Cancer patients are prone to develop different kinds of complications. In time intervention improves outcomes and quality of life.

1. Muhammad Asim Rana
Department of Critical Care Services
King Saud Medical City
Oncologic Emergencies

2. Case 1
• 77 yrs male
• PMHx of CAD s/p CABG, DM, bipolar disorder,
• 5 year history of CLL comes to ER with severe
fatigue, nausea, mild abdominal discomfort.
• Pt admitted by heme/onco and started on
oral hydroxyurea after diagnosis of acute
blastic transformation.
• ICU physician was called by the oncologist to
review the case as he was worried about jerky
movements & the neuro status of the patient

3. …On Reviewing
• Patient was unconscious, jittery with a
GCS of 10/15, vitals were borderline except
HR…58
• potassium 6.3 mEq/L
• calcium 6.1 mg/dL
• phosphate 5.5 mg/dL
• lactate dehydrogenase (LDH) 28,900 U/L
• uric acid 14.3 mg/dL
• Creatinine was normal, at 1.1 mg/dL

4. and this was the ECG

5. Your Impression….?
…..TUMOR LYSIS SYNDROME

6. …Tumor Lysis Syndrome: Pathophysiology

7. …Tumor Lysis Syndrome: Who gets it?
• High tumor cell proliferation rate, large tumor
burden, tumor is chemosensitive
• ALL, AML, NHL, Burkitt’s Lymphoma, Small
cell> Hodgkin’s disease, Multiple Myeloma,
• Solid Tumors ( breast, GI, prostate etc.)
• Signs and Symptoms are non-specific:
– usually within 12 to 72hrs after starting
chemotherapy
Nausea
Vomiting
Diarrhea
Anorexia
Syncope
Lethargy
Edema
Fluid overload
Cramps
Sudden death

8. …Tumor Lysis Syndrome: Who gets it?
• Usually develops after chemotherapy
• paclitaxel,fludarabine,etoposide,thalidomide,hydroxyurea
• Can occur after
–
–
–
–
–
radiation therapy
corticosteroids
chemoembolization
intrathecal chemotherapy
rarely from spontaneous necrosis
• LDH is considered by some a measure of
tumor load and a marker of TLS risk

9. Cairo-Bishop Definition
• In 2004, Cairo and Bishop defined a classification system for
tumor lysis syndrome.
• Laboratory tumor lysis syndrome: abnormality in two or more
of the following, occurring within three days before or seven
days after chemotherapy.
–
–
–
–
uric acid > 8 mg/dL or 25% increase
potassium > 6 meq/L or 25% increase
phosphate > 4.5 mg/dL or 25% increase
calcium < 7 mg/dL or 25% decrease
• Clinical tumor lysis syndrome: laboratory tumor lysis
syndrome plus one or more of the following:
– increased serum creatinine (1.5 times upper limit of normal)
– cardiac arrhythmia or sudden death
– seizure

10. …Tumor Lysis Syndrome: Prevention &Management
• “The best management is prevention.”
• FLUIDS and HYDRATION:
– Aggressive hydration and diuresis
– Improve intravascular volume, renal blood
flow, GFR (decrease [solute] in distal
nephron/renal microcirculation)
– +/- diuretics (contraindicated in hypovolemia
and obstructed uropathy)

11. …Tumor Lysis Syndrome: Prevention & Management
• ALKALINIZATION OF URINE:
-Uric acid > 10x’s more soluble in pH of 7.0
compared to pH of 5.0
-Xanthine/hypoxanthine is also significantly
more soluble in basic urine
- Historically used, but not based on EBM.
NOT RECOMMENDED
Complications of alkalinization outweighs benefits
(calcium phosphate precipitation, metabolic alkalosis)

12. …Tumor Lysis Syndrome: Prevention & Management
• ALLOPURINOL:
– Competitive inhibitor of
xanthine oxidase which ↓
conversion of purine
metabolites to uric acid.
– Used prophylactically for TLS
-BUT
Option for pts with medium risk
Ineffective in reducing uric acid
levels before chemoTx
Xanthine and hypoxanthine
precipitateobstructive uropathy
reduces clearance of some chemoTx
(azothiopurine & 6-mercaptopurine)

