Correct!
3. Supportive treatment

Treatment of re-expansion pulmonary edema is supportive. Placing the patient with the  affected side up is recommended which, in unilateral cases, contributes to reducing the pulmonary shunt and improving oxygenation. Noninvasive ventilation should be considered.

Our patient was treated with BiPAP and oxygen and gradually improved.

Prescriber Pearls (physicians/PAs/NPs) (Theodore Loftsgard R.N., C.N.P.)

 

Respiratory Therapy Pearls (Adam Frost R.R.T., C.R.T.)
Underlying respiratory disease (asthma): usually treat with albuterol, but monitor heart rate (tachycardia). Our patient's heart rates were from 110-170 so we should treat with ipratropium which does not affect heart rate as much as epinephrine.

When looking at that chest CT the patient was found to have a pleural effusion and atelectasis. The ICU service tapped the effusion which should in return help with patient work of breathing, lung expansion, and the atelectasis. Respiratory can assist with improving the atelectasis by performing bronchial hygiene with the patient by working with incentive spirometry (I.S.) to help the patient reinflate the alveoli in the lung to eliminate the atelectasis. If the patient is not strong enough to use the I.S., the respiratory therapist could try EZPAP, which utilizes a fluidic process to augment spontaneous breathing to provide higher inspiratory flow and larger tidal volumes than on unsupported ventilation. The patient also exhales against resistance, creating PEEP (Positive End Expiratory Pressure) to stent the airways open and promote lung recruitment. The flow to the device should be initiated at a lower flow and increased slowly as the patient tolerates. Patient should be assessed pre and post therapy and monitored for any signs of distress as therapy will temporarily increase patient’s work of breathing. Patient should be allowed to take rest periods during the treatment.

When the patient arrived in the ICU she was having increased work of breathing, to help the patient out we started her on 30% FiO2 and CPAP 7. CPAP is Continuous Positive Airway Pressure is a spontaneous breath mode during which there are no mechanically delivered inspirations. Advantages of CPAP include significantly lower peak airway pressures for a given tidal volume, spontaneous breathing throughout the ventilatory cycle for patient comfort, due to the presence of spontaneous breathing, hemodynamic compromise such as can occur with PEEP during mechanical ventilation rarely occurs, decreased sedation, and elimination of neuromuscular blockade use. Contraindications for CPAP include apnea or hypoventilation, increasing sedation or administration of a paralytic, and impaired ventilatory drive.

During the patients stay in the ICU while she was using CPAP for support, the patient had a decrease in mental status and was having periods of apnea due to some side effects of the medicines she had received earlier before coming to the ICU. To help the patient out we placed her on BIPAP, is delivering IPAP (Inspiratory Positive Airway Pressure) and EPAP (Expiratory Positive Airway Pressure). Also referred to as bi-level PAP therapy. BIPAP therapy is used to treat sleep related disorders including severe COPD, OSA and nocturnal hypoventilation. We placed the patient on BIPAP with settings, 30% FiO2 S/T 4 (spontaneous/timed: this mode lets you breath at your own rate with giving you the support the therapist sets or if the patient does not take a breath in the allotted time the machine will give the patient a breath,) with an IPAP of 14 and EPAP of 7 giving the patient a pressure support of 7. Contraindications for BIPAP are patents unable to protect airway or adequately clear secretions, with a high risk for aspiration, acute sinusitis, severe respiratory therapy patients without a spontaneous respiratory drive, pneumothorax, recent gastric, laryngeal, or esophageal surgery, significant facial fractures, nausea and vomiting, and cardiac ischemia or acute myocardial infarction. This patient had none of these. The patient was oxygenating well just not ventilating that is why we made the Switch to BIPAP from CPAP.

Pharmacy Pearls (Karen C. Kolbet, Pharm.D., R.Ph.)
Thalomid® (thalidomide): known in the 1950-60s as a sedative and hypnotic.
Mechanism of action: In the treatment of multiple myeloma patients, thalidomide is thought to work through several mechanisms including induction of apoptosis, inhibition of vascular endothelial growth factor, modulation of immune surveillance, and decreased adherence of myeloma cells to bone marrow stromal cells.
Indications for use: It is FDA approved for use in multiple myeloma as monotherapy and in several combination regimens.
Black Boxed Warning: Thalidomide does contain a black boxed warning for an increased risk of venous thromboembolic events when used in patients with multiple myeloma. This risk is increased when thalidomide is used in combination with other chemotherapeutic agents.
Incidence of pulmonary/respiratory adverse effects: Prescribing information: Based on results from a Celgene-sponsored controlled clinical trial (4):
i. Respiratory system adverse effects were reported in 3 (12.5%) of patients:
-Pharyngitis: 1 (4.2%)
-Rhinitis: 1 (4.2%)
-Sinusitis: 1 (4.2%)
ii. Treatment-emergent adverse effects occurred in >/=10% of all patients
-Grade 3/4 pulmonary adverse events occurred in 52 (51%) of patients
a) Dyspnea: 43 (42.2%)
b) Cough: 15 (14.7%)

