Oncological emergencies

ONCOLOGICAL EMERGENCIES
Dr.N.Vasu Babu

INTRODUCTION
• CARDIOVASCULAR- 1)SUPERIOR VENACAVA SYNDROME
2)PERICARDIAL EFFUSION
• CENTRAL NERVOUS-1)SPINAL CORD COMPRESSION
2)CARCINOMATOUS MENINGITIS
• METABOLIC- 1)HYPERCALCEMIA
2)TUMOR LYSIS SYNDROME
3)SIADH
4)HYPOGLYCEMIA
5)HYPERURECEMIA
6)ADRENAL FAILURE
• HEAMATOLOGICAL- 1) LEUCOSTASIS
2) HYPERVISCOSITY SYNDROME
3) POLYCYTHEMIA AND LEUKOCYTOSIS
• OTHERS- 1)NEUTROPENIC FEVER

1.SUPERIOR VENACAVA SYNDROME
• Superior vena cava syndrome (SVCS) is the clinical
expression of obstruction of blood flow through the
SVC. Characteristic symptoms and signs may develop
quickly or gradually when this thin-walled vessel is
compressed, invaded, or thrombosed by processes in
the superior mediastinum.
• The first pathologic description of SVC obstruction, in a
patient with syphilitic aortic aneurysm, appeared in
1757.
• cancer of the lung -approximately 70% of patients with
SVCS.

SUPERIOR VENACAVA SYNDROME
• Before antibiotics the most common causes were
from complications of untreated infection
– Syphilitic thoracic aneurysms
– fibrosing mediastinitis
• Malignancy is presently the most common cause
• Malignant disease can arise in weeks to months
– Not enough time to develop collaterals
• Fibrosing mediastinitis can take years to have
symptoms

• Lung cancer is the most common
• Lymphoma is second most common together represent
94% of cases
• 2-4% of bronchogenic cancer patients develop SVC
syndrome by extrinsic compression or direct invasion.
• Thymoma
• primary mediastinal germ cell neoplasm
• solid tumors with mediastinal nodal metastases
– breast cancer most common type
• Post radiation local vascular fibrosis can also be considered
in oncology patients
• Thrombosis
• Indwelling central venous catheters

• Small cell-38%
• Squamous cell-26%
• Adenocarcinoma-14%
• Large cell-12%
• Unclassified-9%

SIGNS AND SYMPTOMS
• Central venous pressures remain high even in collaterals
– High pressures cause the characteristic clinical picture
• Shortness of breath is the most common symptom
• Facial swelling or head fullness
– exacerbated by bending forward or lying down
• Cough
• Arm edema
• Cyanosis
• Venous distension
– neck
– chest wall

SYMPTOMS-
• DYSPNEA-63%
• FACIAL SWELLING AND HEAD FULLNESS-50%
• COUGH-24%
• ARM SWELLING-18%
• CHESTPAIN-15%
• DYSPHAGIA-9%
PHYSICAL FINDINGS-
• VENOUS DISTENSION OF NECK-66%
• VENOUS DISTENSION OF CHEST WALL-54%
• FACIAL EDEMA-46%
• CYANOSIS-23%
• PLETHORA OF LUNG-19%

SUPERIOR VENA CAVA SYNDROME
Patient who presented with progressively enlarging veins over the anterior chest wall.
A diagnosis of a right-sided superior sulcus (Pancoast) tumor compressing the SVC was
made.

DIAGNOSIS-
• Diagnostic procedures, such as
bronchoscopy,mediastinoscopy, thoracotomy, or
supraclavicular lymph node biopsy, were often avoided
because they were considered to be hazardous in the
presence of SVCS.
• The clinical identification of SVCS is simple because the
symptoms and signs are typical and unmistakable.
• The chest film shows a mass in most patients.
• Only 16% of the patients studied by Parish had normal
chest films.
• The most common radiographic abnormalities are
superior mediastinal widening and pleural effusion.

• CT phlebography provides excellent imaging
information on the site and extent of obstruction
and the status of collaterals.
• Helical CT phlebography replaced the
combination of CT and digitalphlebography that
was advocated in the past.
• Contrast venography provides important
information for determining if the vena cava is
completely obstructed or remains patent and
extrinsically compressed

• Radionuclide technetium (Tc) 99m venography
is an alternative, minimally invasive method of
imaging the venous system
• Gallium single photon emission CT may be of
value in selected cases.
• In 58% of 107 patients reported by
Schraufnagel et al. the SVCS developed before
the primary diagnosis was established.