13. …Tumor Lysis Syndrome: Prevention & Management
RASBURICASE
(recombinant urate oxidase)
-promotes catabolism of uric acid:
Uric acid  allantoin (10x more soluble
than uric acid)
100 adult pt (w/ aggressive NHL) got 3
to 7 days of rasburicase beginning
day 1 of chemo:
• Uric acid levels decreased within 4
hrs of rasburicase initiation
• Normal uric acid levels maintained
throughout chemotherapy
• No increase in creatinine observed
• No patient required dialysis

14. Patient at risk
Serum
Uric Acid
Normal
(<8mg%)
High
(>8mg%)
Initiate therapy
Intravenous hydration
Allopurinol
?Rusburicase
Uric acid < 8mg%
Follow labs Q8 hrs
PO4, Ca+2,LDH,UA,BMP
Uric acid> 8mg%
Correct hyperkalemia
Maintain urine out put >100ml/hr
Consider CRRT if poor response
Add
Rusburicase !!
……….
Review

15. Case2
• 64 y/o male w/o significant past medical history comes to
ED w/ complaints of progressive LBP.
• He notes pain initially started approx 6-8 weeks ago w/o
any inciting event.
• He is normally very active and enjoys jogging/biking ;
currently still working as a chef.
• He went to local out patients two weeks ago and got
routine lumbosacral films which were essentially normal.
He was sent home w/ course of high dose NSAIDS.
• He comes to KSMC ER w/ complaints of persistent and
progressive band like lower back pain.
• He notes new unsteadiness when he walks for the last two
days, which prompted him to come to accidents &
emergency

16. • In ED: vitals and labs
were within normal
limits
• Exam showed legs
weakness 4/5
• Urgent MRI of spine
showed metastatic
disease diffusely noted
with thecal sac
impingement at level of
L3-L4
• ICU physician requested
PSA & it came 68 ng/mL

17. Your Impression?
…SPINAL CORD COMPRESSION

18. … Spinal Cord Compression
• Neoplastic epidural
spinal cord
compression
• Defined as thecal
sac indentation
radiographically
(spinal cord or
cauda equina)
• Thoracic spine: 60%
• Lumbar spine: 30%
• Cervical spine: 10%

19. … Spinal Cord Compression
• Cord compression is a common complication
in oncology patients
– (5-10% of all cancer patients: prostate, lung, breast)
• … is a cause of pain and irreversible loss of
neurologic function.
• Back pain is the precursor to spinal cord injury
in almost all (96%)patients w/ spinal mets.
Pain similar to disc disease: except ↑ pain
supine, ↓upright
• NOT immediately life threatening unless it
involves C3 or above

20. …Spinal Cord Compression: Epidemiology
•
•
•
•
•
•
•
Vertebral mets are common than ESCC
Prostate cancer: 90%
Breast Cancer: 74%
Lung Cancer: 45%
Lymphoma: 29%
Renal cell: 29%
Gastro-: 25%
Posner, JB. Neurologic Complications of Cancer. FA Davis, Philadelphia, 1995

21. …Spinal Cord Compression: Epidemiology
• Many cases of unrecognized ESCC
• Difficult to define incidence
• Autopsy review studies suggest around 5%
of cancer patients die with ESCC
Barron, KD, Hirano, A, Araki, S, Terry, RD. Experiences with metastatic
neoplasms involving the spinal cord. Neurology 1959; 9:91.

22. …Spinal Cord Compression:
Diagnosis
Back pain + known malignancy
= SCC until proven otherwise
– Plain films NOT enough
– Exam has poor accuracy
with localizing level
– MRI without contrast is the
best test for SCC when
suspected
– Can do CT (myelography) if
pt cannot tolerate MRI, or
not candidate for MRI, or
not available.

