There are various causes of dysfunction of the diaphragm.1 Diaphragm dysfunction can be caused by surgical injury or infection, but an indirect procedural injury such as tension pneumoperitoneum is rare as a cause of diaphragm dysfunction. Here, we report a case in which a gastrointestinal endoscopic procedure caused an excessive pneumoperitoneum (tension pneumoperitoneum) that resulted in bilateral diaphragm dysfunction.
Written consent for this case report was obtained from the patient.
A 65-year-old woman (height, 158 cm; weight, 65 kg; body mass index [BMI], 26 kg/m2) who had no medical history presented at a clinic complaining of abdominal pain. Gastrointestinal endoscopy was performed under light sedation. She became pale and unresponsive during the examination 2 hours before she came to our institution. Noninvasive blood pressure could not be measured and respiratory arrest occurred. Tracheal intubation was immediately performed. Fluid resuscitation was commenced, and drainage to the abdomen by a 18 G needle was also performed. A computed tomography (CT) scan was then performed. An extraordinary amount of free air was still seen in the abdominal space with the air occupying more than half of the intraperitoneal space, and the excessive abdominal pressure had compressed and flattened the descending aorta (Figure 1).
Gastrointestinal perforation was suspected; she was taken to our hospital for urgent laparotomy.
When she arrived at our hospital, laboratory examination showed severe lactic acidosis (pH 7.079; base excess [BE], −16.7 mEq/L; HCO3, 12.0 mEq/L; lactate, 14.05 mEq/L) and profound anemia (hemoglobin, 5.9 g/dL; hematocrit, 20.3%). In the emergency department, her blood pressure was 105/60 mm Hg and heart rate was 110 beats per minute. Mechanical ventilation was initiated. We did not measure intraabdominal pressure, but her abdomen was severely distended. High abdominal pressure might have continued for about 3 hours. The patient was assessed as American Society of Anesthesiologists physical status IV E. She was immediately taken to the operating theater for laparotomy.
General anesthesia without an epidural was induced with propofol, rocuronium, and fentanyl. Sevoflurane was administered intraoperatively. The surgeons made a diagnosis of gastric perforation during the operation. Although the direct cause of the pneumoperitoneum was unclear, there was the possibility of direct endoscopic injury to the gastric wall or spontaneous perforation of the gastric wall that had been damaged by an ulcer due to endoscopic insufflation into the gastrointestinal tract. Distal gastrectomy and reconstruction of the tract by the Roux-en-Y method were performed. During surgery, packed red blood cells and crystalloids were administered and appropriate mechanical ventilation was applied (inspiratory pressure, 13 mm Hg; positive end-expiratory pressure, 7 mm Hg; fraction of inspired oxygen [Fio2], 0.6; respiratory rate, 12/min). At the end of the operation, metabolic acidosis was dramatically improved (pH 7.342; BE, −5.1; lactate, 3.9 mEq/L). She was transferred to the intensive care unit (ICU) with her trachea remaining intubated.
Mechanical ventilation was applied with pressure-controlled ventilation (inspiratory pressure, 12 mm Hg; positive end-expiratory pressure, 5 mm Hg; Fio2, 0.4; respiratory rate, 12/min) at the time of admission to the ICU. In the process of weaning from mechanical ventilation, respiratory rate gradually increased. Eight hours later, respiratory rate was more than 30/min in continuous positive airway pressure mode with pressure support of 6 cm H2O (Fio2, 0.4; positive end-expiratory pressure, 5 cm H2O). Although the patient had tachypnea, oxygenation was satisfactory (Pao2, 94.3 mm Hg; Paco2, 34.6 mm Hg), tidal volume was sufficient (TV, 400 mL), and her consciousness was clear under light sedation with propofol. Tracheal extubation was successfully performed. After extubation, a paradoxical breathing pattern appeared in addition to tachypnea (respiratory rate, >30/min). Oxygenation worsened and she complained of dyspnea with 3 L/min oxygen through a facemask (Pao2, 54.7 mm Hg; Paco2, 49 mm Hg). We administered oxygen via a nasal high-flow cannula (40 L/min; Fio2, 0.6). Oxygenation immediately improved (Pao2, 85 mm Hg; Paco2, 45 mm Hg; respiratory rate, 23/min; Spo2, 98%) and her symptoms improved.
