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ACUTE ONCOLOGIC EMERGENCIES, DR. AHMAD TARHINI
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Good morning. Today’s grand rounds is on oncological emergencies, diagnosis and management
will be given by Dr. Ahmad Tarhini. Dr. Tarhini is Assistant Professor in the Department of
Medicine and Oncology. He went to medical school at Quantas University in Lithuania and was
recruited here as a resident at UPMC and then did a fellowship in hematology and oncology. He
also was a master level student and now a clinical research training program and subsequently as a
faculty has joined our PhD program. So he has really done well as a resident as well as a faculty at
UPMC, and it’s a pleasure to have him give grand rounds.
Thanks, Dr. Tapur, it’s an honor to be invited for a second time to do grand rounds. Today’s topic is
oncologic emergencies. So it’s going to be kind of a simple discussion of the diagnosis and
management primarily of spinal cord compression, hypercalcemia of malignancy, superior vena cava
syndrome and the tumor lysis syndrome.
I’m going to talk with a clinical case, this is a 42 year old gentleman with a history of stage 3B
surgically resected melanoma, treated after surgery with adjuvant Interferon Alpha, completed 2
years ago. Stage 3B disease, this is a patient who had lymph node involvement, in other words he
had a high risk, a risk of more than 50% of recurrence and death at 5 years. The patient presented to
a walk-in health clinic with back pain, initially associated with heavy lifting but later at rest. The
pain was getting worse over the past 2 months, radiating down the right leg and worsens with
recumbency.
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On physical exam he was tender to palpation at T12 and L1, had lumbar pain with straight leg
raising and a diagnosis was made as lumbar strain or sprain, was treated with Ibuprofen and they
recommended bed rest. Four weeks later the pain continued to worsen, interfering with his sleep,
decreased appetite and weight loss, progressive weakness of the lower extremities and this time he
goes to his primary care physician. The physical exam showed objective multiple weakness of the
lower extremities. What would you recommend as the next step in the management of this patient?
Spinal films, thoracic lumbar, bone scan, MRI, thoracic lumbar CT scan or stat consult with
neurosurgery? You can hit your answer now.
Okay. So 60% chose the right answer, which is MRI thoracic and lumbar spine and we are not
saying that spinal films are useless, probably in a patient with a regular back pain a spinal film
would be good as a screening and less expensive, readily available. But somebody with a compelling
clinical picture, a high risk for recurrent cancer and such physical findings and where there is an
urgency to make a decision in terms of the next step in management probably getting the MRI is the
most efficient way of moving forward with this patient.
And it has been shown that MRI and myelography actually are important terms of decision making
and treatment planning. And in a retrospective series of 130 patients with suspected spinal cord
metastases the choice of therapy based on MRI findings was changed in 45% of patients. And the
MRI findings influenced the addition or modification of radiation in 33% of patients. In a smaller
series of 24 patients initial radiation treatment fields based on x-rays were changed in 69% of
patients after doing myelography.
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So our patient would have an MRI that probably would look something like this, this is a sagittal T1
weighted MRI through the thoracic spine. You can see tumor involving at T5 and T12 levels and
compression into the spinal canal. So epidural spinal cord compression, it is a neoplastic invasion of
the space between the vertebrae and the spinal cord, usually from bone metastases, it compresses the
thecal sac of the spinal cord and defined radiologically as an indentation of the thecal sac.
Graphically it would look something like this, a metastatic lesion within the bone causing bone
destruction and then compressing the, the dura and obviously the spinal cord. In 2.5 to 6% of
patients with cancer it may come, may present with a spinal cord compression as a complication. It
can cause pain and irreversible loss of neurologic function. All cancers by definition can cause
spinal cord compression, but 2/3 are reported from patients with breast, lung and prostate cancer.
Less commonly 5 to 10% renal cell non-Hodgkin’s lymphoma or multiple myeloma.
In terms of pathophysiology most develop from metastases to the vertebral bodies, thoracic spine is
the most common location. Less commonly lymphoma sarcoma and lung tumors occupy the
paraspinous space and enter the spinal canal through the intervertebral foramen and cause cord
compression. Very little metastases will occur directly that the spinal cord or meningis.
A epidural tumor causes direct compression of the neural elements leading to interruption of the
axonal flow. Venous plexus obstruction causing marked cord edema and occlusion of the arterial
blood supply creating an acute infarction leading to abrupt and irreversible cord ischemia. Multiply
inflammatory mediators increase the edema and ischemia resulting in irreversible neuronal injury.