23. …Spinal Cord Compression:
Treatment
• TREATMENT
– Steroids
– Radiation Therapy
– Surgery

24. …Spinal Cord Compression:
Treatment
• Corticosteroids
–
–
–
–
Provides pain relief and are anti-inflammatory
Dexamethasone:
Loading 10mg-16mg; followed by 4mg q 4hrs.
Higher doses (100mg) may be associated w/
slightly better outcome in exchange for higher
incidence of adverse effects.
– Reserved for paraplegia/paraparesis generally.
(low vs high dose studies = equivocal)
– Taper once definitive treatment is underway

25. …Spinal Cord Compression:
Treatment
• Surgery---evolving science
– THEN:
Previous studies: Laminectomy w/ or w/o RT vs
RT alone = NO difference in outcome
– Decompressive resection reserved for unstable spine, life
threatening compression, unknown etiology, tumors that
are not reliably radiosensitive or chemosensitive.
– NOW: Newer studies show surgical
intervention + XRT show BETTER functional
status than XRT alone
– (anterior approach, improvements in
instrumentation)

26. Surgery + XRT vs. XRT alone
• Recent controlled trial comparing aggressive
surgery followed by radiation vs. radiation
alone
• Improvement in surgery+rads
– Days remained ambulatory (126 vs. 35)
– Percent that regained ambulation after therapy
(56% vs. 19%)
– Days remained continent (142 vs. 12)
– Less steroid dose, less narcotics
– Trend to increase survival
Patchell, R, Tibbs, PA, Regine, WF, et al. A randomized trial of direct decompressive
surgical resection in the treatment of spinal cord compression caused by metastasis
(abstract). proc Am Soc Clin Oncol 2003; 22:1.

27. Surgery + XRT vs. XRT alone
Surgery preserves ability to walk in patients
presenting with cord compression versus
radiation

28. All outcomes better with surgery
Patchell et al, Lancet 2005; 366

29. …Spinal Cord Compression:
Treatment
• Other Management issues
– Quickly involve
• Rad/oncology and Neurosurgeon / Ortho
–
–
–
–
Analgesia: opioids, steroids
Bed rest: controversial
Anticoagulation: DVT prophylaxis
Bowel regimen: because
• autonomic dysfunction, opioids, limited mobility all
contribute to constipation
– Spinal bracing:
• only in patients with refractory pain

30. …Spinal Cord Compression:
Treatment
• Best predictor is pre-treatment
functional/neurologic status
– Rapid onset and quick progression = poor
Prognosis
– 75% of patients treated correctly while still
ambulatory, will remain ambulatory
– Only 10% of patients presenting with
paraplegia will regain ambulatory status

31. Important to recognize
• Early recognition leads to better outcomes
• Efficacy of treatment depends most on
patient’s neurological function at
presentation
• Median time from symptoms to diagnosis
is around 2 months
• More than half of patients who present to
hospital are non-ambulatory
Husband, DJ. Malignant spinal cord compression: Prospective study of delays in referral
and treatment. BMJ 1998; 317:18.

32. Important to recognize: Red Flags
Red Flag 1: Pain
Red Flag 2: Motor loss
Usually firstSensory loss
Red Flag 3: symptom
80-90% 60-85%
Weakness:of the time Bladder function loss
Red Flag 4: Bowel and
At or common than motor findings
Usually precedes other neurologic symptoms
Less above conus medularis
Extensors of the upper extremities
by seven weeks
Loss is late finding
Above the thoracic spine
Increases in intensity
Still present in majority of cases
Weakness from corticospinal dysfunction
Severe localneuropathy presents usually as
Autonomic back pain
affects flexorsrecumbency extremities
Aggravated by in the lower
urinary retension hyperreflexic below the
Patients mayvenous plexus parathesias
Ascending numbness and
Distension of be
Rarely sole finding
lesion and have extensor plantars
May become radicular