SUPERIOR VENA CAVA SYNDROME
TREATMENT-
RADIATION THERAPY-
• Radiotherapy is an optional treatment for most patients
with SVCS.
• It is also used as an effective initial treatment if a histologic
diagnosis cannot be established and the clinical status of
the patient is deteriorating.
• Some reviews suggest that SVC obstruction alone rarely
represents an absolute emergency that requires
radiotherapy without a specific diagnosis, and endovascular
stenting may be used as an alternative to radiotherapy for
obtaining immediate relief of the obstruction

• The fractionation schedule of radiation that has been
recommended includes two to four large initial fractions of
3 to 4 cGy, followed by conventional fractionation to a total
dose of 30 to 50 cGy.
• No data clearly support a particular fractionation scheme.
In one study, patients treated with initial high-dose
fractions showed a slightly faster symptomatic
improvement than patients receiving conventional-dose
radiation.
• Improvement within 2 weeks or less was observed in 70%
of those treated with initial high-dose fractions and in 56%
of patients receiving conventional-dose therapy. This
difference was not statistically significant

ENDOVASCULAR STENTING AND ANGIOPLASTY-endovascular
therapy—thrombolysis, angioplasty, and stent therapy.
SURGERY-
• It was recommended that autologous grafts of almost the
same size as the SVC should be used.
• Doty et al. used a composite spiral graft, which was
constructed from the patient's saphenous vein.
• Dacron protheses
• polytetrafluoroethylene prosthesis
• The preferred bypass route is between an innominate or
jugular vein on the left side and the right atrial appendage,
using an end-to-end anastomosis.

THROMBOLYTIC THERAPY-
• Successful experience with thrombolytic
agents was also obtained in the treatment of
catheter-induced SVCS.
• Urokinase was more effective than
streptokinase, and a delay administering
therapy beyond 5 days of symptom onset was
associated with a treatment failure.

General measures-
• Bed rest with the head elevated and oxygen
administration can reduce the cardiac output
and venous pressure.
• Diuretic therapy and a reduced-salt diet to
reduce edema may have an immediate
palliative effect, but the risk of thrombosis
enhanced by dehydration should not be
ignored.

SPINAL CORD COMPRESSION
• Malignant spinal cord compression is defined as the
compressive indentation, displacement, or encasement of
the spinal cord's thecal sac by metastatic or locally
advanced cancer.
• Compression can occur via posterior extension of a
vertebral body mass, resulting in compression of the
anterior aspect of the spinal cord, or through anterior or
anterolateral extension of a mass arising from the dorsal
elements or invading the vertebral foramen, respectively.
• Intramedullary spinal cord metastases produce edema,
distortion, and compression of the spinal cord parenchyma,
resulting in symptoms and signs that are similar to epidural
spinal cord compression

• In adults, metastatic spinal cord compression
occurs in roughly 3.0% to 7.4% of patients
with lung, prostate, and breast cancer and the
overall frequency of malignant spinal cord
compression has been reported to be
approximately 5%.

• Spinal cord damage and loss of neurologic
function result from venous stasis, spinal cord
edema, reduced capillary blood flow, ischemia,
and mechanical compression culminating in
infarction.
• Prostaglandins, cytokines, excitatory
neurotransmitters, and inflammatory mediators
regulate the sweeping pathophysiologic changes
associated with hypoxia, edema, ischemia, and
injury resulting from malignant compression

CLINAICAL PRESENTATION
• The most frequently involved site is the
Thoracic spine (59% to 78%)
Lumbar spine (16% to 33%)
Cervical spine (4% to 15%).
• Multiple epidural sites of compression can occur in
26% to 49%.
• Intramedullary cord compression, accounting for only
1% to 4% of cases, is usually solitary and is often
associated with parenchymal brain metastases

• PAIN-96%
• WEAKNESS-86%
• SENSORY DYSFUNCTION-80%
• AUTONOMIC DYSFUNCTION-64%

• The pain may be local, radicular, or both.
• Local pain is present in the vast majority of cases and
is caused by expansion, destruction, or fracture of the
involved vertebral elements.
• The site of compression can usually be localized to the
site of back or neck pain.
• Local back or neck pain is usually dull, aching,
constant, and progressive.
• Back pain from vertebral destruction resulting in
retropulsion of bone fragment is often worse in the
supine position, a feature distinguishing cord
compression from a herniated disc
• Local back or neck pain can be exacerbated by
movement, sneezing, straining, or neck flexion.

• Bilateral band-like girdle pain is characteristic of
thoracic cord lesions, and unilateral radicular pain
is more characteristic of lumbar or cervical
lesions. Radicular pain from a cervical or lumbar
lesion may involve the shoulder, hip, groin,
perineum, or extremity.
• Complete loss of motor and sensory function
below the affected level (cord shock) can occur
abruptly as vascular insufficiency progresses to
frank ischemia.