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The clinical presentation clearly back pain 90% of patients, usually precedes other neurologic
symptoms by several weeks, increases in intensity and may become radicular, multiple weakness
and gait disturbances and dysfunction of bladder and bowel function follow. Multiple weakness in
patients with epidural spinal cord compression tends to be symmetrical with progressive weakness
followed by loss of gait function then paralysis. The severity of the weakness is greatest with
thoracic metastases, ascending numbness and paresthesias are less common but may, may occur.
Also autonomic dysfunction leading to bladder and bowel function is not uncommon.
Early recognition is essential, neurologic deficits may not improve with treatment and multiple and
synchronous spinal metastases are common which gives the rationale for imaging the whole spine in
patients with high risk of spinal cord compression where the, where the index of suspicion is high.
In terms of radiologic diagnosis, again MRI is the study of choice, CT myelography can be used if
MRI is contraindicated or not available. Plain radiographs of the spine and bone scans have limited
sensitivity and specificity although plain films are readily available and may provide valuable
information if needed. Diagnosis depends on the ability to demonstrate a mass compressing the
thecal sac and again entire imaging of the spine is ideal.
MRI versus CT myelography, both image the thecal sac and spine indentation and encircling of the
sac, roughly equivalent in terms of sensitivity and specificity, although there are no randomized
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studies. CT myelography however involves a lumbar function and contraindicated in patients with
large tumors, thrombocytopenia or coagulopathy.
Inter_____ metastases are less frequent, again pain, weakness and numbness, similar to epidural
compression. Unlike epidural compression often produce a hemicord syndrome although with
continued growth may lead to subsequent bilateral spinal cord dysfunction obviously.
Radiation myelopathy is another – is a thing that needs to be thought of in terms of differential
diagnosis. Patients who have previously received radiation to the spine, latency following
radiotherapy is typically 9 to 15 months, chronic progressive radiation myelopathy is the clinical
picture and MRI or myelography distinguish this from epidural cord compression.
Therapy should be initiated as soon as possible, starting with pain control and then a high dose of
steroids, Dexamethasone 10 to 16 mg IV followed by 4 mg every 4 hours, and high doses of
Dexamethasone up to 100 mg may be associated with a slightly better outcome, but have higher
incidence of adverse events. These are usually reserved for patients with parapareses or paraplegia
and then the dose can be cut in half every 3 days. Now there are no randomized studies to support
the choice of, of treatment. High dose Dexamethasone has been compared to observation and clearly
has been shown to be superior. A small study, only about 50 patients compared low dose to high
dose and didn’t show any significant difference.
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Radiation therapy until recently has been the standard of care and the first choice of treatment. It
relieves pain in most cases, post-neurologic function usually determines the response. Response is
most associated with the tumor type and radiosensitivity. Example, lymphoma for example or
myeloma would be ideal to start with radiation therapy. Dosing is 20 to 40 grade and 5 to 20
fractions. Surgery is now the treatment of choice although for a selected group of patients.
One study, a randomized study of 41 patients with neurologic deficits the functional outcome
including the ability to ambulate and maintain continence was superior in patients who underwent
radical tumor resection followed by radiation therapy compared to patients who received radiation
therapy alone. The improvement in the arm that got surgery included days remained ambulatory,
percentage of patients who regained ambulation after therapy, days remained continent, there was
less steroid use and less narcotics and there was a trend, although an insignificant, to increased
survival.
So patients who would get surgery should be carefully selected for identifiable with an adequate life
expectancy and performance status. Now we have clearly modern techniques that would allow
aggressive management and post-resection, vertebral reconstruction in experienced hands.
Chemotherapy is an option and chemo-sensitive tumors especially lymphomas, Hodgkin lymphoma,
non-Hodgkin lymphoma, multiple myeloma, neuroblastoma, _______ tumors and occasionally in
addition to radiation therapy probably and surgery hormone manipulation is helpful in patients with
breast cancer and prostate cancer.
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Bisphosphonates are important in patients with bone metastases and have been shown in a number of
randomized studies, mostly in patients with lung cancer and prostate cancer and breast cancer
actually to reduce the rate of pathologic fractures, bone pain and there is recent data also improved
survival.
