormonal problems and treatment related
complication
Structural-Obstructive Oncologic Emergencies
Superior Vena Cava Syndrome
 Clinical manifestation of SVC obstruction with
severe reduction in venous return from the head,
neck and upper extremities
 Malignant tumor (e.g. lung cancer, lymphoma and
metastatic tumors)  responsible for the majority of
SVCs cases
 With the uses of intravascular device (.e.g.
permanent central venous access catheters,
pacemakers/defibrillator leads)  the prevelance of
benign causes of SVCs is increasing 40%
 Lung cancer  e.g. small cell and squamous cell
histologies = 85% of all cases of malignant origin
 In young adults  malignant lymphoma is a
leading causes of SVCs
 Hodgkin’s lymphoma  involves the mediastinum
more commonly that other lymphomas but rarely
causes SVCs
 When SVCs is seen in young man with a
mediastinal mass  the differential diagnosis is
lymphoma vs primary mediastinal germ cell tumor
 Metastatic cancers to the mediastinal lymph nodes
 e.g. testicular and breast carcinomas  only small
portion in cases
 Other causes include: benign tumor, aortic
aneyrysm, thyromegaly, thrombosis and fibrosing
mediastinitis (from irradiation, histoplasmosis or
behcet’s syndrome)
 SVCs as the initial manifestation of Behcet’s
syndrome  due to inflammation of the SVC
associated with thrombosis
Clinical Manifestation
 Neck and facial swelling (especially around the
eyes, dyspnea and cough
 Other symptomps include: hoarseness, tongue
sweeling, headaches, nasal congestion, epistaxis,
hemoptysis, dysphagia, pain, dizziness, syncope and
lethargy
 Bending forwards or lying down  may aggravate
the symptoms
Physical Findings
 Dilated neck veins
 Increase number of collateral veins covering the
anterior chest wall
 cyanosis and edema of the face, arms and chest
 Facial swelling and plethora  exacerbated when
the patients is supine
 More severe cases: Proptosis, glossal and laryngeal
edema and obtundation (altered level of
consciousness)
Symptoms: usually progressive
Signs and symptoms of cerebral and/or laryngeal edema 
associated with poorer prognosis and require urgent
evaluation
 Seizure  related to brain metastasis than to
cerebral edema from venous occlusion
Cardiorespiratory symptoms at rest  particularly with
positional changes  suggest significant airway and vascular
obstruction and limited physiologic reserve
 Cardiac arrest or respiratory failure can occurs
Rarely  esophageal varices may develop: these are downhill
varices  based on the direction of blood flow from cephalad
to caudad (beda dengan portal hypertension dari bawah ke
atas)
 If the obstruction to the SVC is proximal to the
azygous vein = upper 1/3 esophagus
  If the obstruction to the SVC is distal to the azygous
vein = varices occur in the entire length of the
esophagus
 Variceal bleeding  late complication of chronic
SVCS
SVC obstruction  may lead to bilateral breast edema with
bilateral enlarged breast
 Unilateral breast dilation may be seen as a
consequences of axillary or subclavian vein blockage
Diagnosis
 Chest radiographic finding  widening of superior
mediastinum, most commonly on the right side
o Pleural effusion occurs in only 25% of
patients often on the right side
 The effusion are exudative and
occasionally chylous (milky bodily
fluid consisting of lymph and
emulsified fats)
 Computed topography (CT)  proved the most
reliable view of the mediastinal anatomy
 MRI  no advantages over CT scan
 Invasive procedure  bronchoscopy, percutaneous
needle biopsy, mediastinocopy and even thoracotomy
 Endobronchial or esophageal ultrasound guided
needle aspiration  may establish the diagnosis
safely
Treatment
 The one potentially is life-threatening complication
of a superior mediastinal mass  tracheal
obstruction
o Diuretics with a low salt diet, head
elevation and oxygen  produce temporary
symptomatic relief
o Glucocorticoid  for shrinking lymphoma
masses
o They are of no benefit in patients with lung
cancer
 Radiation therapy  primary treatment for SVCs
 caused by non-small-cell lung cancer and other
metastatic solid tumors
 Chemotherapy  effective when the underlying
cancers I small-cell carcinoma of the lung, lymphoma
or germ cells tumors
 Early stenting  may be necessary in patients with
severe symptoms; but this could increase the venous
return after stenting may precipitate heart failure and
pulmonary edema
o Other complication: hematoma at the
insertion of the site, SVC perforation, stent
migration in the right ventricle, stent
fracture and pulmonary embolism
 Surgery may provide immediate relief for patients
in whom a benign process is the cause.
Pericardial Effusion/Tamponade
 Malignant pericardial disease  found at autopsy in 5-
10% of patient with cancer
o Most frequently with lung cancer, breast
cancer, leukemia’s, and lymphomas
 Cardiac tamponade initial presentation of extra
thoracic malignancy is rare
 The origin is not malignancy in about 50% of cancer
patient with symptomatic pericardial disease  but
can be related to irradiation, drug-induced pericarditis,
hypothyroidism, idiopathic pericarditis, infection or
autoimmune disease
 Two types of radiation pericarditis occur:
o Acute inflammatory effusive pericarditis 
occur within months of irradiation  which
resolves spontaneously
o Chronic effusive pericarditis  may appear up
to 20 years after radiation therapy  is
accompanied by a thickened pericardium
Symptoms:
 Most patients with pericardial metastasis are
asymptomatic
 Common symtomps: dyspnea, cough, chest pain,
orthopnea and weakness
Physical Findings  A combination of cytology, pericardial and
 Pleural effusion epicardial biopsy and guided pericardioscopy 
 sinus tachycardia give the best diagnostic yield
 jugular venous distention  CT scan: irregular pericardial thickening and
 hepatomegaly mediastinal lymphadenopathy  suggest this is a
 peripheral edema and cyanosis malignant pericardial effusion
 Cancer patient with pericardial effusion containing
Relatively specific diagnostic findings: malignant cells on cytology = very poor survival
 paradoxical pulse, diminished heart sounds about 7 weeks.

