Very few studies have been done on the quality of life following sepsis. Most patients that survive sepsis remain in the hospital. More than half die within 3 months of developing sepsis. Approximately, 60% experience psychological impairments. A few others experience a life similar to the one they had prior to hospitalization and may return. However, most are discharged to nursing homes or rehabilitation facilities. Mortality following discharge from the hospital is highest for older individuals (older than 55) and those that were hospitalized in the intensive care unit for more than 2 weeks. Many patients that survive sepsis experience a syndrome called post-ICU syndrome. This condition is defined by the presence of insomnia, nightmares, fatigue, depression, loss of cognitive function and low self-esteem. At least three of these symptoms are experienced by nearly half of surviving patients. Other observed cognitive deficits include verbal learning and memory impairments for up to 2 years post-hospital discharge, general brain dysfunction, and post-traumatic stress disorder (PTSD). Survivors of sepsis are 10% more likely to experience cognitive impairment and to experience new impairments than individuals that did not have sepsis.
The etiology of impairments resulting from sepsis, much like the quality of life following sepsis, is unknown. It is thought that the following caused of weakness may contribute:
- Inactivity and immobility during hospitalization
- Corticosteroids used to treat sepsis
- Neuromuscular blockers used to treat sepsis
WHAT EFFECT DOES SEPSIS HAVE ON DIFFERENT ORGAN SYSTEMS?
Sepsis often results in a change in mental status. The change can be so severe that the patient can no longer breathe without assistance and thus endotracheal intubation is needed. To determine if these changes are due to sepsis, healthcare providers must rule out that mental change is due to focal neurological deficits (damage to the nerves, spinal cord or brain), hypoxemia (low level of blood oxygen), hypoglycemia (low blood sugar), drug toxicity or infection of the central nervous system.
Respiratory failure is a primary sign of sepsis and septic shock. It is caused by damage to the alveolar-capillary membranes by inflammatory mediators. The damage causes severe pulmonary edema which causes increased ventilation and tachypnea (unusual, rapid breathing). Tachypnea may occur in combination with hypoxemia or hypercarbia (abnormally high levels of carbon dioxide in the blood). These conditions along with respiratory muscle fatigue may require the need for endotracheal intubation. Other pulmonary responses include an increase of water in the lungs. Left ventricular heart failure should be ruled out as the cause to attribute these symptoms to sepsis.
Another common sign of sepsis, severe sepsis, in particular, is myocardial depression—a decrease in ejection fractions from a heart ventricle. Signs of myocardial depression include hypotension. Myocardial depression affects both ventricles of the heart which is different from other conditions in which myocardial depression is a symptom. Patients with sepsis often have high levels of cardiac troponins or regulatory proteins that regulate heart contraction. Oxidative and nitrosative stress (accumulation of reactive oxygen and nitrogen species (ROS, NOS), respectively) may also contribute to cardiovascular failure. During sepsis, inducible nitric oxide synthase is upregulated. Hypoxia-induced factor-α, HIFα, is also active during sepsis. Both factors promote reactive species and may promote organ failure during sepsis.
Sepsis can also induce renal dysfunction that progresses toward renal failure. Many sepsis-related deaths are due to frank renal failure, a severe form of renal failure. It is not clear how sepsis causes renal failure. In some cases, renal failure induced by sepsis can be prevented by volume resuscitation. However, healthcare providers should be cautious about the fluids used for resuscitation since some commonly used fluids could promote renal failure. The kidneys do not fully recover following sepsis-related renal failure.
Severe sepsis patients often experience disseminated intravascular coagulation (DIC). There are two types: one characterized by bleeding from multiple areas, and one with blood clots in small and medium blood vessels. The type of DIC presented depends on the clotting system dominant during sepsis coagulation or fibrinolytic. Either one can be the dominant system in sepsis. A sign of a dominant fibrinolytic system is bleeding from multiple areas. A sign of dominant coagulation system is discoloration of the fingers and toes that may progress to gangrene in the extremities. Since DIC can also be caused by heparin, this cause should also be ruled out before treating.
Similar to renal dysfunction, hepatic dysfunction is very common in sepsis. However, unlike renal dysfunction, it rarely progresses to liver failure. Signs of liver damage include high levels of serum alanine transaminase and bilirubin. Like with many other organ injuries, the cause of sepsis-induced hepatic dysfunction is unknown. It is postulated to be due to centrilobular necrosis of the liver secondary to poor hepatic perfusion. Cells in the liver undergo both necrotic and apoptotic cell death in individuals with sepsis.