I’m going to move onto the second case, this is a 68 year old lady with no significant past medical
history who was brought to the ER by a friend because of weakness, confusion and productive
cough. The patient was noted to be lethargic, confused, she was afebrile, vital signs were stable. She
was noted to be dehydrated and on the physical exam had bilateral coarse crackles. Her labs showed
mildly elevated BUN, creatinine, sodium and potassium, mildly reduced chloride and normal CBC
and liver function tests. Chest x-ray showed bilateral opacities, differential diagnosis clearly includes
malignancy. Calcium was high at 13 mg per dl. So what is the most common underlying mechanism
for this patient’s high calcium level? Osteolytic bone metastases, high PTH, PTH RP, tumor
production of vitamin D analogs, osteoblasts? You can start clicking.
So again, the majority answered the right answer, which is PTH RP, which as most of you may
know, it was actually discovered in 1987 by a group of investigators including the Chief of
Endocrinology Dr. Andrew Stewart, who later sequenced and has done some work in the synthesis
of PTH RP. So this is the most common mechanism for hypercalcemia of malignancy which is
reported in 10 to 30% of patients with cancer, most common with breast, lung and multiple
myeloma. And often portends poor prognosis. So we have 3 main mechanisms, humeral, which is
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tumor secretion of parathyroid hormone related protein, osteolytic metastases, local bone destruction
with local cytokine release and tumor production of vitamin D analogs.
PTH RP, again, it occurs in up to 88% of patients with solid tumors as the mechanism for
hypercalcemia. Ectopic pH secretion may occur at this rate, and PTH RP, again it has structural
similarities to PTH and stimulates PTH actions including increased bone resorption and increased
distal tubular calcium reabsorption. Osteolytic metastases is another mechanism common with
breast cancer, lung cancer, multiple myeloma. There is cytokine secretion which leads to local
macrophage differentiation in the bone and to mature osteoclasts leading to more bone destruction
and release of calcium.
A third mechanism, over-production of vitamin D analogs, including calcitriol, most common with
Hodgkin’s lymphoma, it may also occur with non-Hodgkin’s lymphoma, clearly with nonmalignant
granulomatous disorders like sarcoidosis. And this is a response to glucocorticoid therapy,
somebody with Hodgkin’s lymphoma, hypercalcemia, we start glucocorticoids early.
Clinical presentation, classically lethargy and confusion, anorexia, nausea, constipation, which is
related to autonomic dysfunction, also polyuria and polydipsia, which is because of a defect in
concentrating ability basically, nephrogenic diabetes insipidus.
The clinical picture correlates with the level of hypercalcemia and the rapidity of onset. There is
cognitive dysfunction, delirium psychosis, hallucinations, somnolence, coma, rarely it leads to
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pancreatitis and severe calcemia. And chronic renal failure may be an issue in these patients,
especially if they have long standing hypercalcemia caused by you know calcification, degeneration
and necrosis of the tubules. Cardiogenic or cardiovascular complications may occur, short QT
interval, SVT, V tachs, so these patients should be on a monitored bed. Physical findings
nonspecific, dehydration is most common secondary to diuresis caused by hypercalcemia and
impaired fluid intake. Diagnosis by checking ionized serum calcium or total calcium corrected for
albumin. Must also check creatinine, electrolytes and alkaline phosphatase.
PTH usually is low in patients with hypercalcemia of malignancy. PTH RP may be checked but it’s
not necessary to make the diagnosis. It may help in assessing the mechanism and prognosis and
response to bisphosphonates. Patients in a small study, patients with PTH RP, more than 12
picomole per liter were less responsive to bisphosphonates and associated with a higher risk of
recurrence of hypercalcemia within 14 days, so it portends a poorer prognosis.
The goals of treatment are initially correcting the hypovolemia, lowering the serum calcium and
treating the complications if present, and of course treating the underlying disease. Volume
correction at the expense intervascular volume clearly and establishes the urine output, increases
calcium excretion, inhibiting – inhibition of proximate tubule and loop reabsorption, reducing
passive reabsorption of calcium. Very important to follow the fluid status of these patients to avoid
fluid overload and congestive heart failure. Loop diuretics should be avoided until euvolemia is
achieved. Serum calcium should be measured frequently and we should discontinue medications
that may increase calcium levels such as thiazide, diuretics and vitamin D supplements.