• Neurologic examination of the patient with cord shock reveals
absent motor, sensory, reflex, and autonomic function below the
level of the lesion, and the affected extremities demonstrate
flaccidity and absence of tone.
• Absence of perineal and anal reflexes and painless overflow
incontinence complete the neurologic presentation.
• Flaccidity and areflexia are gradually replaced by paraplegia in
flexion.
• Compression of the upper cervical spinal cord can produce paralysis
of the upper extremities and respiratory failure, if acute.
• Lesions involving the conus medullaris or cauda equina produce
flaccid paralysis of the lower extremities, absent or flexor plantar
responses, saddle anesthesia, urinary retention leading to
incontinence, and male impotence

DIAGNOSTIC EVALUATION-
• Plain film radiographs detect the presence and location of
epidural metastases in 83% of patients complaining of back
pain.
• Vertebral body collapse, destruction of the pedicle, and
blastic or sclerotic changes are characteristic findings
observable with plain film radiography.
• Myelography has the advantage over plain films of
visualizing the level of the compression as indicated by a
blockage of myelographic contrast.
• Multiple sites of compression, which may be present in
greater than 30% of cases, may require more than one
subarachnoid puncture

• Bone scintigraphy is more sensitive than plain films in
detecting metastatic involvement and provides
information about the entire skeleton in a single
examination.
• Bone scintigraphy is not as sensitive and specific in
detecting spinal metastases as MRI and is incapable of
describing the soft tissue and spinal cord anatomy
required for the proper diagnosis and treatment of
cord compression.
• Furthermore, primarily osteolytic metastases produced
by multiple myeloma, lymphoma, and other
malignancies may not be detected by bone scan.

CT SCAN
MRI SCAN-
• MRI has a sensitivity of 93%, a specificity of 97%, and an overall
diagnostic accuracy of 95% in detecting cord compression.
• Paraspinous and neuroforaminal tumors are not as easily identified
with myelography as with MRI. In addition, MRI allows avoidance of
neurologic deterioration following lumbar puncture for
myelography.
• MRI excels in demonstrating intramedullary metastases that can be
missed completely by myelography.
• The advantages of MRI over CT include its ability to distinguish the
spinal cord proper from other soft tissue masses in the spinal canal.

• A sagittal T1 nonenhanced survey of the entire spine
quickly and easily identifies multiple sites of compression
and should guide the acquisition of axial views through
areas of involvement.
• Bone metastases appear as dark botches relative to normal
bone marrow in unenhanced T1 images.
• CSF and edematous tumor appear bright on T2 sequences.
• T2 sequences display CSF brightly, producing images that
are similar to a myelogram.
• Axial T2 sequences can be useful in identifying small tumor
nodules on nerve roots.
• Focal blastic lesions may produce decreased intensity on
T2 images.

MRI with
contrast is the
imaging study of
choice to
diagnose spinal
cord
compression
**CT scans maybe
used if MRI
contraindicated

TREATMENT-
• The results of treatment of cord compression have
improved in recent years as a result of earlier diagnosis
with the greater availability of MRI and due to a heightened
awareness of cord compression as a potential oncologic
emergency.
• The pretreatment degree of neurologic dysfunction is the
strongest predicator of therapeutic outcome.
• Eighty percent to 100% of patients with minimal or no
ambulatory dysfunction retain ambulation post treatment.
• Paraparesis improves with treatment in 34% to 63% of
cases, whereas paraplegia improves in up to 10% to 55% of
cases

CORTICOSTEROIDS-
• Corticosteroids (dexamethasone, methylprednisolone)
Dexamethasone reduces edema, inhibits PGE2
synthesis, and decreases the specific gravity of the
compressed spinal cord. It also was shown to delay the
onset of paraplegia in experimental cord compression.
• A prospective randomized study comparing a single
high dose of intravenous dexamethasone (100 mg)
with conventional dose intravenous dexamethasone
(10 mg), both followed by 4 mg orally every 6 hours,
demonstrated no significant benefit for the initial high-
dose bolus

SURGERY-
• Although radiation therapy is currently the treatment of
choice for most spinal metastases, radioresistant and
recurrent neoplasms remain therapeutic dilemmas.
• Accepted indications for surgery are
(1) unknown diagnosis,
(2) spinal instability or compression by bone,
(3) failure to respond to radiotherapy, and
(4) maximalallowable radiation dose already administered
to the spinal cord.
• LAMINECTOMY
• Anterior decompression

• Anterior decompression with mechanical
stabilization has supplanted laminectomy as the
principal surgical treatment for epidural
metastases arising from the vertebral body.
• This approach allows total removal of the
pathologic vertebral body via thoracotomy or a
retroperitoneal approach.
• The vertebral body is replaced with
methylmethacrylate, which is supplemented with
a metal prosthesis that attaches to the adjacent
vertebral bodies

RADIATION THERAPY-
• Radiation plays a central role in the treatment of newly
diagnosed epidural cord compression.
• Greenberg et al., treated patients with
hypofractionated radiotherapy and initial high-dose
dexamethasone. Patients received 100 mg of
intravenous dexamethasone and 500 cGy per fraction
daily for the first 3 days of treatment. Following a 4-day
rest, radiation was continued in 300-cGy fractions to a
total dose of 3000 cGy. Fifty-seven percent of patients
were ambulatory after treatment.

