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Int J Surg Case Rep
Int J Surg Case Rep
International Journal of Surgery Case Reports
2210-2612
Elsevier

S2210-2612(24)01060-5
10.1016/j.ijscr.2024.110279
110279
Case Series
Composite mesh a novel innovative bridge approach for refractory pancreatic effusion - sequelae of porous diaphragm syndrome: Case series☆
Dantis Klein drkleindantis@yahoo.com
a⁎
Dey Chandan Kumar b
a Department of CTVS, All India Institute of Medical Sciences, Bathinda, India
b Department of Trauma and Emergency Medicine, All India Institute of Medical Sciences, Raipur, India
⁎ Corresponding author. drkleindantis@yahoo.com
11 9 2024
10 2024
11 9 2024
123 11027910 8 2024
5 9 2024
9 9 2024
© 2024 The Authors. Published by Elsevier Ltd on behalf of IJS Publishing Group Limited.
2024

https://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Introduction and importance

Managing refractory pancreatic effusion due to porous diaphragm syndrome (PDS) is a challenge. Various surgical interventions such as repairing the defect, sealing with fibrin glue, performing parietal pleurectomy, and talc pleurodesis have been reported however, the use of composite mesh placement in treating PDS has not been described in the literature.

Case presentation

All three male patients with a low body mass index were diagnosed with pancreatic disease as described in cases 1–3 and associated pancreatic effusion. These patients required medical treatment as an initial approach and surgical intervention in the form of decortication, sterilization of the thoracic cavity with 20 % betadine and normal saline in the ratio 1:4, followed by warm normal saline washes and composite mesh placement for PDS followed by endoscopic retrograde cholangiopancreatography (ERCP) as a pancreatic intervention after 3 weeks. Only one patient underwent sphincterotomy, while the other two patients had no abnormality on ERCP. Post-operative follow-ups at 3, 6, and 12 months were uneventful with no recurrence.

Clinical discussion

The mechanism for pancreatic effusion is explained by pancreatic duct disruption followed by enzyme leak leading to pancreatic-pleural communication mediated by PDS. Various studies have described their role in treating PDS, even thoracoscopic pleurodesis requiring prolong chest tube and repeated talc slurry for better outcome. However, to address this, we performed the above procedure as a bridge approach followed by a pancreatic intervention.

Conclusion

Thoracic intervention with composite mesh can serve as a bridge procedure before future pancreatic intervention or surgery.

Highlights

• Porous diaphragm syndrome (PDS) is a diaphragmatic defect secondary to peritoneal cavity disorders.

• The etiology is pancreatic duct disruption leading to pancreatic effusion.

• Pancreatic effusion is mediated through PDS.

• Persistent respiratory symptoms warrant early thoracic intervention.

• Composite mesh placement serves as a bridge approach for future intervention.

Keywords

Porous diaphragm syndrome
Pancreatic effusion
Decortication
Mesh
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pmc1 Introduction

Porous diaphragm syndrome (PDS) is a diaphragmatic defect secondary to peritoneal cavity disorders resulting in pleural effusion (>500 mL) with no evidence of cardiopulmonary disease [1]. Managing refractory pancreatic effusion due to PDS is a challenge. Various surgical interventions such as repairing the defect, sealing with fibrin glue, performing parietal pleurectomy, and talc pleurodesis have been reported however, the use of composite mesh placement in treating PDS has not been described earlier in the literature. In these cases, we present a simple, innovative bridge approach using composite mesh to seal the diaphragmatic defect, followed by pancreatic intervention in patients requiring early thoracic intervention due to persistent respiratory symptoms despite medical treatment and chest tube drainage. The below work has been reported in line with the PROCESS criteria [2].

