Journal Pre-proof Hepatic Compartment Syndrome Following a Right-Sided Diaphragm Plication Christopher P. Foran, MD, Yuri Genyk, MD, Suzanne Palmer, MD, Anthony W. Kim, MD PII:
S0003-4975(19)31563-2
DOI:
https://doi.org/10.1016/j.athoracsur.2019.09.013
Reference:
ATS 33141
To appear in:
The Annals of Thoracic Surgery
Received Date: 19 May 2019 Revised Date:
22 August 2019
Accepted Date: 14 September 2019
Please cite this article as: Foran CP, Genyk Y, Palmer S, Kim AW, Hepatic Compartment Syndrome Following a Right-Sided Diaphragm Plication, The Annals of Thoracic Surgery (2019), doi: https:// doi.org/10.1016/j.athoracsur.2019.09.013. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 by The Society of Thoracic Surgeons
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Hepatic Compartment Syndrome Following a Right-Sided Diaphragm Plication Running Head: Hepatic Compartment Syndrome Christopher P. Foran, MDa; Yuri Genyk, MDb; Suzanne Palmer, MDc; Anthony W. Kim, MD a,d a
Department of Surgery, Keck School of Medicine, The University of Southern California, Los Angeles, CA b Department of Hepatobiliary Surgery, Keck School of Medicine, The University of Southern California, Los Angeles, CA c Department of Radiology, Keck School of Medicine, The University of Southern California, Los Angeles, CA d Division of Thoracic Surgery, Keck School of Medicine, The University of Southern California, Los Angeles, CA Corresponding Author: Anthony W. Kim, MD Chief & Professor of Clinical Surgery Keck School of Medicine, USC Division of Thoracic Surgery 1510 San Pablo St., Suite 514 Los Angeles, CA 90033
[email protected]
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Abstract We present a case of acute hepatic failure due to hepatic vein outflow obstruction after a unilateral right diaphragm plication requiring reoperation. This complication does not appear to have been reported previously. After reoperation and the removal of several plication sutures, hepatic vein outflow was restored, and hepatic function normalized soon thereafter.
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Diaphragm plication has demonstrated efficacy for unilateral diaphragm paralysis (1,2). We present a unique case of “hepatic compartment syndrome” after an open right-sided, unilateral diaphragm plication resulting in acute hepatic failure due to hepatic vein outflow obstruction and requiring reoperation.
The patient is a 71-year-old male who 30 months earlier underwent an exploratory laparotomy, colectomy, and right-sided rib plating following a motor vehicle collision. He underwent another exploratory laparotomy and ileocolonic anastomosis revision to address enterocutaneous fistulae 6 months following the original trauma laparotomy. During this operation, he was noted to have significant adhesions within his abdomen. His previous medical and surgical history also included hypertension, stage III chronic kidney disease, frequent alcohol consumption, and a cholecystectomy. He presented with progressive shortness of breath affecting his quality of life. Based on his history and the accompanying preoperative chest radiograph (Figure 1a), he was suspected of having a traumatic diaphragm paralysis which was confirmed by a sniff test Preoperative computerized tomography (CT) of the chest demonstrated an elevated right hemidiaphragm. His Forced Expiratory Volume in One Second (FEV1) and Diffusion Capacity of Carbon Monoxide (DLCO) were 35% predicted and 64% predicted, respectively. A perfusion study revealed a 62% and 38% distribution of blood flow to the right and left sides, respectively. A preoperative liver function panel was within normal limits Due to concerns that his paralyzed hemidiaphragm was causing his respiratory issues, he underwent an open right-sided diaphragm plication via right thoracotomy. Upon entry into the chest via the eighth intercostal space an extensive pneumolysis was required to mobilize the right
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lung and expose the eventrated and redundant right diaphragm. During the index operation, a plication was performed using multiple pledgeted 0-Ethibond sutures in an interrupted, horizontal mattress fashion placed radially starting medially and extending laterally. Additional sutures were places between the sutures in our initial layer to further reduce the redundancy and laxity of the diaphragm. . In the same anesthetic setting, an abdominal incisional hernia from his prior surgeries was also repaired during this case, by a different surgical team and the total intraoperative time was approximately 3 hours. His postoperative chest radiograph demonstrated a satisfactory result (Figure 1b). Following an uneventful extubation in the operating room, he was reintubated for respiratory failure in the intensive care unit with a postintubation arterial blood gas revealing a metabolic acidosis: pH 7.23 [range: 7.35-7.45], Bicarbonate 12 [range: 22-27 mmol/liter], pO2 265 [range: 69-110 mmHg], and a lactate 6.2 [range: 0.5-2.2 mmol/liter]. A postoperative liver function panel revealed aspartate aminotransferase (AST)/alanine aminotransferase (ALT) values of 1,046/755 [range: 0-40/0-41 units/liter]. A repeat liver function panel sent 6 hours later demonstrated elevated AST/ALT levels of 1,462/1,236 units/liter. His lactate level continued to increase to 8.6 mmol/liter prompting a liver ultrasound that demonstrated patent, but decreased flow in the main portal vein (Figure 2a) and elevated velocities in the right hepatic vein with decreased pulsatility (Figure 2b). A CT scan of the abdomen and pelvis with IV contrast demonstrated hypoattenuation throughout the right hepatic lobe with attenuation of the inferior vena cava and all three hepatic veins consistent with hepatic necrosis secondary to compression (Figure 3). A subsequent liver function panel demonstrated worsening AST/ALT levels to 5,581/3,347 units/liter.
