CT Pulmonary Angiogram report: what it shows, what it means, and what to do
Patient: Shailesh Umesh Rupwate. Scan date on report: 30/10/2026. Reason for scan: breathlessness on and off.
1. The problem in one line
The scan shows a large, bilateral pulmonary embolism (blood clots in the lung arteries). The clots are saddle-type, and there are signs that the right side of the heart is under strain. This needs urgent medical attention, so please don't wait on it.
2. What the report says, in plain language
| Report finding | What it means |
|---|
| Saddle thrombus at the bifurcation of the main pulmonary trunk, extending into the right and left main pulmonary arteries | A large clot sits across the point where the main lung artery splits into right and left branches. It blocks blood flow to both lungs. |
| A second saddle thrombus at the right/left main artery bifurcation, extending into lobar and segmental branches | The clot burden is extensive. It reaches deep into the smaller branches of the lung arteries. |
| CT pulmonary embolism index = 55 | This is a score for how much of the pulmonary artery tree is blocked. It is most likely the Qanadli obstruction index, shown as a percentage. If so, about 55% of the arterial tree is obstructed, which is a heavy clot load. The report doesn't state the unit, so confirm this with the radiologist. |
| Pulmonary trunk 2.8 cm, right and left pulmonary arteries 2.2 cm each; PA:aorta ratio maintained | The arteries are not enlarged. The upper limit of normal for the trunk is about 2.9 cm. This suggests the clot is acute or recent. Long-standing clots usually enlarge the artery because pressure has been high for a long time. |
| Mild prominence of right ventricle and right atrium | The right side of the heart is stretched because it is pumping against blockage. This is called right ventricular (RV) strain. |
| Dependent densities in both lower lobes | These are likely atelectasis (partial collapse) or gravity-related changes, which are common and usually not serious. |
| Mosaic attenuation in places | Some lung areas get less blood than others because of the blocked vessels. It supports the diagnosis of embolism. If it persists, doctors consider chronic thromboembolic disease. |
| No pleural effusion, consolidation or pulmonary infarct | There is no lung tissue death or fluid yet. This is good news. |
| Small hiatus hernia | A small part of the stomach sits through the diaphragm opening. It is an incidental finding and unrelated to the clots. |
| Trachea, bronchi, mediastinal nodes, ribs and bones normal | No other problems were found. |
Typos in the report: The impression says "right lateral ventricle" and "right ventricular sprain pattern". These almost certainly mean "right ventricle" and "right ventricular strain pattern". The body of the report describes the right ventricle and atrium, so the meaning is clear. Ask the radiology team to correct it.
3. Why this matters
A PE blocks blood flow to the lungs, so oxygen levels fall and the patient feels breathless. The right ventricle has to push harder against the blockage. If it fails, blood pressure can collapse, and that is the main cause of death in PE. Medical textbooks state that RV enlargement on chest CT, together with raised troponin, predicts a higher risk of adverse outcomes despite anticoagulation. Most patients with normal RV function do well (Harrison's Principles of Internal Medicine 22E, Risk Stratification, p. 2205).
Saddle location and RV strain mean this is at least an intermediate-risk PE. The category depends on blood pressure, troponin, BNP and echo. If blood pressure is low, it is high-risk (massive) PE. That is an emergency.
4. What is needed: the solution
A. Immediate (today, in hospital)
- Admit to a monitored setting (HDU or ICU). This is not suitable for outpatient care given the clot burden and RV strain.
- Check these now:
- Blood pressure, heart rate, oxygen saturation, and syncope history.
- Troponin and BNP/NT-proBNP.
- Bedside echocardiogram to assess RV function.
- ECG.
- Baseline CBC, creatinine, coagulation profile and liver function.
- Oxygen to keep saturation above 90%.
- Start anticoagulation immediately if there is no bleeding contraindication:
- Preferred in the sicker patient is unfractionated heparin (IV infusion), because it can be stopped quickly if thrombolysis is needed.
- Alternatives are LMWH (enoxaparin) or fondaparinux.
- Rosen's states that apixaban and rivaroxaban are now first-line for most PE, but have not been extensively tested in severe PE. LMWH is preferred in that situation (Rosen's Emergency Medicine, Standard Anticoagulation).
- Avoid excess IV fluid. Too much fluid overdistends the right ventricle and can worsen collapse. Small boluses of 250-500 mL are acceptable if hypotensive. Norepinephrine is the first-choice vasopressor (Rosen's, Hemodynamic Resuscitation).
- Avoid intubation if possible. Positive-pressure ventilation can precipitate collapse in severe PE (Rosen's).
B. Escalation depends on the patient's status
| Status | Treatment |
|---|
| High-risk: low BP, shock or cardiac arrest | Systemic thrombolysis (for example alteplase) unless contraindicated. If thrombolysis is contraindicated or fails, use catheter-directed or surgical embolectomy. ECMO can bridge. |
| Intermediate-high risk: normal BP, but RV strain and raised troponin | Anticoagulation with close monitoring. Rescue reperfusion if the patient worsens. Catheter-directed therapy (mechanical thrombectomy or low-dose thrombolysis) is considered case by case. |
| Stable with only mild RV strain | Anticoagulation alone, usually with a short monitored stay first. |
C. After the acute phase
- Switch to an oral anticoagulant (apixaban or rivaroxaban, or warfarin or dabigatran/edoxaban after initial parenteral therapy) for at least 3 months.
- Look for the source and cause:
- Leg Doppler ultrasound for DVT.
- Review for recent surgery, immobility, long travel, cancer, hormonal therapy and family history.
- If there was no clear trigger, consider thrombophilia and cancer screening, and decide on extended therapy.
- Antiphospholipid syndrome needs warfarin rather than DOACs.
- Follow-up at 3 months: repeat echo. If breathlessness persists, check for chronic thromboembolic pulmonary hypertension (CTEPH) with V/Q scan. The mosaic attenuation makes this follow-up worthwhile.
- An IVC filter is only for patients who cannot take anticoagulants or who have recurrent clots despite treatment.
5. Recent evidence note
My quick PubMed check found two recent meta-analyses on how to treat intermediate- and high-risk PE:
Also, a 2026 AHA/ACC multisociety PE guideline (PMID 41712677) appears to replace the older low/intermediate/high categories with a graded A-E severity scale. The exact thresholds and recommendations come from search snippets only. I did not read the guideline itself. The treating team should apply whichever guideline their hospital follows.
6. Warning signs: go to the emergency room immediately
- Worsening breathlessness or chest pain
- Fainting or near-fainting
- Coughing blood
- Racing heart or low blood pressure
- Bluish lips
- Any bleeding on blood thinners
7. Limits of this explanation
I only have the written report. I haven't seen the images, vital signs, labs or echo. This is an explanation, not a prescription. Drug choice and dose, and whether thrombolysis is needed, must be decided by the treating physician (cardiologist, pulmonologist or intensivist) after bedside assessment. The report was referred by Dr. Nandkumar Chonkar, so share it with him or a hospital emergency team today.
If you tell me the patient's blood pressure, oxygen saturation, troponin and echo findings, I can explain which risk category applies and what that means for treatment.