 pulsus alternans (pulse waves alternating between

those of greater and lesser amplitude with successive Treatment:
beats)  Acute pericardial tamponade with life-threatening

 friction rub are less common than with nonmalignant hemodynamic instability  requires immediate

pericardial disease drainage of fluid

o this can be quickly achieved by

Diagnosis pericardiocentesis

 Chest radiograph and EKG  reveal abnormalities  The recurrence rate after percutaneous catheter

in 90% of patients; but half of these abnormalities are drainage is about 20%

nonspecific o Sclerotherapy: e.g. pericardial instillation of

o Chest radiograph: enlargement of the belomycin, mitomycin C or tetracycline 

cardiac silhouette or a “water bottle” may decrease recurrence

configuration  Thoracopic pericardial fenestration  use in

 Echocardiography  most helpful diagnostic test; benign causes; but 60% of malignant pericardial

detect little as 15ml of fluids effusion recur after this procedures

o Findings on echocardiogram of right atrial o In subset of patients  drainage of the

and ventricular collapse in diastole strongly pericardial effusion is followed by worsening

suggest tamponade hemodynamic instability  this is called

 Cardiac catherization  gold standard for “postoperative low cardiac output syndrome”

diagnosis and monitoring; equalization of pressures  carries a poor short term survival

across the chambers defines tamponade

 Pericardial fluid: serious, serosanguineous or Hypercalcemia

hemorrhagic  Results from excessive bone resorption relative to

 Cytologic examination of pericardial fluid is bone formation

diagnostic in most patients 1. Bone Metases

a) Most tumors capable of bone
 Measurement of tumor markers in the pericardial
metastasis can also produce
fluid are not helpful in the diagnosis of malignant
hypercalcemia
pericardial fluid
b) Local production of various
 Pericardioscopy (not widely available)  with
substances by tumor cells may
targeted pericardial and epicardial biopsy may
stimulate osteoclastic bone
differentiate: Neoplastic and Benign pericardial
resorption
disease
 c) Local production of various  Slowly rising serum calcium levels may produce only mild
substance by tumor cells  may symptoms, even with serum levels exceeding 15 mg/dL.
stimulate osteoclastic bone a. Early symptoms
resoprtion (1) Polyuria, nocturia, polydipsia
2. Ectopic parathyroid hormone (PTH)  (2) Anorexia
rare (3) Easy fatigability
3. Humoral hypercalcemia of malignancy (4) Weakness
a) Caused by production of a PTH lie b. Late symptoms
substances  called PTH-related (1) Apathy, irritability, depression, decreased ability to
peptide (PTH-RP), by a variety of concentrate, mental obtundation, coma
carcinomas (2) Profound muscle weakness
 PTH-RP has bone- (3) Nausea, vomiting, vague abdominal pain,
resorbing activity and constipation, obstipation
interacts with the renal (4) Pruritus
PTH receptor  to (5) Abnormalities of vision
stimulate renal calcium
resorption Differential diagnosis:
 PTH-RP is not measured in  Idiopathic hypercalcemia is not a tenable diagnosis in
serum PTH assays adult patients.
4. Vitamin D metabolites  More and more often, benign causes of hypercalcemia
a) May be produced by some are recognized to occur in patients with cancer.
lymphomas  these metabolites  The possible etiologies of hypercalcemia include the
promotes intestinal calcium following:
absorption a. Malignancy
5. Prostaglandin and interleukin-1 (1) Metastases to bone
a) Produced by various tumors may (2) Secretion of PTH-like or other humoral factors
occasionally cause  (3) Production of vitamin D metabolites
hypercalcemia; perhaps by b. Primary hyperparathyroidism
