Oncologic emergencies asim


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

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  • Large volume of normal Saline administrationExpands intravascular volumeIncreases calcium excretionInhibition of proximal tubule and loop reabosrptionReduces passive reabsorption of calicumFollow fluid status b/c of danger of fluid overload
  • Salmon calcitoninIncreases renal excretion of calciumDecreases bone reabsorption by interfering with osteoclast maturationWeak agentWorks the fastest
  • More potent than calcitoninMaxium effect occurs in 2 to 4 daysTrend to use of IV zoledronic acid in the acute situationBoth can be renal toxicMore potent than pamidronateAdministered over a shorter period of time (15 minutes vs. 2 hours)Prophylactic Pamidronate use in patients with known lytic lesionsLess episodes of hypercalcemiaLess pathologic fracturesLess painLess spinal cord compressionLess need for radiation or surgeryStudy: Hortobagyi, GN, Theriault, RL, Porter, L, et al for the Protocol 19 Aredia Breast Cancer Study Group. Efficacy of pamidronate in reducing skeletal complications in patients with breast cancer and lytic bone metastases. N Engl J Med 1996; 335:1785. Recent case reports of jaw bone necrosis in patients on pamidronate
  • Oncologic emergencies asim

    1. 1. Muhammad Asim Rana Department of Critical Care Services King Saud Medical City Oncologic Emergencies
    2. 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. 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. 4. and this was the ECG
    5. 5. Your Impression….? …..TUMOR LYSIS SYNDROME
    6. 6. …Tumor Lysis Syndrome: Pathophysiology
    7. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 17. Your Impression? …SPINAL CORD COMPRESSION
    18. 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. 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. 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. 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. 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. 23. …Spinal Cord Compression: Treatment • TREATMENT – Steroids – Radiation Therapy – Surgery
    24. 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. 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. 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. 27. Surgery + XRT vs. XRT alone Surgery preserves ability to walk in patients presenting with cord compression versus radiation
    28. 28. All outcomes better with surgery Patchell et al, Lancet 2005; 366
    29. 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. 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. 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. 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. 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. 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. 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. 36. ….SVC Syndrome: Signs & Symptoms
    37. 37. …Chest X-rays of the patient
    38. 38. Your Impression….? …..SUPERIOR VENA CAVA SYNDROME
    39. 39. ….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.
    40. 40. ….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
    41. 41. ….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
    42. 42. ….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
    43. 43. ….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
    44. 44. ….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.
    45. 45. …SVC Syndrome: before stent
    46. 46. … SVC Syndrome: After stent
    47. 47. … SVC Syndrome: After stent
    48. 48. 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
    49. 49. 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.”
    50. 50. • 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
    51. 51. Your Impression….? …..NEUTROPENIC FEVER/SEPSIS
    52. 52. …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
    53. 53. …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
    54. 54. …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)
    55. 55. ...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)
    56. 56. ...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
    57. 57. …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.
    58. 58. …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
    59. 59. …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
    60. 60. …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.
    61. 61. 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
    62. 62. 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
    63. 63. …You would ask Labs & Radiology • • • • • • • Sodium – 130 Potassium – 4.6 Chloride – 100 Bicarb – 25 Creatinine – 1.0mg% Glucose – 80mg% Calcium – 16.5 mg%
    64. 64. Your Impression….? …..HYPERCALCEMIA
    65. 65. …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.
    66. 66. ...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.
    67. 67. …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
    68. 68. …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
    69. 69. …Hypercalcemia: Treatment • Lower serum calcium concentration • Treat complications if present • Treat underlying disease Inhibition of Rx Volume underlyingCRRT Bone Replacement resorption disease
    70. 70. …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
    71. 71. …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)
    72. 72. …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)
    73. 73. …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
    74. 74. …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
    75. 75. Thank you for your patience ALWAYS FEEL COMFORTABLE CALLING THE FELLOW!