eMedicine Specialties > Emergency Medicine > Hematology & Oncology

Neoplasms, Lung: Treatment & Medication

Author: Mityanand Ramnarine, MD, Resident Physician, Department of Emergency Medicine, Albert Einstein College of Medicine at Long Island Jewish Medical Center
Coauthor(s): Gino A Farina, MD, Program Director, Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine
Contributor Information and Disclosures

Updated: Oct 21, 2009

Treatment

Prehospital Care

  • No specific prehospital care is needed for patients with lung cancer.
  • All prehospital personnel should inquire about the patient's resuscitation directives.

Emergency Department Care

All patients thought to have lung cancer should be encouraged to obtain follow-up care with their primary care physician. In almost all cases, document the possible diagnosis and discuss it with the patient. Definitive treatment of the underlying cancer is not the purview of the ED.

Treatment is based on symptoms, as follows:

  • Upper airway obstruction
    • Admit the patient to the intensive care unit.
    • Prepare for intubation and/or cricothyrotomy.
    • Obtain ears, nose, and throat and/or surgical consultation for fiberoptic laryngoscopy or intraoperative tracheostomy.
  • Hemoptysis
    • Administer supplemental oxygen and perform suctioning.
    • If a threat of imminent demise exists, consider placing a double-lumen endotracheal tube.
    • Position the patient with the bleeding hemithorax in a dependent location.
    • Perform ABG and CBC (type and crossmatching) coagulation studies if the bleeding is more than trivial.
    • A pulmonologist may have to perform fiberoptic bronchoscopy.
    • Admit patients, except those with the most minor bleeding, to the intensive care unit.
  • Pain control: See Special Concerns for workup and treatment of patients with CNS metastasis and cancer; infections in those with immunosuppression, Pancoast tumor, or Ogilvie intestinal pseudo-obstruction; or pain in those with severe cancer.

Consultations

  • Consult an oncologist if cancer is present.
  • Ear, nose, and throat; thoracic; general; orthopedic; vascular; and/or neurosurgical or neurological services may be required to address complications caused by spread of the disease.

Medication

Treatment differs according to the histologic type of cancer, the stage at presentation, and the patient’s functional status.

Chemotherapeutic agents

Because of a greater emphasis on outpatient therapies, patients taking chemotherapeutic agents frequently are seen in the ED.


Gemcitabine (Gemzar)

Cytidine analog, after intracellular metabolism to active nucleotide, inhibits ribonucleotide reductase and competes with deoxycytidine triphosphate for incorporation into DNA. Cell-cycle specific for S phase.

Adult

1000 mg/m2 IV given over 30 min on days 1, 8, 15 of a 28-d cycle or 1250 mg/m2 IV on days 1 and 8 of a 21-d cycle

Pediatric

Not established

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause myelosuppression (particularly thrombocytopenia); toxicities include flulike syndrome, LFT abnormality, maculopapular rash, pruritus, nausea, vomiting, dyspnea, hematuria, proteinuria, and hemolytic uremic syndrome; clearance reduced in women and elderly individuals


Cyclophosphamide (Cytoxan, Neosar)

Chemically related to nitrogen mustards; as an alkylating agent, the mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

Adult

40-50 mg/kg IV in divided doses over 2-5 d; other IV regimens include 10-15 mg/kg q7-10d or 3-5 mg/kg twice weekly; oral cyclophosphamide doses usually are 1-5 mg/kg

Pediatric

Administer as in adults

Allopurinol may increase risk of bleeding or infection and enhance myelosuppressive effects; may potentiate doxorubicin-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones; chloramphenicol may increase the half-life while decreasing metabolite concentrations; may increase the effect of anticoagulants; coadministration with high doses of phenobarbital may increase the rate of metabolism and leukopenic activity; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity

Documented hypersensitivity; severely depressed bone marrow function

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Regularly examine the hematologic profile (particularly neutrophils and platelets) to monitor for hematopoietic suppression; regularly examine the urine for RBCs, which may precede hemorrhagic cystitis; adverse effects include SIADH and pneumonitis


Doxorubicin (Adriamycin, Rubex)

Inhibits topoisomerase II and produces free radicals, which may cause destruction of DNA; combination of these two events can, in turn, inhibit growth of neoplastic cells.

