Diaphragm Dysfunction in Critical Illness

Abstract

The diaphragm is the major muscle of inspiration, and its function is critical for optimal respiration. Diaphragmatic failure has long been recognized as a major contributor to death in a variety of systemic neuromuscular disorders. More recently, it is increasingly apparent that diaphragm dysfunction is present in a high percentage of critically ill patients and is associated with increased morbidity and mortality. In these patients, diaphragm weakness is thought to develop from disuse secondary to ventilator-induced diaphragm inactivity and as a consequence of the effects of systemic inflammation, including sepsis. This form of critical illness-acquired diaphragm dysfunction impairs the ability of the respiratory pump to compensate for an increased respiratory workload due to lung injury and fluid overload, leading to sustained respiratory failure and death. This review examines the presentation, causes, consequences, diagnosis, and treatment of disorders that result in acquired diaphragm dysfunction during critical illness.

Keywords: ICU acquired weakness; diaphragm weakness; mechanical ventilation; ultrasound.

Figure 1

Effect of mechanical ventilation on the diaphragm. A, In vitro force- frequency relationships in diaphragms from rats undergoing mechanical ventilation (MV). As shown, MV induced significant (P < .05) and progressive reductions in the diaphragm specific force-generating capacity (force/cross-sectional area) when compared with control animals. B, Comparison of a representative diaphragm biopsy specimen from a mechanically ventilated brain-dead organ donor (case subject) and a control patient undergoing surgery and mechanical ventilation for 2 to 3 hours. As shown, diaphragm fiber size was reduced in the case subject, affecting both slow and fast twitch fibers, indicating that prolonged controlled mechanical ventilation induces diaphragm fiber atrophy in humans.

Figure 2

Effect of infection on diaphragm function. A, In vitro force- frequency relationships for control and septic mice. Sepsis was induced with cecal ligation puncture; control mice were animals who were operated on and underwent the same protocol without ligating the cecum or performing puncture and evaluated 24 hours later. As shown, sepsis induced marked reductions in the diaphragm specific force generation (force per cross-sectional area) (P < .001 for all comparisons). B, Transdiaphragmatic twitch pressure (PdiTw) measurements in 57 critically ill mechanically ventilated patients. Patients were classified as uninfected or infected on the basis of whether they were actively receiving treatment for an infection. Data from individual patients are shown for each group on the right, whereas plots on the left for each group show mean (filled squares), median levels (middle line of box), 25% and 75% confidence intervals (upper and lower borders of the box), and 1% and 99% intervals (whiskers above and below the box). Infection was associated with significant lower PdiTw values; *, statistical significance).

Figure 3

Diaphragm excursion. A, Appropriate probe position for B- and M-mode diaphragmatic excursion measurements using a 1- to 5-MHz probe. B, Path of the ultrasound beam as it travels to image the diaphragm. C, B-mode diaphragm ultrasonography; the bright line reflects the diaphragm using the anterior subcostal approach. D, M-mode tracing showing the amplitude of excursion during deep breathing. The arrows indicate the beginning and end of diaphragmatic contraction, and the distance between the arrows indicate diaphragm displacement (excursion).

Figure 4

Diaphragm paralysis. A, Paralysis in the right hemidiaphragm of a 15-year-old boy. As indicated, the M-mode tracing shows no diaphragmatic motion. B, M-mode tracing in another patient with right hemidiaphragm paralysis. Note that there is paradoxical (upward) diaphragm motion during inspiration (arrow).

Figure 5

Diaphragm thickening. A, Probe position for B- and M-mode diaphragmatic thickness measurements in the zone of apposition using a 6- to13-MHz probe. B, Position of transducer at the zone of apposition and the path of the ultrasound beam. C, B-mode ultrasonography of the diaphragm in the zone of apposition, the diaphragm is visualized as a three-layered structure composed of two parallel echogenic layers of diaphragmatic pleura and peritoneal membranes sandwiching a nonechogenic layer of diaphragm muscle. Lung artifact is seen on the left side of the image. D, M-mode tracing, where 1 is the thickness at end expiration (1.6 mm) and 2 is the thickness at end inspiration (2.2 mm).