• Radioresponsive tumors, such as neuroblastoma,
can be treated with 2000 to 3000 cGy.
• Epidural cord compression caused by lymphoma
more often responds completely when total
doses greater than 2500 cGy are employed.
• Patients with cord compression by malignant
melanoma are more likely to respond to total
doses greater than 3000 cGy.

• Complete recovery is more often associated with
higher total doses, rather than with the use of large
doses per fraction.
• some radiotherapists continue to recommend delivery
of large doses per fraction (400 to 500 cGy) on the first
3 days of treatment to achieve rapid lysis of tumor,
followed by smaller doses (200 to 300 cGy) for the
remainder of the treatment.
• By convention, patients usually receive 200 to 300 cGy
per fraction to a total dose not exceeding 3000 to 4000
cGy to the spinal cord in 2 to 4 weeks.

CHEMOTHERAPY-
• In adults, cytotoxic chemotherapy and hormonal
therapy have been used to successfully alleviate
spinal cord compression from prostate cancer,
Hodgkin's disease, myeloma, germ cell tumors,
lymphoma, and breast cancer.
• The use of chemotherapy combined with
radiation was associated with a prolonged
survival in patients presenting with epidural cord
compression from non-Hodgkin's lymphoma.

NEUTROPENIC FEVER
• Extremely common emergency in oncology
• Up to 70% mortality rate at 48 hours
Neutropenic:
• ANC (polys and bands) < 500
Fever:
• One reading of 101.3 (38.3)
• 100.4 (38) for more than one hour
steroids, sick, hypotension even in the absence
of fever

NEUTROPENIC FEVER
• Sources
– Enteric Bacteria
– Skin Flora
– Community Acquired Agents
– Iatrogenic/Instrumentation
• Agents
– Gram Negative Rods
– Gram Positive Cocci
– Fungi
– Other

NEUTROPENIC FEVER
Treatment
• Begin therapy within 4 hours of fever spike
• Monotherapy cheaper, safer equaly effective as
dual therapy in uncomplicated neutropenic
fever(Cefepime, Imipenem, Meropenem)
• Dual therapy offers synergy against GNR and
may be preferred in sicker patients or those with
focal infections requiring broader coverage
(pneumonia).
• Regimen must always include anti-pseudomonal
coverage

NEUTROPENIC FEVER
Risk stratification
Need for vancomycin
• – Cellulitis, severe mucositis
• – Infected catheter
• – Hypotension, signs of sepsis
• – Known MRSA colonization
• – Prior quinolone prophylaxis
Need for anaerobic coverage
• – Gingivitis
• – Bowel involvement/rectal abscess

NEUTROPENIC FEVER
Addition of antifungal
• Incidence rises after 7 days of antibiotics with
persistent
fever and neutropenia
• Antifungal added at 5-7 days of persistent F+N
• – Liposomal ampho as effective as ampho, less toxic,
fewer breakthrough fungal infections
• – Voriconazole vs ampho: same mortality,
• – Caspofungin vs ampho: better mortality and fewer SE
• – Intraconazole (avoid in renal insufficiency and for
longer than 14 days)
• When patient’s ANC resolves and afebrile, one can
discontinue meds one by one
– Amphotericin → vancomycin → cefepime

NEUTROPENIC FEVER
Duration of therapy
• If pathogen identified: treat as indicated
• If ANC rises and F stops: can stop A
• If F resolves but N persists:
– Consider stopping with early signs of
hematologic recovery, but watch closely.

NEUTROPENIC FEVER
Growth factors (CSFs) for febrile neutropenia-
• Minor clinical benefit documented
– Shorter duration of neutropenia
– Quicker resolution of fever
– Shorter hospital stay
– No difference in mortality
• May be more effective in high risk

HYPERCALCEMIA
• Hypercalcemia is the most common life-
threatening metabolic disorder in patients with
cancer.
• The prevalence of this disorder approximates 15
to 20 cases per 100,000 persons.
• The incidence varies depending on the underlying
cancer diagnosis, being highest in myeloma and
breast cancer (approximately 40%),intermediate
in non–small cell lung cancer, and uncommon in
colon, prostate, and small cell lung carcinomas

HYPERCALCEMIA
CLINICAL FEATURES-
• GENERAL-dehydration,weight loss,anorexia,polydipsia
• NEUROMUSCULAR-fatigue,lethargy,muscle
weakness,hyporeflexia,confusion,psychosis,
seizure,coma.
• GASTROINTESTINAL-nausea,vomiting,constipation,ileus
• GENITORENAL-polyurea,renal insufficiency
• CARDIAC-bradycardia,prolonged P-R intervel,shortened
Q-T interval,wide T wave,atrial or ventricular
arrhythmias.