Adult

40-75 mg/m2 IV, depending on whether drug is used alone or in combination

Pediatric

Administer as in adults

May decrease phenytoin and digoxin plasma levels; phenobarbital may decrease plasma levels; cyclosporine may induce coma or seizures; mercaptopurine increases toxicity; cyclophosphamide increases cardiac toxicity

Documented hypersensitivity; severe heart failure; cardiomyopathy; impaired cardiac function; preexisting myelosuppression

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Irreversible cardiac toxicity and myelosuppression may occur; extravasation may result in severe local tissue necrosis; reduce dose in patients with impaired hepatic function; adverse effects include pancytopenia, ECG changes, nausea, and vomiting


Vincristine (Oncovin)

Mechanism of action is uncertain; may involve a decrease in reticuloendothelial cell function or an increase in platelet production. However, neither of these mechanisms fully explains the effect in thrombotic thrombocytopenic purpura and hemolytic uremic syndrome.

Adult

1.4 mg/m2 IV qwk

Pediatric

<10 kg: 0.05 mg/kg IV qwk
>10 kg: 2 mg/m2 IV qwk

Acute pulmonary reaction may occur when taken with mitomycin-C

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with severe cardiopulmonary or hepatic impairment and patients with preexisting neuromuscular disease; adverse effects include leukopenia, peripheral neuropathy, constipation, and abdominal pain


Etoposide (Toposar)

Inhibits topoisomerase II and causes DNA strand breakage, causing cell proliferation to arrest in the late S or early G2 portion of cell cycle; do not administer IT.

Adult

Ranges from 35 mg/m2/d for 4 d to 50 mg/m2/d for 5 d IV; PO route is twice the IV dose rounded to the nearest 50 mg

Pediatric

Administer as in adults

May prolong the effects of warfarin and increase the clearance of methotrexate; cyclosporine and etoposide have additive effects in the cytotoxicity of tumor cells

Documented hypersensitivity; IT administration may cause death

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Bleeding, severe myelosuppression, alopecia, and nausea may occur


Cisplatin (Platinol)

Inhibits DNA synthesis and, thus, cell proliferation by causing DNA cross-linking and denaturation of the double helix.

Adult

120 mg/m2 IV

Pediatric

Administer as in adults

Increases toxicity of bleomycin and ethacrynic acid

Documented hypersensitivity; preexisting renal insufficiency; myelosuppression; hearing impairment

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Ensure adequate hydration before and 24 h after cisplatin administration to reduce risk of nephrotoxicity; myelosuppression, ototoxicity, neurotoxicity, nausea, and vomiting may occur

Antineoplastic Agent, Alkylating Agent


Carboplatin

Analog of cisplatin. This is a heavy metal coordination complex that exerts its cytotoxic effect by platination of DNA, a mechanism analogous to alkylation, leading to interstrand and intrastrand DNA crosslinks and inhibition of DNA replication. Binds to protein and other compounds containing SH group. Cytotoxicity can occur at any stage of the cell cycle, but cell is most vulnerable to action of these drugs in G1 and S phase.
Has same efficacy as cisplatin but with better toxicity profile. Main advantages over cisplatin include less nephrotoxicity and ototoxicity not requiring extensive prehydration, less likely to induce nausea and vomiting, but more likely to induce myelotoxicity.

Dose is based on the following formula: total dose (mg) = (target AUC) x (GFR+25) where AUC (area under plasma concentration-time curve) is expressed in mg/mL/min and GFR (glomerular filtration rate) is expressed in mL/min.

Adult

Can be dosed on basis of body surface area, but current formulas take into account patient's renal function; one such formula is Calvert formula

Pediatric

Not established

Nephrotoxicity increases with aminoglycosides and other nephrotoxic drugs

Documented hypersensitivity; bone marrow suppression

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor bone marrow function

More on Neoplasms, Lung

Overview: Neoplasms, Lung
Differential Diagnoses & Workup: Neoplasms, Lung
Treatment & Medication: Neoplasms, Lung
Follow-up: Neoplasms, Lung
Multimedia: Neoplasms, Lung
References

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Further Reading

Keywords

lung neoplasm, bronchogenic carcinoma, lung cancer, lung malignancy, adenocarcinoma, squamous cell carcinoma, SCC, oat cell carcinoma, large cell carcinoma, smoking, tobacco, passive smoke, secondhand smoke, SCLC, NSCLC

Contributor Information and Disclosures

Author

Mityanand Ramnarine, MD, Resident Physician, Department of Emergency Medicine, Albert Einstein College of Medicine at Long Island Jewish Medical Center
Mityanand Ramnarine, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Gino A Farina, MD, Program Director, Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine
Gino A Farina, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Edmond A Hooker II, MD, DrPH, FAAEM, Assistant Professor, Department of Health Services Administration, Xavier University; Associate Clinical Professor, Department of Emergency Medicine, University of Louisville; Assistant Clinical Professor, Department of Emergency Medicine, Wright State University
Edmond A Hooker II, MD, DrPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Public Health Association, Society for Academic Emergency Medicine, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Jeffrey L Arnold, MD, FACEP, Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center
Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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