Because the patient had tachypnea and paradoxical breathing, we suspected that there was a problem in the diaphragm. A chest X-ray taken immediately after extubation showed that the bilateral diaphragm was slightly elevated (Figure 2). In ultrasonography, the thickness ratio (diaphragm thickness of maximal inspiration/that of end-expiration) of the patient was 1. There was no obvious diaphragmatic movement on the right side and right diaphragmatic thickness did not change during the respiratory phase (Figure 3). Observations in the left diaphragm were similar. We made a diagnosis of dysfunction of the bilateral diaphragm. Her symptoms, oxygen saturation, and respiratory rate gradually improved on a day-by-day basis (respiratory rates were 18/min 2 days later and 16/min 3 days later). Three days later, nasal high-flow cannula therapy was discontinued, and she was discharged from the ICU to a general ward on postoperative day 3. On postoperative day 4, oxygen therapy was also discontinued. Ten days later, another ultrasound examination of the chest showed normal diaphragmatic movement (the thickness ratio was 1.5; Figure 4). Two weeks after surgery, she was discharged from the hospital without any further complications.
We presented a case of bilateral diaphragm dysfunction diagnosed by ultrasonography after urgent laparotomy. Tension pneumoperitoneum was considered as the cause. There was a case report showing that circulatory failure was caused by an excessive pneumoperitoneum when colonoscopy was performed.2 However, there was no problem with diaphragm function in that case.
Dysfunction of the diaphragm can be diagnosed by chest radiographs, pulmonary function test, fluoroscopy, sniff nasal inspiratory pressure, and electromyography.1 Recently, several studies have shown the usefulness of ultrasonography for diagnosis.3,4 Diaphragmatic movement is assessed by M-mode ultrasonography, and diaphragmatic thickness is assessed by B-mode ultrasonography. M-mode is technically more difficult than B-mode, particularly in patients who are obese. However, it is easy to diagnose a paradoxical breathing pattern. Although the patient’s BMI was 26 kg/m2, she was obese compared with the average BMI in Japanese women. The diaphragm thickness ratio is defined as the diaphragm thickness of maximal inspiration/that of end-expiration. A normal diaphragm thickness ratio is considered to be >1.2. The thickness ratio in our patient was 1 immediately after extubation on B-mode. However, 10 days after surgery, the ratio had improved to 1.5. Diagnosis of diaphragmatic dysfunction was easily made by ultrasonography in our case.
Previous reports have shown various causes of dysfunction of the diaphragm.5–8 Causes of diaphragm dysfunction include cervical spine damage, cardiovascular surgery, infection, neuromuscular disease, and injury. Although the course of diaphragmatic dysfunction varies depending on the underlying disease, about two-thirds of patients show improvement in diaphragmatic paralysis caused by an injury or infection.1 Our case might have been caused by excessive abdominal pressure that resulted in hyperextension of the diaphragm or phrenic nerve damage. It has been reported that patients who underwent laparoscopic cholecystectomy showed decreased diaphragmatic function.9 Although the mechanism of postoperative inhibition of diaphragmatic function is unclear, an animal study showed that local trauma in the abdomen is associated with inhibition of phrenic nerve output.10 The diaphragmatic dysfunction in our case might have been caused by a phrenic nerve disorder. Given the fact that diaphragm dysfunction completely recovered within 2 weeks, phrenic nerve injury caused by local trauma or excess intraperitoneal pressure might have been the main reason for the respiratory problem in our patient. However, another report showed that patients who underwent laparoscopic hernia repair had no reduction in diaphragmatic activity.11 It is uncertain whether the site of surgery (upper abdomen or lower abdomen) is a reason for the difference in the incidence of local phrenic nerve injury. Furthermore, it is difficult to determine whether the surgery performed in our case was a cause of the bilateral phrenic nerve injury. There was no sign of infection in our patient, and she had no history of cervical spine disease or neuromuscular disease.
We suspected dysfunction of the diaphragm based on her symptoms. Generally, when the diaphragm is paralyzed on both sides, patients have tachypnea and paradoxical breathing.1 Of course, postoperative respiratory muscle obstacle caused by residual neuromuscular blocking agents should be considered. When our patient complained of dyspnea, we monitored her by acceleromyography (TOF-Watch SX; MSD, the Netherlands). Because her TOF ratio was over 100%, there was no problem with neuromuscular blocking agents.
In conclusion, we experienced a case of dysfunction of the diaphragm caused by tension pneumoperitoneum. Diagnosis was made by ultrasonographic examination. We should keep in mind that diaphragm dysfunction after excessive abdominal extension can be a cause of respiratory failure. Because ultrasonography is noninvasive, it is recommended for diaphragm examination in patients with respiratory failure.
Name: Keita Hazama, MD.
Contribution: This author helped manage the case and write the manuscript.
Name: Yuichiro Toda, MD, PhD.
Contribution: This author helped review and complete the manuscript.
Name: Hideki Nakatsuka, MD, PhD.
Contribution: This author helped review the manuscript.
Name: Yoshihisa Fujita, MD, PhD.
Contribution: This author helped review the manuscript.
This manuscript was handled by: BobbieJean Sweitzer, MD, FACP.
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