Symptomatic hemidiaphragm paralysis after uncomplicated laparoscopic cholecystectomy
Authors: Parker Robert J , Wathen Christopher G 
Published: May 2014

A 55-year-old man was referred to the outpatients clinic for investigation of unexplained exertional dyspnoea. The condition had progressed over 3 months and resulted in a markedly reduced exercise capacity. Before admission the patient reported to be fit and well with no significant medical history. He took no medications and was a non-smoker. Five months previously he had undergone an uncomplicated laparoscopic cholecystectomy. His preoperative chest radiograph was normal (Figure 1). In the months that followed he had multiple episodes of transient breathlessness and was investigated by his surgical team. No pulmonary embolus was seen on computed tomography pulmonary angiography and the mediastinum was normal. Ultrasound and computed tomography imaging of the upper abdomen did not demonstrate a subphrenic collection. Routine blood tests and electrocardiogram were also normal. His breathlessness continued and he was started empirically on warfarin therapy and referred for respiratory opinion. In clinic he was comfortable at rest with a normal temperature, heart and respiratory rate and an oxygen saturation of 97% breathing room air. Cardiovascular and abdominal examinations were unremarkable. The respiratory system revealed decreased breath sounds on auscultation and dullness to percussion at the right base posteriorly. An arterial blood gas breathing room air had normal range partial pressures of oxygen and carbon dioxide and the A-a gradient was 2.3 kPa. A repeat radiograph (Figure 2) showed a grossly elevated right hemidiaphragm when compared to Figure 1. Pulmonary function tests showed a forced expiratory volume in 1 second =1.81 (55% predicted), standing vital capacity (VC) =2.31 (56% predicted), lying VC 1.71 (a fall of 26% compared to the standing VC), total lung capacity =4.71 (70% predicted), residual volume =2.31 (101% predicted), the transfer factor for carbon monoxide was 73% predicted which corrected to 125% when alveolar volume was allowed for. Maximal inspiratory pressure was reduced at 54 cmH2O (normal >80). A diagnosis of hemidiaphragm paralysis resulting in exertional dyspnoea was made. Unilateral diaphragm paralysis was confirmed by twitch transdiaphragmatic pressure measurement, right =0 cmH2O and left =7.3 cmH2O (normal >7 cmH2O). Further questioning did not elicit a history of orthopnoea although the patient was breathless on bending over. Sleep was undisturbed without the daytime symptoms of nocturnal hypoventilation. There was no evidence of paradoxical abdominal movement on inspiration. He had not suffered neck, arm or shoulder pain, or trauma. Neurological examination of the upper limbs was normal. After discussion with the surgical consultant who performed the laparoscopic procedure, injury during surgery to the diaphragm or the phrenic nerve supplying it was ruled out. The patient had no evidence of intra-abdominal post surgical complications. His anaesthetic and postoperative recovery were uncomplicated, no central venous catheter was inserted and his electrolytes were always appropriate. The above are all recognized as causes of diaphragm or phrenic nerve injury, none of them were thought to be causative for this patient. When seen in the clinic 1 year later he was less limited by exertional dyspnoea. The standing VC had risen to 2.91 indicating partial recovery of inspiratory muscle strength. Given the absence of an alternative cause and evidence of spirometric resolution with time, the diaphragm paralysis was felt to be caused by neuralgic amyotrophy preferentially affecting the phrenic nerve triggered by recent laparoscopic surgery.