enhancing bone resorptions c. Thiazide diuretic therapy
6. Tumors  rarely or never associated with d. Vitamin D or vitamin A intoxication
hypercalcemia despite high frequencies of e. Milk–alkali syndrome
bone metastases f. Familial benign hypocalciuric hypercalcemia
a) Small cell lung cancer g. Others:
b) Prostate cancer (1) Immobilization of patients with accelerated bone
c) Colorectal cancer turnover (e.g., Paget disease or myeloma)
Diagnosis (2) Sarcoidosis, tuberculosis, and other granulomatous
 Symptoms of hypercalcemia depend both on the serum diseases
level of ionized calcium and on how fast the level rises. (3) Hyperthyroidism
 Rapidly rising serum calcium levels tend to produce (4) Lithium administration
obtundation and coma with only moderately elevated (5) Adrenal insufficiency
serum calcium levels (e.g., 13 mg/dL). (6) Diuretic phase of acute renal failure
 (7) Severe liver disease
(8) Theophylline intoxication (6) Radiographs of the abdomen and bones
 Nephrolithiasis is rare in hypercalcemia
Laboratory studies. caused by malignancy and suggests
 All patients with cancer and polyuria, mental status hyperparathyroidism.
changes, or gastrointestinal symptoms should be  Nephrocalcinosis and other ectopic
evaluated for hypercalcemia. calcifications are common in long-standing
a. Routine studies hypercalcemia.
(1) Serum calcium, phosphorus, and albumin levels  Subperiosteal bone resorption
 Ionized calcium constitutes about 47% of the
serum calcium and calcium bound to albumin. Management
 calcium can be corrected (to a normal albumin 1. Acute, symptomatic hypercalcemia should be treated as
concentration of 4 g/dL) using the following an emergency.
formula: a. Hydration and saline diuresis.
Corrected serum calcium (mg/dL) = measured calcium + 0.8  Normal saline containing potassium.
(4.0 − measured albumin) (1) Fluid intake and output and body weight are carefully
monitored.
(2) Serum alkaline phosphatase. (2) Blood levels of calcium, potassium, and magnesium are
 Elevated levels may be due to either measured every 8 to 12 hours, and concentrations of cations
hyperparathyroidism or metastatic disease to (3)Treatment is continued until the blood calcium
the bone or liver. concentration is below 12 mg/dL.
 Normal levels are typical in cases of (4) More vigorous administration of fluids (e.g., 12 to 14 L
hypercalcemia produced by myeloma. over 24 hours) and diuretics (e.g., every 1 to 2 hours) requires
excellent cardiac and renal function
(3) Serum electrolytes.
 Serum chloride concentrations are frequently b. Bisphosphonates
elevated in primary hyperparathyroidism.  potent inhibitors of osteoclast activity and are
effective in the treatment of hypercalcemia of
(4) Blood urea nitrogen (BUN) and serum malignancy.
creatinine.  Zoledronate (Zometa) is the most effective of the
 The direct effect of hypercalcemia on the available drugs; it is given as a single IV infusion of 4
kidneys can result in nephrogenic diabetes mg in 100 mL of normal saline over 15 minutes.
insipidus with defective renal tubular water
conservation Common side effects of both drugs include:
 fever, nausea, and constipation; both drugs may
5) Electrocardiogram (ECG). also cause hypocalcemia, hypophosphatemia, and
 Hypercalcemia results in relative shortening increased serum creatinine.
of the QT interval and prolongation of the PR
interval A potential adverse effect of bisphosphonates is osteonecrosis
of the jaw.
 b. Bisphosphonates.
c. Gallium nitrate (Ganite),  Zoledronate (4 mg IV) or pamidronate (60 to 90 mg
 a potent inhibitor of bone resorption, is given IV) may be given every 7 to 30 days as needed to
intravenously in a dose of 200 mg/m2 daily for 5 days. control hypercalcemia