HYPERCALCEMIA
PATHOPHYSIOLOGY-
1. Parathyroid Hormone and the Parathyroid
Hormone–Related Protein-
• Many patients with cancer-related hypercalcemia
have biochemical characteristics suggestive of
PTH stimulation, including increased tubular
reabsorption of calcium, hypophosphatemia with
phosphaturia, and elevated levels of
nephrogenous cyclic adenosine monophosphate

HYPERCALCEMIA
• PTH-RP appears to be the most common
mediator of cancer-related hypercalcemia.
Increased blood levels of PTH-RP are commonly
found in patients with solid tumors , particularly
patients with squamous (epidermoid)
carcinomas.
• Several studies have shown that patients with
high levels tend to have an inferior response
when treated with bisphosphonates and a
poorer life expectancy

HYPERCALCEMIA
Vitamin D3-
• Elevated serum 1,25 (OH)2-vitamin D3 levels have
been reported in patients with Hodgkin's disease,
non-Hodgkin's lymphoma, myeloma, and
occasional patients with solid tumors.
• This effect probably results from increased
enzymatic conversion of 25-OH-vitamin D 3 by
1a-vitamin D-hydroxylase, similar to well-
documented processes that occur in patients
with granulomatous disease.

HYPERCALCEMIA
Prostaglandins-
• Prostaglandins have long been implicated as circulating
mediators of cancer-related hypercalcemia, and certain
prostaglandins (notably of the E series) have potent bone-
resorptive activity in vitro
Cytokines-
• TGF-a shares partial amino acid homology with epidermal
growth factor, binds to the epidermal growth factor
receptor, and is a potent inducer of bone resorption in
vitro, both alone and in combination with PTH-RP.
• Interleukin-6 increases bone resorption in vitro, acts as an
autocrine growth factor in myeloma, and may be
associated with hypercalcemia in kidney cancer.

HYPERCALCEMIA
TREATMENT OF CANCER-RELATED HYPERCALCEMIA-
• Where possible, immobilization should be minimized
because inactivity tends to aggravate hypercalcemia
• Patients should be carefully interviewed with respect
to dietary aberrations, and medications containing
calcium, vitamin D, vitamin A, or other retinoids should
be stopped.
• Intravenous Fluids and Diuretics , this approach is
outdated
• Most patients benefit substantially from the early
introduction of specific antihypercalcemic therapy, and
this approach leads to more rapid clinical
improvement, lower overall toxicity, and decreased
cost.

HYPERCALCEMIA
SPECIFIC MEASURES-
Intravenous Fluids and Diuretics-
• Assuming renal and cardiac functions are adequate, saline
infusion at a rate of 300 to 400 or more mL/h can be used
for 3 to 4 hours in severely dehydrated patients.
• Slower hydration is indicated for less severe disturbances
or in patients with congestive heart failure or oliguria
• Such treatment is excessively toxic since it frequently
causes fluid overload and occasionally life-threatening
pulmonary edema.
• The resulting weight gain and lower extremity edema that
occurs in hypoproteinemic patients with advanced cancer
may not resolve during the life of that individual and can be
severely disabling.

HYPERCALCEMIA
• Furosemide also increases the risk for
developing hypovolemia; the resultant
decrease in glomerular filtration may actually
stimulate renal calcium reabsorption,
inadvertently reinduce dehydration, and
worsen the clinical condition.

HYPERCALCEMIA
Bisphosphonates-
• Bisphosphonates adsorb to the surface of crystalline
hydroxyapatite and inhibit calcium release from bone
by interfering with the metabolic activity of
osteoclasts.
• There are numerous bisphosphonates available or
undergoing clinical investigation, including etidronate,
clodronate, pamidronate, zoledronate, alendronate,
tiludronate, ibandronate, and risedronate.
• Bisphosphonates have low oral bioavailability (less
than 1%), and none of these agents is currently
recommended as an oral therapy for hypercalcemia

HYPERCALCEMIA
• Intravenous pamidronate has become the most
widely prescribed drug for treatment of
hypercalcemia.
• This drug is well-tolerated and its side effects are
usually limited to infusion-site irritation, fever,
and flu-like symptoms that occur after the first
infusion in approximately 20% of patients.
• Although multiple doses and schedules have
been tested, pamidronate is most commonly
given at doses of 60 or 90 mg infused over 2
hours.

HYPERCALCEMIA
Gallium Nitrate-
• Gallium nitrate is a potent inhibitor of bone
resorption. Elemental gallium is incorporated
into bone and renders hydroxyapatite less
soluble and more resistant to cell-mediated
resorption.
• Following administration as a continuous
intravenous infusion (200 mg/m 2/d over 24
hours for up to 5 days), gallium nitrate induces
normocalcemia in 70% to 90% of patients.