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In terms of inhibition of bone resorption, this can be achieved by bisphosphonates, calcitonin and
other agents such as Plicamycin and Galium nitrate. Bisphosphonates, these interfere with osteoclast
function, they are cytotoxic to the osteoclasts, inhibit calcium release from bone, control
hypercalcemia in most cases but the repetitive onset is not that fast, so the maximum effect occurs in
2 to 4 days. Commonly used are either Pamidronate or Zoledronic acid. Zoledronic acid is more
potent but it’s – and it’s also given in shorten time, about 15 minutes, although the clinical
significance is uncertain. We may use either one although Pamidronate is cheaper.
Calcitonin can be given sub-Q RIM. It works the fastest, so this is for acute kind of reduction in the
calcium level. It lowers calcium to a modest degree, a fact usually short-lived, increases renal
excretion of calcium and decreases bone resorption by interfering with osteoclast maturation.
Glucocorticoids, again particularly effective in hypercalcemia caused the tumor secretion of vitamin
D, especially in Hodgkin’s lymphoma but may also in – maybe also in non-Hodgkin’s lymphoma.
Galium nitrate, which is also cytotoxic to the osteoclasts primarily, it’s effective but has more
potential for nephrotoxicity, it has to be given by a continuous infusion, so it’s a little bit more
cumbersome, not often used. Dialysis is the last resort, primarily patients with renal failure or
congestive heart failure, when aggressive fluids and bisphosphonates cannot be used safely and
when patients cannot tolerate large volume, if calcium needs correction emergently as well.
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Chemotherapy is important as an kind of secondary measure, correcting the acute hypercalcemia,
which gives the direct treatment of the cancer, palliation of symptoms and reduces the recurrence of
the hypercalcemia by treating the underlying problem.
Prophylactic bisphosphonates are important, in truth use of bisphosphonates is now used for all
patients who have bone metastases. Patients with metastatic bone disease will have decreased
episodes of hypercalcemia, decreased rate of pathologic fractures, spinal cord compression,
decreased need for additional surgery and less incidence of pain.
One complication with bisphosphonates that we have to be careful about is osteonecrosis of the jaw,
or avascular necrosis of the jaw. It’s patients who are at high risk for osteonecrosis are those who
had recent dental extraction during a period of bisphosphonate treatment, or had sequential therapy
with Pamidronate and Zoledronic acid, longer follow-up time and older age at diagnosis, presents as
an infection and necrotic bone in the mandible and maxilla must be treated by conservative measures
and observation, rarely patients may need surgery for it.
Now I’ll move onto the third case. This is a 62 year old gentleman with history of 40 pack years
smoking and COPD who presents to the primary care physician with increasing shortness of breath,
worsening chronic cough and occasional blood in sputum and epistaxis, noted to have facial swelling
and venous distention on the anterior chest wall.
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Physical exam, dullness to percussion on the right lower lobe, increased tactile fremitus at the right
lower lobe, decreased breath sounds and he had no neurologic deficits. Chest x-ray showed right
pleural effusion and CT scan showed paratracheal tumor invading the superior vena cava. What is
the most important next step in the management of this patient? SVC stenting, bronchoscopy and
biopsy, sedation and intubation, broad spectrum antibiotics, immediate initiation of radiation
therapy?
So the majority said immediate initiation of radiation therapy, which may not be wrong. Although in
this case we mentioned that there were no neurologic symptoms. And there is no kind of respiratory
compromise, it’s not a true emergency. I think it would be important first to establish the diagnosis,
and the histology what we are dealing with exactly if it’s cancer, for example, before we start
treatment. So in the absence of neurologic symptoms or compromise of the airways such as stridor
histologic diagnosis should be performed to guide the treatment. You may give him radiation and it
turns out to be tuberculosis for example, or syphilis. Superior vena cava syndrome, when the
superior vena cava becomes occluded or compressed restricting blood return to the heart, impaired
venous drainage from the head, neck and upper extremities, if the occlusion occurs gradually
collaterals may form and mitigate the symptoms. Most common are malignancies as a cause
including lung cancer and lymphoma primarily. Intraluminal thrombus indwelling central venous
catheters, prior to modern antibiotics, infectious causes like syphilis, tuberculosis and fungus
infections.
