ICU-Acquired Hypernatremia Is Associated with Persistent Inflammation, Immunosuppression and Catabolism Syndrome

Rysz

et al. 2021

Endocrine Connections

Acute systemic diseases, such as severe infections, can lead to electrolyte and acid-base alterations. To study the presence of electrolyte imbalance in severe COVID-19, we investigated the frequency and consequences of changes in electrolyte and acid-base patterns over time. We performed a retrospective cohort study including 406 patients with severe COVID-19. Levels of electrolytes, base excess, pH, serum osmolality and hematocrit, the first two weeks of hospitalization, were collected daily from the laboratory database and clinical data from patients’ medical records. We found that hyponatremia was present in 57% of the patients at admission and hypernatremia in 2%. However, within two weeks of hospitalization 42% of the patients developed hypernatremia, more frequently in critically ill patients. Lower levels of sodium and potassium at admission was associated with need of mechanical ventilation. Decreased pH at admission was associated with both death and need of mechanical ventilation. Hypernatremia in the ICU was combined with rising base excess and a higher pH. In the group without intensive care, potassium levels was significantly lower in the patients with severe hypernatremia. Presence of hypernatremia during the first two weeks of hospitalization was associated with 3.942 (95% CI 2.269–6.851) times higher odds of death. In summary, hypernatremia was common and associated with longer hospital stay and a higher risk of death, suggesting that the dynamics of sodium is an important indicator of severity in COVID-19.

Section: Discussionmentioning

confidence: 99%

Electrolyte and acid-base imbalance in severe COVID-19

Rysz

et al. 2021

Endocrine Connections

“…Moreover, apart from sodium, other solutes also need to be excreted. Many critically ill patients exert osmotic diuresis due to a disturbed glucose metabolism, osmotic therapies or increased urea levels caused by (hyper)alimentation and ongoing catabolism [27,28]. The necessity of excreting solutes is the main reason why it is not desirable to omit hypotonic maintenance fluids when other sources of water are absent.…”

Section: Excreting Solutes Is Difficult If Not Enough Free Water Is Providedmentioning

confidence: 99%

Fluid-induced harm in the hospital: look beyond volume and start considering sodium. From physiology towards recommendations for daily practice in hospitalized adults

Regenmortel

Moers

Länger

et al. 2021

Ann. Intensive Care

Purpose Iatrogenic fluid overload is a potential side effect of intravenous fluid therapy in the hospital. Little attention has been paid to sodium administration as a separate cause of harm. With this narrative review, we aim to substantiate the hypothesis that a considerable amount of fluid-induced harm is caused not only by fluid volume, but also by the sodium that is administered to hospitalized patients. Methods We show how a regular dietary sodium intake is easily surpassed by the substantial amounts of sodium that are administered during typical hospital stays. The most significant sodium burdens are caused by isotonic maintenance fluid therapy and by fluid creep, defined as the large volume unintentionally administered to patients in the form of dissolved medication. In a section on physiology, we elaborate on the limited renal handling of an acute sodium load. We demonstrate how the subsequent retention of water is an energy-demanding, catabolic process and how free water is needed to excrete large burdens of sodium. We quantify the effect size of sodium-induced fluid retention and discuss its potential clinical impact. Finally, we propose preventive measures, discuss the benefits and risks of low-sodium maintenance fluid therapy, and explore options for reducing the amount of sodium caused by fluid creep. Conclusion The sodium burdens caused by isotonic maintenance fluids and fluid creep are responsible for an additional and avoidable derailment of fluid balance, with presumed clinical consequences. Moreover, the handling of sodium overload is characterized by increased catabolism. Easy and effective measures for reducing sodium load and fluid retention include choosing a hypotonic rather than isotonic maintenance fluid strategy (or avoiding these fluids when enough free water is provided through other sources) and dissolving as many medications as possible in glucose 5%.

“…Some patients experience chronic inflammation, which is also known as persistent inflammation, immunosuppression, and catabolism syndrome [ 90 ]. This condition may be caused by various conditions including disseminated intravascular coagulopathy [ 91 ] and electrolyte imbalance [ 92 ]. Chronic inflammation is known to cause muscle atrophy [ 93 ].…”

Section: Picsmentioning

confidence: 99%

Urinary Titin N-Fragment as a Biomarker of Muscle Atrophy, Intensive Care Unit-Acquired Weakness, and Possible Application for Post-Intensive Care Syndrome

Nakanishi

Tsutsumi

Hara

et al. 2021

JCM

Titin is a giant protein that functions as a molecular spring in sarcomeres. Titin interconnects the contraction of actin-containing thin filaments and myosin-containing thick filaments. Titin breaks down to form urinary titin N-fragments, which are measurable in urine. Urinary titin N-fragment was originally reported to be a useful biomarker in the diagnosis of muscle dystrophy. Recently, the urinary titin N-fragment has been increasingly gaining attention as a novel biomarker of muscle atrophy and intensive care unit-acquired weakness in critically ill patients, in whom titin loss is a possible pathophysiology. Furthermore, several studies have reported that the urinary titin N-fragment also reflected muscle atrophy and weakness in patients with chronic illnesses. It may be used to predict the risk of post-intensive care syndrome or to monitor patients’ condition after hospital discharge for better nutritional and rehabilitation management. We provide several tips on the use of this promising biomarker in post-intensive care syndrome.