HYPERCALCEMIA
Calcitonin-
• Pharmacologic doses of calcitonin reduce
serum calcium by increasing renal calcium
excretion and inhibiting bone resorption.
Calcitonin is especially advantageous due to
its rapid onset of action (2 to 4 hours).
• High doses of calcitonin (6 to 8 IU/kg every 6
hours) should be employed for acute
treatment of hypercalcemia

HYPERCALCEMIA
CORTICOSTEROIDS-
• Corticosteroids acutely inhibit osteoclast-
mediated bone resorption in vitro and decrease
gastrointestinal calcium resorption.
• Prednisone (40 to 100 mg/d or its equivalent) is
usually effective in controlling hypercalcemia
caused by hematologic cancers; lower doses (15
to 30 mg/d) may suffice for patients with
hypercalcemic flares caused by breast cancer.

HYPERCALCEMIA
Phosphates-
• An increase in serum phosphorus
concentration decreases osteoclastic activity,
inhibits calcium resorption from bone, and
causes a significant reduction in urinary
calcium excretion.
• Oral phosphate (0.5 to 3.0 g/d) may be highly
effective, particularly in mild forms of
hypercalcemia

HYPERCALCEMIA
Plicamycin-
• Plicamycin (formerly mithramycin) induces
hypocalcemia by a direct cytotoxic effect on
osteoclasts, thereby decreasing cell-mediated bone
resorption.
• Plicamycin is administered at doses ranging from 10 to
50 μg/kg of body weight.
• The usual dose is 25 μg/kg or a total dose of 1.5 to 2.0
mg given as a brief infusion.
• Since the onset of action occurs after 24 to 48 hours,
doses should not be repeated more frequently than
every 2 days

TUMOR LYSIS SYNDROME
• The tumor lysis syndrome occurs as a result of the rapid
release of intracellular contents into the blood stream,
which then increase to life-threatening concentrations.
• The syndrome is characterized by hyperuricemia,
hyperkalemia, hyperphosphatemia, and hypocalcemia.
• Lethal cardiac arrhythmias are the most serious
consequences of hyperkalemia. Hyperphosphatemia may
result in acute renal failure.
• Elevated serum phosphorus may also decrease renal
function, which can lead to further reductions in urinary
potassium and phosphate excretion. Hypocalcemia, a result
of hyperphosphatemia, may cause muscle cramps, cardiac
arrhythmias, and tetany.

Tumor lysis: definition
Cairo-Bishop
• Lab: 2 or more
• – Uric acid >8
• – K >6
• – Phos >4.5
• – Calcium <7
• Clinical
• – Lab + creat > 1.5 x ULN
• – Cardiac arrhythmia/sudden death
• – Seizure

• The tumor lysis syndrome occurs most commonly in
diseases with large tumor burdens and high
proliferative fractions that are exquisitely sensitive to
cytotoxic treatment.
• These disorders include high-grade lymphomas,
leukemias with high leukocyte counts, and (much less
commonly) solid tumors.
• The syndrome has been observed not only with agents
that have potent myelosuppressive activity, but also
with drugs such as interferon-a, tamoxifen, cladribine,
and intrathecal methotrexate

• Treatment should be preventive! Chemotherapy
should be delayed until all metabolic
abnormalities are corrected
• Ideally patients should be pretreated with
allopurinol and high rate hydration with IV Fluids.
Urine may be alkalinized as well
• In patients with active tumor lysis, High Rate IV
Fluids, allopurinol and holding chemotherapy are
the initial steps
• If severe electrolytes abnormalities are present
(or life-threatening hyperkalemia), hemodyalisis
should be instituted immediately

Management-
Prophylaxis
• Pre-treat for at least 2 days before chemotherapy
with:
• Allopurinol
• Aggressive hydration (with NS) to maintain urine
output > 2.5L/day
• Alkalinization is no longer recommended as it
can enhance calcium/phosphate deposition

• Once therapy has begun Check lytes, Ca, Mg,
Po4 BID until stable
• Phosphate binders: lower serum phos either
with calcium carbonate (taken with meals) or
aluminum based binders (amphogel,
alternagel)
• Kayexalate for hyperkalemia
• Dialysis when required

– Consider dialysis for
• Potassium > 7
• Uric Acid > 10
• PO4 > 10
• Hypertension
• Volume overload
• Other symptomatic electrolyte abnormalities

SIADH
• Inappropriate or ectopic secretion of ADH
– Tumors
40% of small cell lung cancer pt (poor
prognosis)
– Cytotoxic agents
Vincristine, cyclophosphamide, cisplatin
– Drug, fluids to prevent cystitis
– brain lesions, narcotics