d. Mithramycin (plicamycin). c. Phosphates

 This drug inhibits bone resorption by reversibly  given orally lower blood levels by binding calcium
poisoning osteoclasts. in the gut.
 Mithramycin, 25 μg/kg, is given by rapid infusion  Diarrhea nearly always accompanies phosphate
into a well-established IV line; serum calcium levels therapy
are lowered in 24 to 48 hours
d. Prostaglandin inhibitors
e. Calcitonin  such as aspirin and indomethacin,
 Is useful for rapid reduction of blood calcium  produce variable and inconsistent lowering of calcium
levels. levels
 The drug inhibits bone resorption and increases
renal calcium clearance. Hyponatremia
 Akibat SIADH yang merupakan paraneoplastic
f. Dialysis. syndrome. Meningkatnya retensi air dengan
 Peritoneal dialysis and hemodialysis rapidly lower natrium yang rendah.
blood calcium levels but are rarely used.  Biasa disebabkan oleh SCLC (small cell lung
carcinoma), CNS tumours.
2. Chronic hypercalcemia.  Can also be iatrogenic: usually thought to be
 Ambulation is encouraged to minimize bone secondary to chemotherapeutic agents used;
resorption that accompanies immobilization. o Cisplatin, cyclophosphamide, and vincristine
 Liberal fluid intake (2 to 3 L/d) is prescribed. are common causative agents.
 Foods containing large amounts of calcium, such as  ADH promotes water uptake in the distal convoluted
milk products, are avoided. tubules; the problem is compounded by increased
 Thiazide diuretics aggravate hypercalcemia and water intake due to lack of thirst inhibition (high
should not be taken. levels ADH induce thirst).
 Treatment of the underlying malignancy may be Manifestasi Klinis:
beneficial.  Headache, fatigue, confusion, coma, seizure, death.
Laboratory studies.
a. Glucocorticoids. a. In all patients with hyponatremia
 Prednisone, 20 to 40 mg PO daily, or hydrocortisone, (1) Serum electrolytes, creatinine, urea nitrogen,
100 to 150 mg IV every 12 hours, calcium, phosphate, glucose, total protein, and
 Glucocorticoids also increase renal calcium excretion. triglycerides
(2) Urine sodium
b. In patients with hyponatremia and without an elevated BUN
(1) Serum and urine osmolality
 (2) Chest radiograph or CT scan to look for evidence Laboratory studies
of lung cancer and brain CT or MRI to look for CNS  Blood glucose concentration of <55 mg/dL =
lesions hypoglycemia
c. In patients with evidence of endocrine hypofunction
(1) Thyroid function tests Management/treatment
(2) Adrenal function tests  IV glucose  rapid IV infusion of 50ml of 50%
(3) Pituitary gland function tests, as necessary dextrose solution
Diagnostic criteria for SIADH include all five of the  Glucagon - 1mg IM or IV
following:
 Octreotide  a somatostatin analog, it decrease
a. Hyponatremia with a disproportionately low
insulin hypersecretion
BUN (often <10 mg/dL)
b. Absence of intravascular volume contraction
Leukostasis
c. Absence of abnormal fluid retention, such as
peripheral edema or ascites  Gara-gara acute leukemia, dimana WBC bisa
d. Normal renal, thyroid, and adrenal function mencapai 50.000-100.000, CNS bleeding, respiratory
e. Serum hypotonicity along with urine that is not distress, abnormal chest radiograph, confusion,
maximally dilute. banyak sel blast.
Treatment: Hypertonic saline, treat underlying cause, fluid Manifestasi Klinis: Dyspnea, hypoxia, fever, CNS
restriction, oral salt tablets, Demeclocyclin and vasopressin involvement, DIC, thrombocytopenia. CXR diffuse alveolar or
receptor antagonist. interstitial infiltrates
Treatment: Cytoreduction + Chemotherapy decreasing WBC,
Hypogylcemia hydroxyurea, leukapharesis if blast >100.000 tapi ga boleh
 Insulin-like substances (e.g. pro-IGF2)  produced by diberikan pada APL.
some tumors (e.g. retroperitoneal sarcomas)
 Hepatocellular carcinoma and extensive liver Tumor Lysis Syndrome