33. Pt with clinical
suspicion of cord
compression
Review
Neurological
Examination
Normal
Abnormal
Start
Steroids
Plain X- rays
Normal
Abnormal
MRI
No
compression
Follow Clinically
Cord
compression
Surgery
?
No
Chemosensitive
?
Yes
Chemo +/radiations
Yes
Surgery +/- post
op radio Rx
No
Radiotherapy

34. Case 3
• 56 yrs male with past medical history of
pulmonary embolism in 2005 when he was in
the hospital for a traumatic femur
fracture, no longer on coumadin.
• PMH: HTN
• Social history: Denies alcohol, but smoker
with 60 pack year history (2 ppd x 30 yrs)
• Presented with facial swelling for 2 weeks and
bilateral upper extremity swelling for the past
week.

35. • Referred to ICU for
– Swollen face
– Decreased mentation
– Fear of upper airway obstruction
• When examined
– Edema of face, arms, neck and supraclavicular
region
– Collateral veins on the upper chest
– Hoarse voice

36. ….SVC Syndrome: Signs & Symptoms

37. …Chest X-rays of the patient

39. Your Impression….?
…..SUPERIOR VENA CAVA SYNDROME

40. ….SVC Syndrome: Eitiology
• Malignant tumors are cause of
SVC syndrome in 78-85% of
cases.
• Malignancy
– Lung CA – caused by extrinsic
compression or intrinsic invasion
• Greatest risk is with small cell lung
ca (up to 20% will develop SVC
syndrome)
– Lymphoma – typically caused by
compression by lymph nodes
– Thymoma, primary mediastianal
germ cell neoplasms
– Solid tumors with mediastinal
nodal metastases
• Breast CA is the most common
solid tumor.

41. ….SVC Syndrome: Diagnosis
• 60% of pt’s with malignancy related SVC
syndrome do not have a previous diagnosis
of cancer
• Radiographic Studies – majority have
abnormal chest x-rays
– (mediastinal widening and pleural effusion)
• CT chest is preferred once the diagnosis is
suspected
– Helical CT chest with b/l upper extremity
contrast injection or upper extremity
venography
• Histologic diagnosis

42. ….SVC Syndrome: Treatment
• Historically SVC syndrome was considered
a potentially life-threatening emergency
• Standard of care was immediate
radiotherapy
• The emergent approach is not appropriate
for most patients

43. ….SVC Syndrome: Treatment
Emergent to urgent
• Symptomatic obstruction is usually a
prolonged process
• Most patients are not in immediate danger
at presentation & have time for a full
diagnostic work up
• Prebiopsy radiation can obscure the
diagnosis
• Current strategies aim at accurate
diagnosis of underlying etiology before
therapy

44. ….SVC Syndrome: Treatment
Exception to the rule
• Stridor
– Central airway obstruction or laryngeal edema
• True medical emergency
• Immediate action needed
– Possible intubation and ICU admission
– Immediate therapy to target obstruction
needed

45. ….SVC Syndrome: Treatment
• Tumors with good response: Non Hodgekin’s
lymphomas, germ cell neoplasms and limited-stage small
cell cancer (usually responsive to chemo with or without
radiation). Symptoms improve in 1-2 weeks.
• Anticoagulation
• Intraluminal metal stents –
– Used in cases where unable to give chemo or radiation
– Now some data showing that placing a stent better when patient
first diagnosed because of quicker resolution of symptoms.
– Combination endovascular therapy (thrombolysis, angioplasty
and stent placement)
Rowell, NP, Gleeson, FV. Steroids, radiotherapy, chemotherapy and stents for superior vena
caval obstruction in carcinoma of the bronchus: a systematic review. Clin Oncol (R Coll Radiol)
2002; 14:338.

