Orris

give impression - initial history - Te, Maria Vivian Pe 63/F 5107 DOA: AUG 1, 2026 Patient is a known case of Invasive Breast Carcinoma STAGE IV with lung metastasis. Referred to our service for possible chest pigtail insertion. HPI: Patient was previously admitted last July 14-16 2026 and underwent thoracentesis right for pleural effusion. She tolerated procedure well with no untoward events. Eventually discharged stable. In the interim, patient had noted progression from baseline exertional dyspnea with occasional dry cough. Sought consult at a clinic in Davao noted Chest UTZ findings Chest ultrasound revealed Non loculated pleural effusion Right approximately 770ml with passive atelectasis, right. No complaints of chills, fever, hemoptysis. COURSE IN THE WARD Stable pulmowise and no subjective complaints upon admission. s/p chest pigtail insertion right and pleurodesis (8/3) 8/4-8/16: With intermittent increase work of breathing and exertional dyspnea, non-productive cough, no significant desaturation (lowest 91%). Hooked to HFNC. Started on Levopront and morphine for cough. 8/5-11/26: Noted new onset infiltates. Started on TZP and LVX and referrred to IDS. Decreasing pigtail output from bloody to serosanguneous. CTPA was requested however cannot tolerate to lie down flat. 8/17: With increase effort of breathing, hooked to BIPAP but cannot tolerate hence intubated. Pulmo profile: non smoker with 2nd hadn smoke exposure to husband no previous PTB treatment No BA/COPD 7/28 Chest US (Davao) ULTRASOUND - THORAX Remarks: MRM, Left; With digital xray images from SLMC 2026 Technique: Patient was scanned while sitting upright with her back towards the sonologist. A comparison with the ultrasound dated May 31, 2023 pleural fluid is now seen in the right hemithorax with an approximate volume of 609.4 ml to 770.5 ml. Pneumonia with consolidation and passive atelectasis are seen in the right lower lobe. There are no low level internal echoes, loculations, or septations present in both hemithoraces. Normal excursion of the diaphragm is evident. 8/17 CXR postintubation Unchanged bilateral lung hazy and reticular-streaky densities; and scattered bilateral lung patchy confluent densities. Pulmonary vascular markings remain obscured. Apparent regression of the bilateral lower chest homogeneous density with increased apical capping. Minimal bilateral apical pleural thickening is again observed. Left hemidiaphragm and bilateral are obscured. Right hemidiaphragm is now partially visualized. Interval placement of an endotracheal tube with tip approximately 3 cm above the carina at the level of T4-T5. Feeding tube, right chest pigtail catheter, and right implantable central venous access port and catheter are noted in place.   IMPRESSION Unchanged bilateral pneumonia and areas of consolidation. Unchanged pulmonary congestion. Apparent regression of the bilateral lower chest homogeneous density with increased apical capping may suggest posterior layering of the bilateral pleural effusion. 8/17/26 Relaying ABG at FI02 30% 7.40 / 50 / 105 / 32.5 / 6.2 / 99% dFI02: 22 PFR 350 —> Compensated metabolic alkalosis with suspected underlying respiratory acidosis more than adequate oxygenation 8/3 PF cell block: positive malignant PF GS: no microorganism 8/7 CBC 11.3(9.9)/34.8/3.24/35980(31670)/N92 L2 M2/397K(313K) 8/7 CXR -Bilateral pleural effusion and,or atelectasis, with regression on the RIGHT and unchanged on the LEFT 8/4 Crea 0.58 Albumin 4.21 A: ARF Type II Malignant recurrent bilateral pleural effusion s/p pigtail inertion right (8/30 SEC TO  1. MALIGNANT from Invasive Breast Carcinoma 2. Parapneumonic process from HAP T/C ILD drug induced (ICP inhibitor), t/c Aspergilloma  Encephalopathy prob drug induced (Morphine) vs septic T/C Acute pulmonary embolism, high risk s/p Thoracentesis right (7/15/26, 8/3/26) Invasive Breast Carcinoma STAGE IV (TxNxM1 - NRLN) (2023) ER + PR - HER2neu 1+  s/p Cycle 17 Enhertu (6/24/26) Rule Out Progressive Disease to Pleura (7/10/26) DVT at risk (WS 1 PADUA 8) > eventually intubated Good eveniing, sir! Update on Patient Te, Maria Vivian, now transferred to ICU 8 On Precedex 0.2mkh Received on CMV TV 280 (5.9ml/kg) PEEP 5 BUR 14 FiO2 50 Seen with triggered breaths Able to follow commands No MV asynchrony BP 101/57 HR 74 RR 15 sO2 100 at 50FiO2 > 98 at 40FiO2 Ppeaks 25 VTEs 253-264 Min vol 4.0 Decrease