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Clinical presentation, symptoms onset depends on how fast the SVC obstruction develops. Onset
usually is fast but may occur rapidly – if insidious it may occur rapidly, such as a rapidly growing
tumor or thrombosis. It is a true medical emergency when neurologic symptoms or compromise of
the airways are present. High central venous pressure usually causes the characteristic clinical
picture. Symptoms include shortness of breath, facial swelling, cough that may be aggravated by
bending forward or stooping. We would see facial edema, plethora, extended neck and chest wall
veins, and edema of the lower extremities just like in our case.
A chest x-ray at presentation usually shows widening of the mediastinum and pleural effusion. CT
scan would rule out venography as preferred, it defines the level of obstruction and maps out
collateral pathways and can identify underlying – the underlying cause of obstruction. This is a
spiral CT angiogram which shows SEC obstruction and collaterals including the left mammary veins
in this case.
MRI may be used in patients with IV contrast allergy, for example. Histologic diagnosis should be
performed to guide treatment, sputum with pleural fluid cytology, for example, bronchoscopy,
mediastinoscopy, depending on the case. Target – in terms of treatment target the underlying cause.
In terms of malignancy, radiation and/or chemotherapy may achieve long term remission for
sensitive tumors such as lymphomas, small cell lung cancer, germ cell tumors and some palliation
for non-small cell lung cancer.
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SVC stenting may be helpful especially in patients who have recurrent disease and previously
irradiated fields, we cannot give more radiation. Tumors refractory to chemotherapy, full tolerance
for chemotherapy/radiation or and there is a study that showed potential benefit from stenting in
patients with non-small cell lung cancer since these are relatively less responsive to radiation and
chemotherapy. And in this case, it was shown to have more rapid relief of the symptoms for these
patients.
Our final case is a 76 year old gentleman who presents 10 months after being diagnosed with diffuse
large B cell lymphoma with weakness, low appetite, 20 pound weight loss. He had received 6 cycles
of chemotherapy CHOP regimen which is cyclophosphamide, doxorubicin, vincristine and
prednisone achieving a complete remission. Repeat CT revealed abdominal and pelvic lymph
adenopathy, repeat biopsy a week later confirmed recurrent lymphoma. The patient was fatigued
with low appetite and decreased performance status.
Laboratory studies showed hemoglobin 11.9, BUN 38, creatinine 2.4. The decision was made to
treat with single agent rituximab, which is as you know a monoclonal antibody against CD 20
antigen and B lymphocytes.
The patient presents the second day after rituximab treatment with weakness, nausea, vomiting,
diarrhea, decreased urine output and bilateral pedal edema. Blood pressure was 170/105, pulse 72,
temperature 101, 22 respiratory rate, hemoglobin 11.6, sodium 139, potassium 6.3, BUN 90,
creatinine 5.4 now and uric acid elevated at 20. So what caused this patient’s severe metabolic
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derangements? Diffuse large B cell lymphoma, initiation of immunotherapy, elevated BUN and
creatinine, H CT with contrast.
So the majority answered the right answer, which is the initiation of immunotherapy rituximab in a
patient with high tumor burden, it is a widely kind of lymphoma with systemic lymph adenopathy
and high response to rituximab, which is CD 20 antibodies.
So tumor license syndrome
characterized by several metabolic derangements, most commonly seen after therapy for aggressive
hematologic malignancies such as high grade lymphomas and acute leukemias, and may be seen
after the treatment of kinetically active solid tumors such as lymphoma and may occur
spontaneously.
Pathophysiology is cause by massive release of intracellular contents after tumor cell death and
nucleic acid products released result in hyperuricemia. A high concentration of uric acid can lead to
crystallization within the renal tubules resulting in obstruction of tubular flow and acute renal
failure. Renal failure is further exacerbated by hypovolemia. The release of intracellular potassium
along with decreased renal function lead to hyperkalemia that may cause life threatening
arrhythmias. Increasing levels of phosphorous result in hypocalcemia and sometimes tetany,
seizures and arrhythmias.
There is no kind of accepted, widely accepted definition of what kind of forms tumor lysis syndrome
but there are some classifications like the Cairo-Bishop definition of clinical and radiologic, or
clinical and laboratory findings which look at the uric acid level, potassium, phosphorous, calcium,
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the presence of arrhythmia, sudden death or seizures. But primarily it’s a clinical presentation and
most of the time you don’t need any of these to make your diagnosis.
