Ann Thorac Surg 2006;82:334-336
© 2006 The Society of Thoracic Surgeons
Case report
Abdominal Compartment Syndrome: A Rare Complication of Plication of the Diaphragm
Joideep Phadnis, MD
a
,
John E. Pilling, MD
a
,
Timothy W. Evans, MD, PhD
b
,
Peter Goldstraw, MD
a
,
*
a Department of Thoracic Surgery, Royal Brompton Hospital, London, United Kingdom
b Department of Intensive Care, Royal Brompton Hospital, London, United Kingdom
Accepted for publication August 22, 2005.
* Address correspondence to Prof Goldstraw, Department of Thoracic Surgery, Royal Brompton Hospital, Sydney Street, London, SW3 6NP United Kingdom (Email: p.goldstraw{at}rbh.nthames.nhs.uk).
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Abstract
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Abdominal compartment syndrome is an increasingly recognized phenomenon. We report the case of an otherwise fit and healthy 42-year-old man who underwent plication of the right hemidiaphragm for idiopathic phrenic paresis. His postoperative recovery was complicated by abdominal compartment syndrome, which was managed conservatively. We believe this is the only report of this complication after diaphragmatic plication and one of very few reported thoracic causes of abdominal compartment syndrome.
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Introduction
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Plication of the hemidiaphragm for nonmalignant unilateral phrenic paresis has been shown to provide sustained relief of symptoms with objective improvement in lung function and hypoxemia [1]. Complications, including pneumonia and persistence of dyspnea, are unusual in published series [1–5]. We report a case in which plication of the hemidiaphragm resulted in the development of a transient abdominal compartment syndrome (ACS).
A 42-year-old man presented with a 2-year history of sudden onset dyspnea after an influenza-like illness. He was otherwise fit and healthy and a lifetime nonsmoker. His symptoms were persistent and forced him to adopt a sedentary lifestyle with associated weight gain. Chest roentgenogram demonstrated significant elevation of the right hemidiaphragm (Fig 1A). Computed tomography confirmed this elevation; the thorax was otherwise normal. Spirometry illustrated positional variation in pulmonary function. Forced vital capacity fell from 3.33 L to 2.55 L with a change from upright to supine position, respectively, and forced expiratory volume in 1 second fell from 2.76 L (70% predicted) to 1.97 L. Arterial oxygen tension was 9.05 kPa on air. Nerve conduction studies revealed right phrenic nerve paresis of unknown cause. It was postulated that the patient had suffered a viral mononeuritis.
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Fig 1. (A) Preoperative erect chest roentgenogram showing raised right hemidiaphragm. (B) Postoperative erect chest roentgenogram showing successful plication of the right hemidiaphragm.
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After explanation of the risks and benefits, the patient requested surgical intervention. Right lateral thoracotomy was performed by entering the chest through the eighth intercostal space. Although macroscopically normal, the phrenic nerve did not respond to either mechanical or electrical stimulation. Plication was undertaken by imbrication with several successive rows of continuous nonabsorbable sutures radiating from the phrenic nerve insertion to the costal origin of the muscular diaphragm, achieving a tight repair. Postoperative chest roentgenogram showed the right hemidiaphragm in an improved position (Fig 1B).
In the immediate postoperative period the patient developed a tense, distended abdomen and became oliguric. Abdominal ultrasound revealed an empty bladder with a urinary catheter in situ, kidneys of normal size and echogenicity with no hydronephrosis. Despite intravascular fluid replacement to an adequate mean arterial pressure (75 mm Hg) and passage of a nasogastric tube to decompress the stomach, oliguria persisted. Intra-abdominal pressure was measured via a urinary catheter [6] and was shown to be 27 mm Hg, which confirmed ACS. Mean arterial pressure was augmented with noradrenaline, intravascular volume was maintained, and the patient underwent regular aspiration through a nasogastric tube. Despite these factors, his renal function and hepatic transaminases deteriorated (Table 1). During the ensuing 24 hours, his abdominal distension reduced, oliguria resolved, and the inotropic support was weaned. Subsequent intra-abdominal pressure measurements were progressively lower, and renal and hepatic function was normalized with time (Table 1). Release of the plication was thus avoided. Postoperative computed tomographic scan of the abdomen revealed no intra-abdominal complication, an intact plication, and a large quantity of intra-abdominal fat. His postoperative clinic visit 4 weeks after surgery demonstrated symptomatic improvement, and spirometry showed a forced vital capacity of 3.5 L and a forced expiratory volume in 1 second of 3.0 L.
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Comment
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Abdominal compartment syndrome is an increasingly recognized clinical entity [6, 7]. It is defined by an intra-abdominal pressure of greater than 25 mm Hg (or 30 cm H20) with signs of end-organ compromise, confirmed by alleviation of symptoms on abdominal decompression. Abdominal compartment syndrome most commonly occurs after abdomino-pelvic surgery and trauma. More rarely, ACS has been reported in patients with pancreatitis, ascites, or abdominal tumors [7]. The most prevalent non-abdominal predisposing factors are severe burns, non-abdomino-pelvic trauma and prolonged, aggressive resuscitation [6, 7]. A large study based at a level 1 trauma center reported ACS of non-abdomino-pelvic cause in 14 patients during a 66-month period [6].
Abdominal compartment syndrome has also been described in a ventilated patient after caesarean section who suffered multiple pneumothoraxes and consequent pneumoperitoneum. The patient had an intra-abdominal pressure of 31 mm Hg and required a laparotomy. It must be noted that in this case the patient had undergone prior abdomino-pelvic surgery, although the cause of ACS was ascribed to her thoracic condition [8].
Complications of diaphragmatic plication including pneumonia and persistence of symptoms are reported in 0 to 30% of patients [1–5]. Mortality, when reported, tends to be due to progression of the pathology underlying the raised hemidiaphragm, rather than the plication itself and shows a wide variation in a series of between 0 and 50%, depending on patient selection [7]. Abdominal complications have not been reported [1, 2, 4, 5].
The usual treatment of ACS is by decompression of the abdomen, often by laparotomy, in those with moderately elevated intra-abdominal pressure is growing in vogue [6, 7], although conservative treatment is comprised of supportive therapy and abdominal decompression with nasogastric tube and flatus tube. We speculate that our patient had ACS develop as a consequence of downward hepatic shift and reduced intra-abdominal volume. This was inferred by changes in the patient's hepatic transaminases and was manifested by his oliguria and raised intra-abdominal pressure. As far as we are aware, this is the first report of ACS as a complication of diaphragm plication.
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References
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Abstract
Introduction