breath sounds left mid to base Running I/O: 1014 vs 750 Review of latest labs 8/17 CBC Hgb 9.1 WBC 17500 N 90 L 2 Plt 246k Crea 0.24 BUN 12 Na 139 K 4.3 Cl 102 HCO3 30 iCa 1.10 Mg 2.1 CXR post intubation -Follow-up study shows unchanged bilateral lung hazy and reticular-streaky densities; and scattered bilateral lung patchy confluent densities. Pulmonary vascular markings remain obscured. Apparent regression of the bilateral lower chest homogeneous density with increased apical capping. Minimal bilateral apical pleural thickening is again observed. -Heart is normal in size. Aorta is calcified. -Left hemidiaphragm and bilateral are obscured. Right hemidiaphragm is now partially visualized. ABG 1hr post intubation Combined metabolic and respiratory alkalosis with more than adeuate O2 for age 7.602 pCO2 30.6 pO2 186 HCO3 32.2 sO2 100.7 PFR 186 DFiO2 44 Initial HRCT Follow-up study shows the following findings:   The patient is status-post LEFT mastectomy with relatively stable post-surgical changes. No discrete mass lesion or fluid collection in the mastectomy bed observed. Stable prominent LEFT axillary lymph node still measuring 0.5 cm. The RIGHT breast is heterogeneously dense with stable calcifications, still measuring up to 0.5 cm.   Stable non-calcified solid subpleural nodule in the medial segment of the middle lobe still measuring 0.6 cm (image 4-121). Other smaller non-calcified solid nodules are seen in both lungs, measuring up to 0.2 cm in the anterior segment of the RIGHT upper lobe (image 4-88). Non-calcified perifissural nodules are again observed along the LEFT major fissure measuring up to 0.4 cm, with some of the previously noted perifissural nodules obscured by the overlying pleural effusion.   There is progression of the focal consolidation in the apicoposterior segment of the LEFT upper lobe, with interval demonstration in the anterior segment of the LEFT upper lobe, the lingula, the superior segment of the LEFT lower lobe as well as the RIGHT upper, middle and the anterior and lateral segments of the lower lobe. Progression of the ground glass densities in both lungs is noted. Linear densities in the lingula, middle lobe and both lower lobes are seen.   Stable prominent lower paraesophageal lymph node still measuring 0.8 cm.   Interval demonstration of LEFT-sided pleural effusion. Minimal regression in the RIGHT-sided pleural effusion.   Mediastinum is midline in location. The trachea and proximal airways are patent without definite endobronchial lesions. The intrathoracic esophagus is intact. A RIGHT-sided implantable catheter device, tracheostomy tube and a nasogastric feeding tube are partially visualized.   Heart is enlarged with minimal pericardial effusion. The great vessels are normal in size and configuration. Intimal calcifications are seen along the thoracic aorta.   Compression deformity with mixed lytic and blastic lesions are seen in the T9 vertebral body. Lytic lesions are again seen in the medial end of the LEFT clavicle. Sclerotic foci are again noted along the T4, T6-T8, T12 and L1 vertebral bodies. Cortical irregularities, likely old/healed fractures, are seen along the RIGHT 4th-6th anterolateral, RIGHT 8th-10th lateral, LEFT 6th anterior and the LEFT 3rd lateral ribs. Degenerative changes in the form of spurs are also seen along the visualized osseous structures.   The visualized upper abdomen is grossly unremarkable.   IMPRESSION:   The following findings may relate to an infectious/inflammatory process. Clinical correlation is recommended Progression of the bilateral lung consolidation, as detailed Interval demonstration of LEFT-sided pleural effusion Mild regression of the RIGHT-sided pleural effusion   Status-post LEFT mastectomy with no signs of tumor recurrence or fluid collection   Progression in size of the non-calcified perifissural nodules along the RIGHT major fissure   Stable non-calcified subpleural nodules, medial segment of the RIGHT middle lobe   Stable non-calcified perifissural nodules along the LEFT major fissure   Relatively stable in size and number in the small-sized non-calcified solid nodules in both lungs   Stable prominent lower paraesophageal and LEFT axillary lymph node   Compression deformity and mixed lytic and blastic lesions, T9   Lytic lesions, LEFT clavicle   Sclerotic foci along the T4, T6-T8, T12 and L1 vertebral bodies, worrisome for metastasis.