Symptoms and signs usually are nonspecific, urine output may decrease with symptoms of uricemia
or volume overload, seizures and arrhythmias can occur, labs usually show elevated uric acid,
phosphorous, potassium, LDH and low calcium. EKG in all patients with electrolytic abnormalities
should be done to rule out arrhythmias and conduction abnormalities. Every attempt should be made
to anticipate and prevent tumor lysis syndrome in patients at risk, so all patients won’t have tumor
lysis because the preventive measures were not taken. It can be prevented in most of the patients of
course.
So patients at risk are those with tumors of high proliferative rate, high based on uric acid, large
tumor burden, let’s say leukemia, so with WBC more than 50 or patients with large solid tumors, and
chemo-sensitive disease, mostly hematologic malignancies.
In terms of prevention allopurinol should be started 2 to 3 days before the planned chemotherapy. It
can be given IV in patients unable to take PO. We should maintain good hydration for these patients
before we start the treatment and during treatment, and some patients may benefit from rasburicase
or which is recombinant uric acid oxydase. Of course allopurinol it inhibits exanthem oxydase
which prevents the conversion of hypo-exanthem to exanthem to uric acid, so in other words it
prevents the, or reduces the production of uric acid. Rasburicase, it leads to the conversion of uric
acid into allantoin, which is an inactive and soluble metabolite. So this works much faster in
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somebody with let’s say 20 or relatively high uric acid level, but this should be used for prevention
at the outset and then continued during treatment. Rasburicase is clearly much more expensive than
allopurinol.
Patients with established tumor lysis syndrome need hospital admission.
Consider cardiac
monitoring, IV fluids to maintain a urine output of more than equal 100 ml per liter square per hour,
infusion rate of 3 liters per meter sq per day is appropriate if cardiovascular status allows. But
clearly aggressive treatment of hyperkalemia using calcium gluconate, sodium bicarbonate, insulin,
dextrose, Kayexalate as needed. Patients with hyperkalemia and renal insufficiency or volume
overload may in some cases need hemodialysis. Alkalinization of the urine is routinely used by us
and most of the treating oncologists although it is controversial. It is – the purpose is to convert uric
acid to more soluble urate salt and this can be done at maintaining a pH of 6.5 to 7. However if we
use allopurinol and we are inhibiting exanthem oxidase we are increasing the levels of exanthem
which may crystalize within the tubules, so we have to maintain the pH higher in that case when we
are using allopurinol at 7.4 or more.
There was one randomized study actually that compared urine alkalization to just using normal
cyanine and showed no difference in outcome between the two in terms of renal function.
Diuretics such as furosemide can be used cautiously to increase urine output if not hypovolemic,
and hyperphosphatemia can be treated by restricting phosphate intake and with phosphate binders
ACUTE ONCOLOGIC EMERGENCIES, DR. AHMAD TARHINI
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This is indicated in severe cases, such as oliguric renal failure,
congestive heart failure, severe hyperkalemia, patients who do not respond to medical therapy.
I think I finished way early, I apologize. And welcome any questions.
Questions for Tarhini?
Can you comment on the first case? It looks like the patient went for a while before a diagnosis was
made. How can one – can you talk about early detection perhaps early interventions?
So for patients, this was a case of high risk melanoma. As I said, it was more than 50 to 60% risk of
recurrence and death at 5 years. So this patient should normally be followed in clinic every 3 months
with a medical oncologist or a primary care physician every 3 months for the first year after
diagnosis, every 4 months for the second year, every 6 months after 5 years and then yearly
afterwards. In this case it looks like the patient was lost to follow-up and was seen in a walk-in
clinic, did not take into consideration the high risk, you know the history of cancer and the high risk
of recurrence and that’s why this delayed things and fortunately in the case of spinal cord
compression early detection is very important in terms of maintaining neurologic function.
Was your first case _______ radiation therapist out of bed if you discover that early in the morning?
Absolutely.
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And if it wasn’t radiosensitive would you have chosen the neurosurgeon as next?
What we usually do is get both the neurosurgeon and the radiation, but the neurosurgeon I think is
more important. They will assess the, you know the neurologic function, the kind of ______ of the
tumor and that would be my first choice is to surgery first. And but I would consult them both, but
usually the neurosurgeons they are very good, they come in in the middle of the night to see these
patients.
Other questions? Well, if no other questions, thank you very much.
Thanks so much.
Next week will be Dr. John Crike, giving the review on acute management of shock.