2 Case series

2.1 Case 1

A 41-year-old male with body mass index (BMI) 17.5 kg/m2 and alcohol consumption of 180 mL/day for 20 years presented with complaints of pain abdomen, fever, vomiting, and associated dyspnea for one week. On examination pulse (P) was- 92/min, blood pressure (BP)-110/70 mmHg, temperature (T)- 1010 F, respiratory rate- 24/min and oxygen saturation (SpO2)- 96 % with 3 L oxygen. He appeared pale, lethargic with haemoglobin (Hb)- 9.8 g/dl, total count (TC) 16,000 cells/mm3, C-reactive protein 48.3, serum albumin 1.6 g/dl with mildly deranged liver function tests (LFT), electrolytes and kidney function tests (KFT) while, serum amylase and lipase were 5445 U/L and 6250 U/L respectively. He was negative for viral markers. Chest examination revealed decrease air entry on the right hemithorax, while abdomen examination had tenderness with sluggish bowel sound. Chest x-ray posterior-anterior (PA) view showed a massive right pleural effusion (Fig. 1A) requiring intercostal tube drainage (ICD) and contrast-enhanced computed tomography (CECT) thorax and abdomen revealed acute pancreatitis with pancreatic pseudocyst (<6 mm thickness), pancreatic-pleural communication and right-hydropneumothorax (Fig. 1B-C). He received intravenous (IV) 4.5 g of Piperacillin and Tazobactam combination thrice daily (TDS) with IV Pantoprazole 40 mg once daily (OD), parental nutrition, octreotide infusion and non-opioid analgesics IV with adequate hydration for 14 days and followed by thoracic intervention (described under surgical technique), (Fig. 1D-E). The postoperative course was uneventful, with drains removed on days 6 and 8, and discharge on day 9 with well expanded lung at discharge and 6 months follow-up (Fig. 1F). The pancreatic duct appeared dilated with diffuse irregularity on endoscopic retrograde cholangiopancreatography (ERCP). He underwent sphincterotomy however, stent placement was unsuccessful. Follow-up visits were uneventful with no recurrence.Fig. 1 A: Chest x-ray showing opacity in the right lung, indicating a large effusion. B: Contrast-enhanced computed tomography (CECT) of the chest and abdomen showing acute pancreatitis with a pancreatic pseudocyst (thickness < 6 mm), pancreatic-pleural communication, and a right-sided hydropneumothorax. C: Intraoperative image of the diaphragmatic surface after extensive decortication with an extensively diseased pulmonary parenchyma. D: Intraoperative image showing composite mesh secured over the diaphragmatic surface. E: Follow-up chest X-ray at 6 months follow-up.

Fig. 1

2.2 Case 2

A 22-year-old male with a BMI-18.9 kg/m2 and a history of alcohol consumption of 400 mL/day for three years presented with chest pain, cough, and dyspnea for two weeks. On examination, P-112/min, BP-110/65 mmHg, T-97.60 F, RR-22/min and SpO2–97 % on room air. Chest examination revealed reduced air entry in the right hemithorax. His blood counts were 10,300 cells/mm3, Hb-10.2 g/dl, serum albumin 1.5 g/dl, and serum potassium 2.4 mmol/l with mildly deranged LFT and KFT, positive serology for hepatitis B only while serum amylase and lipase were 8992 U/L and 5225 U/L respectively. The chest x-ray showed right hemithorax opacity, while an ultrasound-guided aspiration revealed pleural pus which on culture further detected pseudomonas-aeruginosa, requiring ICD insertion and IV Piperacillin- Tazobactam combination 4.5 g TDS and Clindamycin 300 mg twice daily (BD) for 14 days and 100 mL human albumin infusion (20 %-25 mL/h OD) and potassium-chloride solution 2.5 mL BD (five days) for low albumin and potassium levels. His CECT thorax and abdomen revealed acute necrotizing pancreatitis, splenic vein thrombosis, pancreatic-pleural communication, and empyema (Fig. 2A-B). He underwent thoracic intervention (described under surgical technique), (Fig. 2C) with an uneventful recovery except for a small pneumothorax improved on day 3 followed by chest drain removal on day 8 (Fig. 2D). ERCP detected no abnormality with no recurrence on follow-up visits.Fig. 2 A: CECT mediastinal window showing a loculated collection with diseased lung parenchyma. B: CECT of the chest and abdomen showing acute necrotizing pancreatitis, splenic vein thrombosis, and pancreatic-pleural communication. C: Intraoperative image of trapped diseased lung with pleural thickening. D: Early postoperative chest X-ray showing right pneumothorax, which improved by day 3.

Fig. 2

2.3 Case 3

A 34-year-old male with a BMI of 20.5 kg/m2 and chronic alcoholic pancreatitis presented with left-sided chest and abdomen pain for one month. On examination, P-92/min, BP-110/70 mmHg, T-99.40 F, RR-22/min, and SpO2–97 % on room air. Further clinical examination revealed reduced air entry in the left hemithorax and a tender abdomen with sluggish bowel sounds. His blood counts were 17,200 cells/mm3, Hb-11.1 g/dl, and C-reactive protein-63.1. His RFT and electrolytes were normal with mildly deranged LFT with serum albumin 2.6 g/dl while, serum amylase and lipase were 6434 U/L and 4991 U/L respectively. He was negative for viral markers. Chest x-ray showed left oblique homogenous opacity while, CECT thorax and abdomen revealed left lower lobe consolidation with pleural thickening and bulky heterogenous distal-body and pancreatic-tail with peripancreatic lymphadenitis and collection suggestive of acute necrotizing pancreatitis (Fig. 3A-B) requiring medical treatment as case 1 followed by a thoracic intervention (described under surgical technique), (Fig. 3C). The postoperative course was uneventful (Fig. 3D) with the chest tube removed on day 18 for persistent air leak and discharge on day 20. ERCP detected no abnormality with no recurrence on follow-up visits.Fig. 3 A: CECT lung window showing lung consolidation with pleural thickening and mediastinal shift to the left due to fibrosis. B: CECT of the chest and abdomen showing left lower lobe consolidation with pleural thickening, and bulky, heterogeneous distal-body and pancreatic-tail with peripancreatic lymphadenitis and collection - acute necrotizing pancreatitis. C: Intraoperative image showing clear demarcation between the diaphragmatic pleura (held with forceps) and diaphragm with diseased lung. D: Chest X-ray in the late postoperative period showing a well-expanded lung. E: Schematic representation of placing a composite mesh over the diaphragm and securing it with prolene 3–0 using seven knots.