Reading File
Finding Sources
Finding Sources
Finding Sources
Searching PubMed

"trastuzumab deruxtecan" AND "interstitial lung disease"

Searching PubMed

malignant pleural effusion pigtail catheter pleurodesis

Reading File
Finding Sources
Finding Sources

Clinical Impression - Te, Maria Vivian Pe, 63/F (5107)

Working Diagnosis:
1. Invasive Breast Carcinoma, Stage IV (TxNxM1, NRLN, 2023), ER+/PR-/HER2 1+, s/p 17 cycles Enhertu (trastuzumab deruxtecan, last 6/24/26), with:
  • Malignant recurrent bilateral pleural effusion (cytology-confirmed, 8/3 PF cell block positive for malignant cells) - s/p thoracentesis right x2 (7/15, 8/3) and right chest pigtail insertion + pleurodesis (8/3), now with new left-sided effusion on repeat imaging (interval development) with only minimal right-sided regression
  • Osseous metastases: compression deformity with mixed lytic/blastic lesion T9, lytic lesion left clavicle, sclerotic foci T4/T6-T8/T12/L1 - diffuse skeletal disease
  • Rule out progressive disease to pleura since 7/10/26
2. Acute Hypercapnic Respiratory Failure (Type II ARF) progressing to intubation on 8/17, now in ICU on CMV. This sits on top of at least three overlapping processes that need to be actively distinguished rather than lumped together:
  • Drug-induced interstitial lung disease/pneumonitis from trastuzumab deruxtecan (T-DXd/Enhertu) - this is a well-recognized, potentially fatal toxicity of T-DXd. Per Goodman & Gilman's Pharmacological Basis of Therapeutics, "interstitial lung disease and pneumonitis, including fatal cases, have been reported as serious adverse effects" of fam-trastuzumab deruxtecan (p. 4528). Recent systematic reviews/meta-analyses confirm ILD/pneumonitis occurs in a clinically meaningful proportion of T-DXd-treated patients and is a leading cause of treatment discontinuation and death, with risk increasing with cumulative dosing (this patient received 17 cycles) - see Li et al., Cancer 2024 systematic review/meta-analysis (PMID 38703012) and Soares et al., ESMO Open 2023 (PMID 37481956). The HRCT pattern described (progressive ground-glass densities and consolidation in multiple lobes bilaterally, not confined to a vascular or lobar distribution) is consistent with this differential, though it is radiographically difficult to distinguish from infection or pulmonary edema.
  • Hospital-acquired pneumonia (HAP)/parapneumonic process - new infiltrates 8/5, leukocytosis (WBC up to 35,980 → 17,500, N90-92%), started on TZP + levofloxacin, IDS referral. This is the most treatable and time-sensitive differential and should not be deprioritized while ILD workup is pending.
  • Cardiogenic/hydrostatic contribution - CXR impression noted "unchanged pulmonary congestion" and follow-up HRCT shows an enlarged heart with new minimal pericardial effusion, raising a component of volume overload or malignant pericardial involvement contributing to the bilateral process.
3. Suspected high-risk (massive) pulmonary embolism - flagged clinically but unconfirmed because CTPA could not be obtained (patient could not tolerate supine positioning). Malignancy is itself a major VTE risk factor, and immobility from progressive dyspnea further raises pretest probability (documented DVT risk assessment: PADUA score 8, "at risk"). This remains an unresolved, high-stakes diagnostic gap - once she is intubated and sedated, a CTPA (or at minimum lower-extremity venous duplex plus consideration of empiric therapeutic anticoagulation if no contraindication) should be pursued, since a missed high-risk PE in this context carries a high mortality risk and is a fully treatable competing diagnosis.
4. Encephalopathy, probable multifactorial - documented as "probable drug-induced (morphine) vs septic." Given she was on morphine and levopront for cough/dyspnea, opioid-related sedation/hypercapnic encephalopathy from Type II respiratory failure itself is highly plausible and may have been the proximate trigger for BIPAP intolerance and intubation, in addition to any sepsis-associated component from HAP.
5. Acid-base/ventilatory course - The serial ABGs are informative:
  • 8/17 pre-intubation on 30% FiO2: pH 7.40/pCO2 50/HCO3 32.5 with PFR 350 - a compensated respiratory acidosis with metabolic compensation, i.e., chronic-on-acute CO2 retention (Type II failure) with adequate oxygenation, consistent with hypoventilation (from encephalopathy/opioids) rather than a primary oxygenation failure at that point.
  • 1 hour post-intubation: pH 7.60/pCO2 30.6/HCO3 32.2, PFR 186 - now a combined respiratory and metabolic alkalosis, most likely from overventilation on the ventilator (iatrogenic hyperventilation correcting the CO2 too fast) layered on the pre-existing compensatory metabolic alkalosis; PFR has also dropped to 186, indicating a real worsening of the ventilation-perfusion/oxygenation status independent of the alkalosis, consistent with progressive bilateral consolidation on imaging.
  • Ventilator settings should be adjusted to slow correction of pCO2 (permissive approach) to avoid rapid pH shifts, and the falling PFR (350→186) should prompt close monitoring for evolving ARDS-pattern lung injury given the multifocal consolidation/ground-glass pattern on HRCT.
6. Chronic disease burden relevant to prognosis and goals-of-care discussion: Stage IV breast cancer with visceral (lung) and osseous metastatic disease, now with respiratory failure requiring mechanical ventilation. Given multiple competing life-threatening processes (possible high-risk PE, drug-induced ILD, HAP, malignant effusions bilaterally), this is a critical, guarded-prognosis presentation. A goals-of-care/palliative care conversation with the family is appropriate in parallel with active treatment, particularly given the intubation occurred acutely after BIPAP failure.