46. …SVC Syndrome: before stent

47. … SVC Syndrome: After stent

48. … SVC Syndrome: After stent

49. SVC syndrome
Review
CT or MRI evidence
of intrathoracic mass
No
Yes
Known cancer
diagnosis?
Central venous
catheter
Yes
Evidence of
thrombosis?
Other causes
of swelling
Yes
No
Yes
Begin
anticoagulation
No
SVC Fibrosis?
Dilatation
/stent
Chemo
sensitive ?
No
Obtain tissue
biopsy
Highly
sensitive
Not highly
sensitive
Chemo +/XRT
XRT +/STENT

50. Case 4
• 45 yrs male Hx of AML s/p stem cell transplant
several months prior.
• Came to ER for scheduled and routine RBC
transfusion.
• He was also receiving outpatient chemo therapy
via PICC line
• Pt complaint of fatigue and constipation.
• ER nurses noted temp of 36.1 C, BP= 82/58, +
orthostasis.
• He was given 1L of NS and had routine labs drawn
as he wass transferred to observation.
• He was referred to ICU for “hypotension.”

51. • Upon admission to floor he denied any
other complaints, and said he had been
compliant with Rx.
• Additionally he had been taking tylenol for
3 days hx of headache and 2 weeks of
bisacodyl suppositories
• His admission vitals :
34.5C, 90/40, 102, 26, 97% on room air but
was vigorously shivering when ICU
physician arrived
• WBC = 0.2 , ANC= 0.06

52. Your Impression….?
…..NEUTROPENIC FEVER/SEPSIS

53. …Neutropenic Sepsis: Definitions
• Neutropenia:
– ANC < 500 or <1000 w/ a predicted nadir of <500
cells
– ANC = (WBC) x (% of neutrophils + % of bands)
– Nadir usually occurs 5 to 10 days after last chemo
dose and usually recovers in 5 days
– (certain leukemia/lymphoma regimens cause longer lasting and
more profound neutropenia)
• Fever:
- Single temp of 38.3oC (101.3oF)
- Sustained Temp of 38.0oC (100.4oF) for > 1 hour

54. …Neutropenic Sepsis: Diagnosis
• Fever is commonly the only symptom.
Common infections present atypically
(asymptomatic UTIs, meningitis w/o nuchal
rigidity, bacteremia with only fatigue as a symptom)
• Avoid digital rectal exams/manipulations
• Careful oral exam and exam of catheter
sites if any
• Pan Cultures

55. …Neutropenic Sepsis: Eitiology
• BACTERIA:
– Until 1980s, GNR (P.aeruginosa) were the most
commonly identified pathogens
– 1995-2000, Gram + organisms = 62-76% of all
bloodstream infections
– Trend toward Gram + due to introduction of long-term
indwelling lines (Hickmans,Mediports)
• FUNGAL:
- Risk increases w/ duration and severity of
neutropenia, prolonged antibiotic use, and number of
chemotherapy cycles
-Candida (lines), aspergillus
(immunocompromised, skin,sinus)
>>>histo, blasto, coccidio,
TB(prolonged steroids, other high risk patients)

56. ...Neutropenic Sepsis: High risk patients
• Already in-patients when fever and neutropenia develop
• Outpatients who need acute hospital care for problems in
addition to the fever and neutropenia
• Outpatients with uncontrolled cancer
(e.g. acute leukaemia not in remission, those with tumours
progressing during anticancer therapy)
• On immunosuppressive agents e.g. cyclosporin A, steroids
• Patients with specific foci of infection e.g. intravascular catheter
infection, tunnel infection, new pulmonary infiltrate
• Neutropenia likely to last for more than 10 days
• Recent fludarabine treatment
• Phase I or II clinical trial patients (inform investigator)

57. ...Neutropenic Sepsis: High risk patients
Presence of any of the following features;
–
–
–
–
–
–
–
–
–
–
–
abdominal pain, nausea and vomiting, diarrhoea
neurological or mental changes
allogeneic BMTs or autologous BMT
pregnancy
HIV
recent treatment with antibiotics (in previous 72 hours)
renal failure (creatinine clearance <30ml/min)
hepatic failure
respiratory insufficiency
haemodynamic instability
inability to take oral medications

58. …Neutropenic Sepsis: Who to treat
• All febrile patients with neutrophil counts
<500/mm3 and those whose counts are
<1000/mm3 but are falling rapidly.
• Afebrile patients with neutrophil counts
<500/mm3 should also be treated if they
have symptoms compatible with infection.