Fig. 3

2.4 Perioperative procedure and surgical technique

All three patients under single lung ventilation underwent posterolateral thoracotomy, decortication, and sterilization of the thoracic cavity with 20 % betadine solution and warm normal saline (0.9 %) mixed in a ratio 1:4 followed by several warm saline (0.9 %) washes. Diaphragmatic examination with high definition thoracoscopic camera not detecting any pores or fistula were classified as grade 1 PDS (Huang and Associates classification) [1]. The composite mesh was shaped as required to fit and placed over the diaphragmatic surface and secured with prolene 3–0 interrupted sutures (Fig. 3E) as a thoracic intervention. Drains, anterior and posterior were placed and connected to a negative suction device (low pressure -1 kPa). All patients underwent endoscopic retrograde cholangiopancreatography (ERCP) after 3 weeks for pancreatic pathology. Patients were followed up at the third, sixth, nine, and twelve months.

3 Discussion

Managing persistent pancreatic effusion with PDS and respiratory issues in debilitated patients poses a clinical challenge. Medical management is mainly targeted at restricting sodium, aggressive use of diuretics, octreotide, and pancreatic enzymes, and eliminating non-steroidal anti-inflammatory medications [3]. Interventional procedures ERCP and stenting for pancreatic duct disruption are favorable. However, severe thoracic disease defers these interventions, making the bridge procedure necessary to preclude the disease process.

The mechanism for pancreatic effusion is explained by pancreatic injury causing pancreatic duct disruption followed by pancreatic enzyme leak leading to pancreatic-pleural communication mediated by trans-diaphragmatic lymphatic blockage, pancreatic-pleural fistula or diaphragmatic defects in the form of pores or fenestration secondary to collagen bundle disruption, further exudating enzymes into the pleural cavity, damaging pulmonary vasculature [3,4]. With no consensus on treatment of choice, ERCP remains the first choice but, ongoing sympathetic pleural effusion leading to empyema, and recurrent respiratory infection, warrants early thoracic intervention [5].

In the study by Mouroux and colleagues for hepatic hydrothorax, diaphragmatic defects were either sewn or sealed with fibrin glue and talc [6]. Similarly, Ferrante, and colleagues, performed talc pleurodesis using video-assisted thoracoscopic surgery (VATS) with an efficacy of 73 % [1]. Later, Cerfolio et al. reported a success rate of 68 % with VATS and talc pleurodesis, which improved to 85 % with repeated talc slurry [1]. The reported side effects were pain and fever due to talc [1]. However, prolonged chest tube placement was necessary for repeated talc slurry and, if talc failed, recurrence was a consequence.

To address this, we decorticated the lung well, sterilized the thoracic cavity with 20 % betadine-warm normal saline (1:4) followed by warm normal saline washes, and placed a composite mesh (Ethicon, Johnson and Johnson, USA) over the diaphragmatic surface to seal the defect as a bridge procedure followed by a pancreatic intervention. As a result, recurrent effusion, its sequelae, and disease progression ceased resulting in the alleviation of respiratory complications with no recurrence at 12 months follow-up. Given poor body mass index, suboptimal pulmonary reserve, late presentation, chronic disease, avoiding prolonged intubation and long operative hours, an open approach was preferred.

Though composite meshes have been deployed for diaphragmatic defects, their role in treating PDS is anecdotal [7]. Their unique properties supporting fibroblast formation, promoting microporous adhesions, providing strong fixation, and maintaining diaphragmatic stability to the thinned diseased diaphragm after decortication have been crucial in the presence of persistent active pancreatic disease and microscopic pancreatic-pleural communication that seem to be the source of recurrence [7,8]. Utilizing these meshes is essential in preventing recurrence, particularly in cases like type 1 PDS.

4 Conclusion

Thoracic intervention with composite mesh can serve as a bridge procedure before future pancreatic intervention or surgery.

Consent

Written informed consent was obtained from the patient for publication and any accompanying images. A copy of the written consent is available for review by the Editor-in-chief of this journal on request.

Ethical approval

As per institutional policy, the ethical approval for case series is not mandatory as ethical principles are not violated and issues such as anonymity of the patient is maintained.

Funding

NA.

Author contribution

Conceptualization: KD.

Data curation: KD, CKD.

Writing original draft: KD.

Writing- review: KD, CKD,

Final approval by both the authors.

Guarantor

Guarantor is the corresponding author: Dr. Klein Dantis.

Research registration number

N/A.

Conflict of interest statement

NA.

☆ Scientific meeting presentation: Presented at European Society of Thoracic Surgery meeting, Milano, Italy (June 4-June 6), 2023 as a poster presentation.
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References

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