SECOND CLINICAL CASE STUDY 1

Bilateral Acute Pulmonary Thromboembolic Disease with

Elevated Right-Sided Cardiac Pressures

Joida Mae Esper I. Canono 22030085

ENP 110 Nursing Practicum II

Clinical Instructor Robbi Martson

February 13, 2023

SECOND CLINICAL CASE STUDY 2

Bilateral Acute Pulmonary Thromboembolic Disease with

Elevated Right-Sided Cardiac Pressures

History of Present Illness

Mr. W. H. is a 73-year-old, male patient who came to the hospital (SAH) for consultation

25 May 2022 c/o prostatism, he was seen and discharge same day. He came back on 25 Sept

2022 to triage c/o UTI. He has a history of multiple urologic issues including BPH, large bladder

calculi as well as severe phimosis. He underwent cystoscopy on 6 August 2022 which

demonstrated a bilobed prostate that was obstructive, 3 large bladder calculi as well as phimosis

with balanitis xerotica obliterans. A staged surgical approach was planned, initially a

circumcision together with the cystolithotomy as a first surgery and a TURP as a second surgery.

He presented to the hospital on 30 November 2022 for his circumcision and

cystolithotomy. Postoperatively, the patient was initially doing well on the surgical ward and his

renal function was improving but he had hyperkalemia. He was ambulating independently. On

2 December 2022, the patient developed chest pain while up on the commode and became

unresponsive. He was pulseless and a CODE BLUE was initiated. He had multiple

PEA/asystolic arrest with some response to epinephrine resulting in brief perfusing rhythms and

subsequent deteriorations. He was transferred directly to the ICU.

Ultimately, he was extubated on 17 December 2022 and made gradual slow medical

improvements. He remained in ICU for monitoring and was noted to be extremely

deconditioned.

He was eventually transferred to the medical unit hemodynamically stable and stable

from a respiratory perspective, and medically stable transferred to 2B rehabilitation 27th January

2023.
SECOND CLINICAL CASE STUDY 3

Past Medical History

1. Bladder calculi

2. Phimosis

3. BPH

4. Remote renal lithiasis

5. Vertigo

6. Tonsillectomy

Social History

 Recent widower. Ex-smoker 10 yrs ago

Medical Diagnosis:

30 November 2022 (3A)

 Bladder Calculi + Phimosis

02 December 2022 (ICU)

 Bilateral Acute Pulmonary Thromboembolic Disease with Elevated Right-

Sided Cardiac Pressures

 Obstructive shock/cardiac arrest

 Post op cystolithotomy/circumcision
SECOND CLINICAL CASE STUDY 4

Bilateral Acute Pulmonary Thromboembolic Disease with

Elevated Right-Sided Cardiac Pressures

Pathophysiology

Pulmonary embolism (PE) is a common and potentially deadly form of venous

thromboembolic disease. It is the third most common cause of cardiovascular death and is

associated with multiple inherited and acquired risk factors as well as advanced age (Turetz,

2018).

Pulmonary embolism (PE) and deep venous thrombosis (DVT) exist on the spectrum of

venous thromboembolic disease (VTE). PE results when thrombus migrates from the venous

circulation to the pulmonary vasculature and lodges in the pulmonary arterial system. The

clinical presentation of acute PE ranges from asymptomatic and incidentally discovered to

massive PE causing immediate death.

Surgery and trauma are known to increase the risk of VTE. Patient underwent

circumcision and chordee repair with open transvesical cystolithotomy, under general anesthesia.

The increased risk is mediated by immobility during and after the surgery as well as by direct

venous injury and inflammation during surgery, although to this patient, surgical interventions

that have been undertaken from a urological perspective was actually reassured that the incisions

were fairly small and that the surgery was very minor and that the incision sites were sutured

closed quite tightly and that there is minimal concern from severe bleeding from a surgical

standpoint which was certainly reassuring. Most PEs originate as thrombi in the deep veins of the

lower extremities. Thrombosis begins in areas of decreased flow such as valve cusps and

bifurcations and then propagates due to local hypercoagulability caused by hypoxia and
SECOND CLINICAL CASE STUDY 5

hemoconcentration. Emboli detach from their point of origin and travel through the systemic

venous system, through the right sided chambers of the heart, and lodge in the pulmonary arterial

system. The physiologic and clinical consequences of PE vary ranging from asymptomatic to

hemodynamic collapse and death. Hypoxemia is the most common physiologic consequence of

acute PE. Two (2) days post operatively, he developed chest pain while up to the commode,

chest pain was felt because by that time large blood clot interferes with the heart and blood

circulation already, and he became unresponsive. He was pulseless and a protected code blue

was initiated. Patient had multiple PEA/asystolic arrests with some response to

epinephrine/cardiac medications resulting in brief perfusing rhythms and subsequent

deteriorations as they wore off. Bedside U/S was done and a dilated RV with hyperdynamic

underfilled LV was noted. CT thorax on pulmonary angiogram performed which demonstrated

massive bilateral pulmonary emboli with elevated right-sided cardiac pressures. According to

Manier, et.al, elevated right atrial pressures in setting of acute PE can open a patent foramen

ovale and cause right-to-left intracardiac shunting. Low mixed venous saturation can also

contribute to hypoxemia. Vascular obstruction leads to increased dead space because lung units

continue to be ventilated despite reduced or absent perfusion. Most patients with PE therefore

have a respiratory alkalosis. Acute respiratory alkalosis results in a clinically significant increase

in plasma potassium, which was seen when patient coded. He was thrombolysed and

subsequently initiated on a heparin infusion.

Initiation of exercise therapy as early as four weeks after acute PE is feasible and safe in

appropriately anticoagulated patients. Exercise intervention may be associated with significant

improvements in physical function. So, the patient now is at the Rehab unit for PT and OT for

this goal.
SECOND CLINICAL CASE STUDY 6

References:

Cires-Drouet, R. S., Mayorga-Carlin, M., Toursavadkohi, S., White, R., Redding, E., Durham,
F., Dondero, K., Prior, S. J., Sorkin, J. D., & Lal, B. K. (2020, December). Safety of
exercise therapy after acute pulmonary embolism. Phlebology. Retrieved February 12,
2023, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8209689/

Manier G, Castaing Y, Guenard H. Determinants of hypoxemia during the acute phase of

pulmonary embolism in humans. Am Rev Respir Dis. 1985;132(02):332–338. [PubMed]
[Google Scholar]

Turetz, M., Sideris, A. T., Friedman, O. A., Triphathi, N., & Horowitz, J. M. (2018, June).
Epidemiology, Pathophysiology, and natural history of pulmonary embolism. Seminars in
interventional radiology. Retrieved February 12, 2023, from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986574/