SIADH
• Mild symptoms include weakness, muscle
cramps, loss of appetite, and fatigue; serum
sodium levels range from 115 to 120mEq/L
• More serious signs and symptoms relate to water
intoxication and include weight gain, personality
changes, confusion, and extreme muscle
weakness
• As the serum sodium level approaches 110mEq/L
seizures, coma, and eventually death will occur,
unless the condition is rapidly treated

SIADH
TREATMENT-
• initiate fluid restriction and increased
sodium intake.
• administer demeclocycline (Declomycin), an
antagonist to ADH
• Monitor serum sodium levels

Malignant Pericardial
Effusions
• Seen most commonly in lung cancer,
lymphoma, and breast cancers.
• Complicates up to 5% of cancers
• May require emergent pericardiocentesis for
CV collapse
• Echocardiography confirms diagnosis of
effusion

Malignant Pericardial
Effusions
• Ultimate treatment is pericardial window for
drainage with 0 to 15% recurrence
• Other definitive therapies can be done
– Radiation with 33% recurrence
– Systemic chemotherapy with 30% recurrence
– Pericardial sclerosis with tetracycline or bleomycin
with 15 to 30% recurrence

Leukostasis
• Leukostasis is a syndrome associated with acute
myelogenous leukemia (AML) and consists of
respiratory distress, abnormal chest radiograph,
confusion, and central nervous system bleeding.
• Patients may be confused or stuporous.
• Gingival hyperplasia or skin lesions may occur
secondary to invasion of blasts in
myelomonocytic (M4) and monocytic (M5) types
of AML

Leukostasis
• Leukostasis is associated with high and rapidly increasing blast
counts, usually more than 50K and often more than 100K.
• Patients in leukostasis are usually hypoxemic
• A nonspecific diffuse infiltrate is often present on CXR.
• There may be impairment of other end organs, including the eye,
kidney, and liver.
• Lactic acidosis may be a late event.
• Symptoms may be fulminant, leading to death in a matter of days
or even hours.
• These patients have a propensity for CNS bleeds after
chemotherapy is begun, often in the absence of disseminated
intravascular coagulation (DIC) or thrombocytopenia.

Leukostasis
TREATMENT-
• Prompt initiation of leukapheresis can be lifesaving for
these patients and should not be delayed.
• Leukapheresis can attenuate or reverse the symptoms
of leukostasis, and patients who receive leukapheresis
have a decreased incidence of CNS bleeds after
beginning chemotherapy.
• Hydroxyurea might be considered as an adjunct to
leukapheresis to decrease cell proliferation before
definitive treatment.
• Intravenous hydration is beneficial.

HYPERVISCOSITY SYNDROME
Clinical Features
• Marked elevations in serum proteins can cause an
increase in serum viscosity.
• This can produce sludging of blood flow and a
reduction of microcirculatory perfusion.
• The most common cause of hyperviscosity syndrome is
macroglobulinemia due to multiple myeloma.
• Early symptoms include fatigue, headache, and
somnolence.
• As viscosity increases, microthromboses occur and
patients may develop visual disturbances, deafness,
seizures, or coma.

HYPERVISCOSITY SYNDROME
• Emergency physicians must suspect this syndrome in patients with
unexplained stupor or coma.
• The most specific physical exam findings are in the ocular fundi and
include “sausage-linked” retinal vessels, hemorrhages, and
exudates. A clue may be provided if the laboratory is unable to run
chemistry tests due to “too thick” blood.
• Patients often are anemic with rouleau formation noted on
peripheral blood smear.
• Measurement of serum viscosity and protein electrophoresis are
diagnostic.
• Initial therapy is IV normal saline (1 to 2 L) and emergency
plasmapheresis. When coma is present and the diagnosis has
been rapidly established, phlebotomy (2U) with saline infusion and
replacement of patients' red blood cells may be used as a
temporizing measure until plasmapheresis can be performed.

POLYCYTHEMIA AND LEUKOCYTOSIS
• An elevated hematocrit (polycythemia) can be due to primary
overproduction of red blood cells by the bone marrow
(polycythemia vera) or as a paraneoplastic syndrome associated
with renal cell carcinoma and hepatomas.
• Patients can develop symptoms such as headache, fatigue, blurred
vision, and thrombotic complications such as stroke or mesenteric
ischemia.
• Both acute and chronic leukemias can produce WBCs, >100,000/μL.
Leukocytosis to this degree can impair circulation and cause
symptoms such as headache, confusion, and dyspnea.
• The treatment of choice in patients with symptomatic polycythemia
is phlebotomy (approximately 500 mL).
• Treatment of symptomatic leukocytosis is by emergent
leukapheresis and chemotherapy.

Carcinomatous Meningitis
• Direct or hematogenous seeding of meninges
• Suspect it if patient has headache or cranial
neuropathy
– Chin numbness is the classic symptom
– Diplopia is most common complaint
• Order of frequency: acute leukemias, NHL, small cell
lung, breast, and prostate cancer.
• Usually a late finding in heavily pre-treated patients.