DTPACE:
i. Pulmonary and renal toxicities and metabolic abnormalities were brief, lasting less than 1 week after completion of 4-day chemotherapy
ii. After the first cycle of DTPACE, 6 patients (3%) died as a result of treatment-related causes:
-Respiratory failure caused by bacterial pneumonia (n=1)
iii. After the second cycle of DTPACE 3 additional patients died:
-Sepsis (n=2)
-Cytomegalovirus pneumonia (n=1)
iv. Overall incidence of pulmonary toxicity of chemotherapy regimen:
-Dyspnea 21 (5%)
-Pulmonary infiltrates 7 (2%)
-Pulmonary edema 5 (1%)

Case Report: Thalidomide-induced pneumonitis:
A 71 year old man with a history of stage IIIB symptomatic multiple myeloma was admitted with fever and dyspnea. He was on oral thalidomide 200mg/day in combination with melphalan, cyclophosphamide, and dexamethasone. After 12 days of therapy with thalidomide, he became febrile and crackles were present on pulmonary exam. After a negative infectious work-up, thalidomide and antimicrobials were discontinued. His symptoms resolved in approximately 1 week. Upon discharge thalidomide was resumed in which case his dyspnea and fever recurred ~8 days later (5).

Case Report: Interstitial pneumonitis as an adverse effect of thalidomide:
A 67 year old man with history of multiple myeloma on thalidomide (approximate duration completed~2 months) in combination with dexamethasone was admitted with progressive dyspnea. CT scan showed diffuse ground glass opacities in both lungs however infectious etiology was ruled out. Thalidomide was discontinued and ground glass opacities and dyspnea resolved (3).

Case Report: Thalidomide-induced reversible interstitial pneumonitis in a patient with recurrent ovarian cancer:
A 58 year old woman with a history of recurrent ovarian cancer on thalidomide 200mg/day (approximate duration completed~5 weeks) in combination with weekly topotecan developed shortness of breath and dyspnea on exertion with a non-productive cough. Work-up for infectious etiology versus PE remained negative despite concerning CT for opportunistic infection. Thalidomide was subsequently held in which her shortness of breath completely resolved without intervention. Repeat CT showed resolution of ground-glass alveolar opacities and micro nodules present on previous image.
Of note, some key contributing factors to note about our patient include a past medical history of asthma, eczema, and h/o pneumonia as well as the concurrent use of narcotics which can decrease respiratory drive putting the patient at an increased risk for respiratory infections. Our patient was also neutropenic which made them more susceptible to not only routine infections, but opportunistic organisms as well.

References

  1. Prekker ME, Scott NL, Hart D, Sprenkle MD, Leatherman JW. Point-of-care ultrasound to estimate central venous pressure: a comparison of three techniques. Crit Care Med. 2013;41(3):833-41. [CrossRef] [PubMed]
  2. Jabot J, Teboul JL, Richard C, Monnet X. Passive leg raising for predicting fluid responsiveness: importance of the postural change. Intensive Care Med. 2009;35(1):85-90. [CrossRef] [PubMed]
  3. Buttin BM, Moore MJ. Thalidomide-induced reversible interstitial pneumonitis in a patient with recurrent ovarian cancer. Gynecol Oncol. 2008;111(3):546-8. [CrossRef] [PubMed]
  4. Lee CK, Barlogie B, Munshi N, Zangari M, Fassas A, Jacobson J, van Rhee F, Cottler-Fox M, Muwalla F, Tricot G. DTPACE: an effective, novel combination chemotherapy with thalidomide for previously treated patients with myeloma. J Clin Oncol. 2003;21(14):2732-9. [CrossRef] [PubMed]
  5. Scholte JB, Potjewijd J, Voogt PJ, Custers FL, Jie KS. Interstitial pneumonitis as an adverse effect of thalidomide. Ned Tijdschr Geneeskd. 2009;153:A452. [PubMed]
  6. Thalomid (thalidomide): Highlights of Prescribing Information. (2014, June 1). Retrieved February 6, 2015, from http://www.thalomid.com/pdf/thalomid_pi.pdf
  7. Wyplosz B, Lerolle U, Israël-Biet D, Dougados J, Lillo-Le Louët A, Ghez D, Pouchot J. Thalidomide-induced pneumonitis. Eur J Intern Med. 2008;19(7):e57-8. [CrossRef] [PubMed]

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