59. …Neutropenic Sepsis: TREATMENT
• Numerous regimens studied:
– monotherapy found equivalent to two drug regimens
– (i.e.: piperacillin/tazobactam, cefepime, meropenem)
• In critically ill, add one aminoglycoside
– (better G -ve coverage)
• Addition of Gram (+) as initial empiric coverage
– In patients with lines and catheters
– in patients without port/catheter/line or mucositis has
no proven clinical benefit instead can↑VRE
• Vancomycin or Linezolid :
-Clinical deterioration
-Hypotension
-Mucositis
-Skin or catheter infection
-Hx of MRSA colonization
-recent quinolone proph

60. …Neutropenic Sepsis: TREATMENT
• Fungal coverage (candida or aspergillus ssp. ):
– Routinely added after 5-7 days of persistent
neutropenic fever w/o clear source
– Post mortem of fatalities after prolonged
febrile neutropenia (1966-1975)
• 69% had evidence of systemic fungal disease
– Rx with liposomal amphotericin B (most common),
voriconazole(? failed noninferiority trial?),
caspofungin (passed noninferiority trial, less nephrotoxic
aspergillus failure?)
– No to fluconazole = ↓ efficacy

61. …Neutropenic Sepsis: TREATMENT
• Colony Stimulating Factors (GM-CSF):
– NOT routinely used for neutropenic fever
unless the patient had previous bout of
neutropenic fever with prior chemo cycle.
– Not shown to decrease mortality
– Beneficial effects are quite modest
– Used in neutropenic septic shock/severe
sepsis (hypotension, organ dysfunction)
– Used in patients whose bone marrow recovery
is expected to be especially prolonged.

62. Case 5
• 55 yrs male with PMH of HTN on Rx came
to A&E complaining of 2 week history of
constipation, recently started having
nausea and vomiting.
• No surgical history
• Social History: Denied alcohol, but 50 pack
year history of smoking
• ROS: weight
loss, polyuria, polydypsia, chronic cough

63. On examination
•
•
•
•
•
•
T: 98.9F BP: 150/90 HR:55 RR:14
General: NAD, thin appearing
CVS: bradycardic, no murmurs
Lungs: clear bilaterally, a few crepts Lt mid zone
Abdomen: soft, normal Bowel Sounds
CNS: AAOx3, no significant weakness, hyper
reflexia +ve

64. …You would ask Labs & Radiology
•
•
•
•
•
•
•
Sodium – 130
Potassium – 4.6
Chloride – 100
Bicarb – 25
Creatinine – 1.0mg%
Glucose – 80mg%
Calcium – 16.5 mg%

65. Your Impression….?
…..HYPERCALCEMIA

66. …Hypercalcemia : approach to patients
• When initially discovering patients with
hypercalcemia first have to rule out
malignancy and PTH
• Occurs in 10-20% of cancer patients
• Most common cancers include lung, breast
and hematologic malignancies.

67. ...Hypercalcemia: Signs & Symptoms
• Acute hypercalcemia:
– nausea, vomiting, constipation, polyuria, polyd
ipsia,Nephrogenic DI, muscle
weakness, arrythmias, short QT, AKI.
• Chronic hypercalcemia:
– kidney stones, bone pain, & psychosis.
• Can also decrease consciouness to coma if
hypercalcemia is very severe
• “stones, bones, groans and psychiatric
overtones”
Heath, H 3d. Clinical spectrum of primary hyperparathyroidism: Evolution with changes
in medical practice and technology. J Bone Miner Res 1991; 6(Suppl 2):S63.