Carcinomatous Meningitis
• Supportive care, steroids if intent is palliative and
patient has minimal symptoms.
• Intrathecal chemotherapy
– Methotrexate
• Radiation therapy
• Systemic high dose methotrexate on the order of 4 to
5 grams with leucovorin rescue

HYPOGLYCEMIA
• Mesenchymal tumors (fibrosarcomas, leiomyomas,
rhabdomyosarcomas, liposarcomas, and
mesotheliomas) account for approximately 50% of
cases; another 25% are hepatomas.
• Classic symptoms of hypoglycemia (e.g., weakness,
dizziness, diaphoresis, and nausea) are nonspecific and
may develop slowly.
• In the initial phases, symptoms tend to be worse in the
early morning (due to overnight fasting) and improve
after ingestion of food.
• Patients may also present acutely with seizures, coma,
and focal or diffuse neurologic deficits

HYPOGLYCEMIA
• Several etiologic mechanisms for cancer-related
hypoglycemia have been proposed:
(1) secretion of insulin-like substances;
(2) excessive glucose use by the tumor that exceeds hepatic
production;
(3) failure of counterregulatory mechanisms that usually
prevent hypoglycemia (e.g., reduction in levels of growth
hormone).
• Accelerated glucose use by large tumors may also account
for cancer-related hypoglycemia in some patients.
• It has been estimated that a 1-kg tumor may use from 50
to 200 g of glucose per day.

HYPOGLYCEMIA
• Many patients with hypoglycemia have
tumors that weigh several kilograms along
with extensive hepatic metastases; thus, the
combination of accelerated glucose use with
impaired production may lead to
hypoglycemia.
• A failure of the usual counterregulatory
mechanisms in patients with large tumors may
also induce hypoglycemia.

HYPOGLYCEMIA
• Mild hypoglycemia can usually be managed by
increasing the frequency of meals.
• In patients with more severe or unpredictable
symptoms, the administration of corticosteroids
and glucagon may afford symptomatic relief.
• Intravenous infusions of glucose provide
temporary support while other specific treatment
is administered (i.e., surgery, chemotherapy, or
radiation)

HYPERURICEMIA
• Renal complications and arthritis are the most important
consequences of acute or chronic hyperuricemia.
• The disorder occurs most commonly in hematologic
neoplasms, particularly the leukemias, high-grade
lymphomas, and myeloproliferative diseases.
• Patients at highest risk include those with bulky high-grade
lymphomas, patients with high leukocyte counts
undergoing remission-induction chemotherapy for acute or
chronic leukemia, and individuals with preexisting renal
impairment (especially those with ureteral obstruction).
• Hyperuricemia is also a side effect of certain agents,
notably diuretics (thiazides and furosemide), and
antituberculosis drugs (pyrazinamide, ethambutol).

HYPERURICEMIA
• TREATMENT-
– Decrease production – allopurinol, Rasburicase
– Promote solubility – alkalinization (goal urine pH
7.0-7.5)
– Reduce concentration – volume expansion with
IVF

ADRENAL FAILURE
• Symptomatic adrenocortical insufficiency due
to destruction of cortical tissue by metastatic
carcinoma is uncommon.
• More common are iatrogenic causes such as
surgical adrenalectomy, treatment with
mitotane and inhibitors of steroid synthesis
such as aminoglutethimide, chronic
corticosteroid therapy, and occasionally
adrenal hemorrhage

ADRENAL FAILURE
• Classic signs and symptoms of adrenal insufficiency
include weakness, weight loss, anorexia,
hyperpigmentation, and postural hypotension.
• One or more of these symptoms are evident in almost
all patients, but the onset of symptoms is frequently
insidious.
• Circulatory collapse and shock are uncommon but may
develop with the onset of infection.
• Biochemical evaluation frequently reveals a mild
acidosis (without an anion gap), hyponatremia, and
hypokalemia.

ADRENAL FAILURE
• Physiologic glucocorticoid replacement is
attained by administration of cortisone acetate
(25 mg in the morning and 12.5 mg in the early
evening).
• During periods of stress (e.g., operative
procedures or infection), these doses may need
to be doubled or tripled.
• Occasionally, mineralocorticoid replacement
(0.05 to 0.1 mg of fludrocortisone) is required in
addition to cortisone acetate.

ADRENAL FAILURE
• In patients with no adrenocortical function
whatsoever, maintenance doses of dexamethasone or
prednisone do not provide adequate mineralocorticoid
coverage and fludrocortisone must be given.
• Pharmacologic doses of parenteral glucocorticoids are
required in the setting of acute adrenal failure and
circulatory collapse.
• Typically, aqueous-soluble forms of hydrocortisone
(e.g., sodium succinate salt) at doses of 100 mg
intravenously every 8 hours are required.

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