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Due to concerns of extrinsic compression of the liver from the diaphragm plication causing hepatic outflow obstruction and congestive hepatocellular injury, or, “hepatic compartment syndrome”, he was returned to the operating room within 20 hours. He was reopened and 50% of the sutures from the previous diaphragm plication were removed while real-time intra-operative doppler ultrasound confirmed the restoration of hepatopedal flow in the portal vein, hepatic veins, and inferior vena cava with normal, antegrade flow (Figure 2c). The overall architecture of the plication remained in place with the repair less taut and the compression on the liver relieved. The patient was returned to the intensive care unit whereupon his liver function panel improved immediately postoperatively. A doppler ultrasound of the liver on postoperative day one from the second procedure demonstrated appropriate inflow and outflow to the entire liver. He recovered without further complication and was discharged home with normal hepatic function on postoperative day seven from the second procedure with both his chest radiograph and preoperative shortness of breath returning to their baseline status (Figure 1c).
Comment This report presents a unique case of “hepatic compartment syndrome” following a right-sided diaphragm plication. Diaphragm plication is a safe and effective procedure for adult patients with dyspnea due to unilateral diaphragm paralysis (1,2). A review of the procedure performed by Groth et al (3) listed many possible complications for all approaches, but not compartment syndrome. Morbidity, including persistence of symptoms, is reported in 0-30% of patients, with mortality tending to be due to progression of the pathology causing the diaphragm paralysis rather than the surgical plication (4). A single case of abdominal compartment syndrome (ACS)
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was reported by Phadnis et al (4); however, in that case report, the condition resolved with conservative measures within 24 hours of diagnosis and did not require reoperation. That compartment syndrome occurred due to a decrease in intra-abdominal volume. We theorize that two concurrent conditions led to acute hepatic failure postoperatively secondary to hepatic outflow obstruction. The first issue was a technical error leading to an overly-taut diaphragm plication. The second was an inability for the liver to experience downward shift within the abdominal compartment (as described by Phadnis et al.) due to the extensive abdominal adhesions. This inability for pedal-oriented intra-abdominal shift contributed to the liver parenchymal compression and impaired hepatic outflow. We describe this condition as “hepatic compartment syndrome” rather than ACS because the liver appeared to be the only end-organ which experienced failure postoperatively. The patient continued to produce urine and was hemodynamically stable throughout the initial postoperative period prior to reoperation and there were no signs of ACS. The mechanism of injury, however, was similar to ACS in that compressive forces led to collapse of lower-pressure venous outflow from the liver leading to a reversal of portal in-flow and organ ischemia. In retrospect, there were no clear technical signs that suggested the repair was overly taut. A closer evaluation of changes in the patient’s central venous pressure and brisk elevation in lactate should have signaled that the repair had caused a venous outflow impairment. With this experience, intraoperative, dynamic ultrasound evaluation of the hepatic vasculature will be used to ensure appropriate hepatic inflow and outflow should there be any concerning physiologic changes observed. Though rare, this condition should be considered in future patients who experience acute hepatic failure after right-sided diaphragm plication in the setting of prior abdominal surgery.
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Patients with known abdominal adhesions, or patients with severe laxity of the diaphragm that will require a high suture burden to achieve an efficacious outcome may benefit from intraoperative ultrasound to confirm hepatic venous outflow prior to completing the case.
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References 1. Freeman RK, Van Woerkom J, Vyverberg A, Ascioti AJ. Long-term follow-up of the functional and physiologic results of diaphragm plication in adults with unilateral diaphragm paralysis. Ann Thorac Surg. 2009;88(4):1112.
2. Graham DR, Kaplan D, Evans CC, Hind CR, Donnelly RJ. Diaphragmatic plication for unilateral diaphragmatic paralysis: a 10-year experience. Ann Thorac Surg. 1990;49(2):248.
3. Groth, Shawn S, Andrade, Rafael S. Diaphragm plication for eventration or paralysis: a review of the literature. The annals of thoracic surgery. 89(6):S2146-S2150.
4. Phadnis J, Pilling JE, Evans TW, Goldstraw P. Abdominal compartment syndrome: a rare complication of plication of the diaphragm. Ann Thorac Surg 2006;82:334–6.
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Figure Legends Figure 1. (A) Preoperative chest radiograph demonstrating right hemidiaphragm elevation. (B) Postoperative chest radiograph from the index case demonstrating near resolution of right hemidiaphragm elevation and a clear costophrenic angle. (C) Postoperative chest radiograph from the reoperation demonstrating increased right hemidiaphragm elevation and an obliteration of the costophrenic angle.
Figure 2. (A) Postoperative liver ultrasound from the index case demonstrating decrease velocities in main portal vein. (B) Postoperative liver ultrasound from the index case demonstrating elevated velocities in the right hepatic vein with decreased pulsatility. (C) Realtime intra-operative doppler ultrasound during the reoperation revealing the restoration of antegrade flow in the patent portal vein.
Figure 3. Postoperative from the index case, the multi-phase CT scan of abdomen demonstrating compression and ischemia of the right lobe of the liver.