metastasis  deplete glycogen store and impair
gluconeogenesis
Symtomps and signs:
 Faituge, convulsion or coma
 Sometimes show fasting hypoglycemia sign  alteed
morning personality (improve after breakfast)
 Tremors, sweating, tachycardia and hungers pangs
 Akibat excessive tumor breakdown either
spontaneously or during therapy.
 Catabolism of nucleic acid to uric acid cause
hyperuricemia, hyperkalemia,
hyperphosphatemia, secondary hypocalsemia 
Biasa pada pasien chemo dan radiasi ALL dan
Burkitt.
Manifestasi Klinis: Nausea, vomiting, diarrhea, anorexia,
congestive heart failure, cardiac arrhythmia, seizures, tetany,
syncope. Bisa bikin renal failure akibat presipitasi fosfat
dengan uric acid di renal tubule.
Treatment: Furosemide, N Saline, mild hyperkalemia pakai
sodium polystyrene sulfate, dan severe hyperkalemia pakai
glucose solution.
Epidural or Spinal Cord Compression  Pulmonary function studies
 Gara-gara metastasis ke spinal column pada pasien  Bronchoscopy
Hodgkin, non Hodgkin lymphoma, prostate ca.
Manifestasi Klinis: Back pain that is not alleviated by
Consideration for surgical resection of metastasis with
recumbent position, ascending numbness and paresthesia,
bowel bladder dysfunction, gait ataxia. specific primary cancers:
Treatment: immediate corticosteroid, surgery, external beam  Head and neck cancers
radiation  Testicular carcinoma
 Sarcomas
Pulmonary Metastases
 Breast cancers
 Lungs are the most frequent site of distant
metastases Management (for nonresectable pulmonary
 Malignnant melanoma, bone and soft tissue metastasis)
sarcomas and etc  tent to spread to vascular  Local control  Radiation theraphy,
routes and produces discrete metastatic lung cyrotheraphy, radiofrequency ablation
nodules
 Chemotheraphy or hormonal theraphy
 Lymphangitic lung metastasis  prednisone,
Types of Metastases:
chemotheraphy
 Endobronchial metastasis
 Solitary pulmonary metastasis
 Isolated pulmonary metastasis
 Lymphangitic pulmonary metastasis
 Central pulmonary metastasis

Sign and symptoms:

 Normally asymptomatic  symtomp patient
have poor prognosis
 Symtomps: cough, chest pain, hemoptysis or
progressive dyspnea
Radiographic studies:
 No current imaging can distuinguish a benign
tumor from a malignant tumor or a primary
tumor from a metastasis
 PET – positron emission tomography: detecting
extrathoracic disease
 Sputum cytology