68. …Hypercalcemia: Pathogenesis
• Osteolytic metastases with local cytokine release
• Tumor necrosis factor & Interleukin-1
• Stimulate osteoclast precursor → mature osteoclasts
• Leading to more bone breakdown and release of calcium
• Tumor secretion of PTHrP (parathyroid hormone-related protein)
• Common in patients with non-metastatic tumors
• Called humoral hypercalcemia of malignancy
• PTHrP binds to same receptor as PTH and stimulates
adeynylate cyclase activity
– Increased bone resorption
– Increases kidney Ca reabsorption and PO4 excretion
• Tumor production of calcitriol

69. …Hypercalcemia: Diagnosis
Corrected calcium >10.3 mg/dL
OR ionized calcium>5.2 mg/dL
PTH appropriately decreased
PTH-independent mechanism;
consider checking Vitamin D levels
Not elevated
PTH-RELATED PEPTIDE:
a) Humoral hypercalcemia of
malignancy
(elevated PTHrP)
BONE RESORPTION:
a) Osteolytic malignancy
b) Paget’s disease
c) Immobilization
d) Hyperthyroidism
e) Adrenal insufficiency
DECREASED Ca EXCRETION
a) Volume depletion
b) Thiazide diuretics
c) Milk-Alkali syndrome
Abnormally elevated
Excess 25-OH
Vit D intoxication
Excess 1,25-OH
Granulomatous
disease
Lymphoma
Calcitriol overdose
Acromegaly
PTH elevated or inappropriately normal
HYPERPARATHYROID STATE:
a) Primary hyperparathyroidism (85%
adenomas, 14% hyperplasia, 1%
carcinoma)-24 hr urine calcium >200 mg
b) Familial hypocalciuric hypercalcemia- 24 hr
urine calcium < 200 mg
c) Tertiary hyperparathyroidism (After renal
transplantation)
d) Lithium use

70. …Hypercalcemia: Treatment
• Lower serum calcium concentration
• Treat complications if present
• Treat underlying disease
Inhibition of
Rx
Volume
underlyingCRRT Bone Replacement
resorption
disease

71. …Hypercalcemia : Treatment
• Three therapies for inhibition of bone
resorption
• Calcitonin
• Bisphosphonates
• Gallium nitrate
• Historical therapy
– Antitumor antibiotic plicamycin (mithramycin)
• Multiple serious side effects
• No longer manufactured

72. …Hypercalcemia: Treatment
• Salmon Calcitonin
– Increases renal
excretion of calcium
– Decreases bone
reabsorption by
interfering with
osteoclast maturation
– Weak agent
– Works the fastest
• Bisphosphonates
– Adsorb to the surface of
bone hyroxyapatite
– Interfere with osteoclast
– Cytotoxic to osteoclasts
– Inhibit Ca release from bone
– Three commonly used
• Pamidronate
• Zoledronic acid
• Etidronate (1st generation, weaker)

73. …Oncologic Emergencies
• 4 Major types
– Metabolic emergencies
– (↑calcemia, ↓natremia, ↓glycemia, adrenal failure, lactic acidosis)
– Hematologic emergencies
– (hyperleukocytosis, DIC, thrombosis )
– Infectious / Inflammatory emergencies
– (typhlitis, pancreatitis, chemo infiltration, hemorrhagic cystitis )
– Mechanical emergencies
– (↑ICP, status epilepticus, cardiac tamponade, SVC syndrome)

74. …Oncologic Emergencies: Urgency Approach
• Right Now This Minute
– Airway obstruction, neutropenic sepsis, tamponade,
cord compression, CNS metastases with symptoms
• Today
– coagulopathies, tumor lysis, DIC, leukostasis, TTP,
hyperviscosity, severe thrombocytopenia, sickle cell
complications, INR over 9
• If Not Today, Tomorrow
– SVC syndrome, most hypercalcemia, most CNS mets
without edema, INR 5-9

75. …Oncologic Emergencies: What
•
•
•
•
you always need to know
Decision Maker: Patient/Relative
Tissue diagnosis: presumptive/bx proven
The time course of the decompensation
Disease status beyond involved site

76. Thank you for your patience
ALWAYS FEEL COMFORTABLE
CALLING THE FELLOW!