UNUSUAL COMPLICATION IN A PATIENT OF CAPD: A CASE REPORT

Introduction:

BACKGROUND: Hemoperitoneum in CAPD patients is a known but infrequent complication, the most common cause being trauma. It may occur in women due to gynecological causes such a follicular cyst bleeding, menstrual reflux, ovulation and endometriosis. Intraperitoneal causes include rupture of hepatic/splenic cyst, catheter or abdominal trauma and vascular anomalies. However, hemoperitoneum from a retroperitoneal source is extremely rare, especially with cyst rupture in patients with ADPKD. In the two prior reported cases of retroperitoneal hemorrhage leading to bloody effluent, one case had intracystic hematoma and the other case had cystic rupture with perirenal hematoma. Among these cases and our case, hemoperitoneum was noted despite the absence of a retroperitoneal to peritoneal communication on abdominal imaging. No other source of hemoperitoneum could be identified.

Another notable observation in spontaneous retroperitoneal hemorrhage secondary to cyst rupture is that there is a remarkable difference in frequencies between peritoneal hemorrhage due to ACKD and ADPKD. Most of the described patients in the literature had underlying ACKD rather than ADPKD. Some putative factors have been put forward to explain this disparity. The more medullary location of cysts in ADPKD compared with cortically residing cysts of ACKD and differences in the speed of cyst growth might account for differences in observed prevalence. Retroperitoneal hemorrhage, in theory, should not find its way through the peritoneal membrane. A possible explanation is an adhesion between the cyst's wall and the peritoneum, favored by their anatomical proximity and inflammation secondary to intracystic hemorrhage. These adjoining structures could then rupture because of the rising intracystic pressure.

Methods:

CASE REPORT:

Patient is a case of ADPKD for 20 years, diagnosed when patient had presented with bilateral loin pain with renal dysfunction (Serum creatinine of 3 mg%). Abdominal imaging at that time showed bilateral polycystic kidneys. Patient initially on medical management but later lost to follow up.

In 2022 Patient had multiple episodes of generalised tonic clonic seizures. MRI brain was suggestive of subarachnoid hemorrhage with rupture of berry aneurysm. Aneurysmal clipping with decompressive craniotomy was done. Patient on T. Levipill 500mg twice a day since then. At this time the serum creatinine was 4.5 mg%, UO 2 lit/day discharged on medical management. 

In 2023, Patient presnted with fluid overload and uremic symptoms, with serum creatinine 15 mg%. Initially Hemodialysis was initiated through the left femoral and then shifted to right Internal Jugular catheter. Left BC AVF done, failed after 4 sessions of hemodialysis. Continued maintenance hemodialysis through non tunneled Right internal jugular catheter and then later from the non tunneled left internal jugular catheter. 

In March 2024, patients presented with fluid overload with uremic symptoms. Patient discontinued hemodialysis from a month as her right IJV catheter was not having blood flow. Doppler was suggestive of complete right IJV, partial left IJV and complete left femoral thrombosis.

Percutaneous insertion of soft PD catheter done. APD cycles initiated with a cycler. After appropriate training for 2 weeks patient shifted to CAPD. Since then patient is on CAPD - 3 cycles/day, Dwell volume 2 liters, Dwell time 4hrs, PD fluid 1.5 % D, Daily ultra filterate of -900ml. Patient was doing well with this prescription.

OBSTETRIC HISTORY:

P2L2, both full term normal vaginal delivery, no history of gestational hypertension or PrAKI, Last child birth was 23 years back. Attained menopause 4 years back.

PRESENTING COMPLAINS: 

Now patient was having PD fluid hemorrhagic outflow followed by complete blockage of PD outflow since 1 week. Hence stopped doing CAPD cycles at home since 1 week. Patient presented to us with anasarca, grade 4 dyspnea and altered sensorium.

Results:

CLINICAL EXAMINATION: 

O/E 

Patient is drowsy, 

GCS- 9,

 Pallor and Pedal edema present

Afebrile

BP- 100/70 mm Hg

PR- 92bpm

P/A soft- no tenderness

Capd cath insitu, No exit site of tunnel site pus/erythema/tenderness

INVESTIGATIONS:

CBP- 7.5/7500/1.75

RFT- 307/20.57

SE- 146/20.57

SCa/SPO4/S UA- 8.3/6.5/6.7

T Bil- 0.7

AST/ALT- 9/14

S Alb/S TP- 2/5.7

PT/INR/APTT- 14/1.2/33 sec

USG Abdomen-

 B/L polycystic kidneys with large intraperitoneal hemorrhage of 16.5* 8cm

CECT abdomen- 

Bilateral enlarged kidneys 17*9*5.2 cm, 15.3*8*4.9.

Evidence of hypodense cystic lesions noted in both the the renal parenchyma with multiple foci of hyperdensities(hemorrhage) noted within the cysts and few of the cysts showing calcification.

Evidence of 23*6.7*18cm well defined intreperitoneal collection of fluid attenuation with air foci noted within superiorly extending from the left subhepatic space, abutting left lobe of liver, greater curvature of stomach, inferiorly extending till the inframesocolic compartment at L5 and S1 vertebral level, laterall collection notes extending the right paracolic gutter.

Evidence of similar collection approximately measuring 6.2*9.7*3.6cm noted in the inferior recess of lesser sac anterior to the body of the pancreas,posterior to distal body of the pancreas.

CECT Abdomen repeated after 3 days

4.7*8*9.2cm collection with air foci noted. Another collection of 3*6.2*6 cm similar collection noted in the inferior recess of lesser sac anterior to the body of the pancreas, posterior to distal body of the pancreas. No active extravasation of contrast noted.

PD FLUID ANALYSIS 

PD fluid cell count - 1100 cells

RBC- plenty of RBC/HPF

Neutrophils - 60%

Malignant cytology- Negative

Malignant cytology- Negative

Peritoneal fluid culture- Negative

TREATMENT GIVEN/COURSE IN THE HOSPITAL:

Saline flushes given through CAPD catheter. PD outflow of 1 liter hemorrhagic fluid noted. PD fluid sent for analysis and CAPD stopped.

Left IJV non tunneled catheter inserted and hemodialysis started. Daily 6 hours of hemodialysis done with good ultrafilterate. One packed cell with two FFPS transfusion done during dialysis. General surgeon and Urology opinion taken. Daily abdominal girth measured. Intraperitoneal Vancomycin and Ceftazidime started.

By 4th day, Patient sensorium improved. Patient is currently admitted with us. Planning to restart CAPD cycles after 2 weeks. Or plan left IJV perm catheter and to continue maintenance hemodialysis. Urologist planned Radical nephrectomy if hemorrhage is persistent

Conclusions:

Our case report exemplifies a rare CAPD patient who developed hemoperitoneum. The reason was rupture of cysts of ADPKD. Cyst rupture is an important and potentially fatal complication. Timely and apt identification of pain abdomen in patients with ADPKD on dialysis can help in salvaging the patient. All patients of ADPKD despite being CKD on maintainence dialyis, radiological surveillance should be continued because of risk of cyst enlargement, rupture and malignancy risk.

I have no potential conflict of interest to disclose.

I did not use generative AI and AI-assisted technologies in the writing process.