Suggested priority actions

  1. Once hemodynamically tolerant, obtain CTPA to rule in/out high-risk PE - this is the most urgent unresolved diagnostic gap given the mortality implications.
  2. Hold further T-DXd; involve oncology regarding grading of possible drug-induced ILD (consider empiric corticosteroids if infection is reasonably excluded/being treated, per T-DXd ILD management algorithms).
  3. Continue/optimize antibiotics for HAP per culture data and de-escalate per sensitivity.
  4. Address new left pleural effusion - consider left thoracentesis/pigtail if compromising ventilation or for diagnostic/cytologic confirmation.
  5. Reassess sedation (Precedex) and ventilator strategy to correct pCO2/pH gradually; trend PFR and repeat imaging to distinguish evolving ARDS from ILD flare vs infection.
  6. Multidisciplinary discussion (pulmonology, oncology, critical care, palliative care) given the multiple overlapping life-threatening differentials in a Stage IV cancer patient.
Recent evidence note: No systematic review/meta-analysis in the last 2 years contradicts the above; the most recent large syntheses (2024-2025, PMIDs 40083848, 40466817, 38703012) reinforce that T-DXd-associated ILD/pneumonitis is dose- and cycle-dependent and remains a leading serious toxicity requiring a high index of suspicion in heavily pretreated patients like this one (17 cycles).
This is a shared conversation. Sign in to Orris to start your own chat.