Critical illness

See ICU(Intensive care unit)

Critical care accounts for 20% of US health costs and 1% of the gross national domestic product.

Protein malnutrition surrounding hospitalization associated with increased morbidity and mortality in hospitalized patients.

Protein energy malnutrition associated with hospital acquired infection, impaired wound healing, prolonged recovery in patients admitted to the ICU.

Critical illness malnurition associated with catabolic hormonal and cytokine response.

During critical illness decreased protein synthesis occurs due to immobility and endotoxin exposure.

Critical illness is associated with an early myelopathic process.

Patients with single organ failure have limited muscle wasting, while those with failure of four organs show much more muscle loss.

Protein synthesis is refractory in the early stages of critical illness and increasing protein delivery is associated with increased muscle wasting.

Inflammation reduces protein synthesis and increases breakdown.

In critically ill individuals on IV insulin treatment, blood glucose level should be maintained between 140 and 180 mg/dL.

In hospitalized patients nutritional support increases caloric and protein intake and body weight but has little effect on clinical outcomes. except for nonelective readmissions (Bally MR et al)

Lung derived inflammatory mediators are associated with muscle wasting chronic lung disease.

In critically ill patients cortisol, catecholamines, glucagon levels are increased and interleukin-1, interleukin-6 and interleukin-8 and tumor necrosis factor alpha are increased in tissues.

Often accompanied by increased cortisol levels appropriate to the severity of illness.

Increase cortisol levels has been attributed to stress induced activation of the hypothalamic-pituitary-adrenal (HPA) axis and increased corticotropin driven cortisol production.

However, during acute critical illness there is reduced cortisol breakdown, related to suppressed expression and activity of cortisol metabolizing enzymes which contributes to hypercortosolemia and causes corticotropin suppression (Boonen E et al).

In the above study of 158 patients in an intensive care unit, total and free circulating cortisol levels were consistently higher in patients than in a control group, whereas corticotropin levels were lower.

In the above study there was a reduction of more than 50% in cortisol clearance accounting for an increase by a factor 3.5 in plasma cortisol level in these patients, as compared with controls.

Most critically ill patients have increased mediators of oxidant stress.

The degree of jaundice is correlated with increased mortality in critically ill patients.

Muscle atrophy associated with low hemoglobin concentrations, and metabolic acidemia in acute illness.

In the critically ill there is peripheral tissue resistance to insulin and insulin like growth factor (Burnham).

With critical illness glycogenolysis and gluconeogenesis occur causing a net breakdown of skeletal muscle, enhanced lipolysis, which provide needed glucose, amino acids and fatty acids required for cellular and organ function and wound healing.

Circulating levels of proteins, such as albumin and prealbumin are often decreased because of inflammation, infection and fluid overload.

During critical illness availability of plasma substrates are diminished by the presence of insulin resistance, lipoprotein lipase inhibition and insufficient levels of certain substrates, such as glutamine to meed metabolic needs.

Associated with decreases food intake before admission to intensive care units related to preexisting anorexia, gastrointestinal dysfunction, depression, anxiety and other medical and surgical processes.

Associated with impaired food intake for diagnostic or therapeutic purposes.

Associated with loss of nutrients from diarrhea, vomiting, polyuria, wounds, drainage tubes, and renal replacement therapy.

Ventilation neuromuscular blockade associated with skeletal muscle wasting and inhibited anabolism.

Bed rest and decreased physical activity that occurs with critical illness associated with impaired anabolic activity.

Drugs administered during hospitalization in ICUs may increase skeletal breakdown from corticosteroids, pressor agents may impair splanchnic blood flow and diuretics may increase urinary losses of mineral, vitamins, electrolytes.

Fever, infections operative trauma may increases energy usage, and micronutrient and protein needs.

Most critically ill patients who require specialized nutrition can be fed enterally through a gastric or intestinal feeding tube and transitioned to oral diet, and this accounts for 85-90% of such patients.

Approximately 10-15% of critically ill patients enteral nutrition is contraindicated .

Optimal caloric requirements in critically ill patients are unknown.

The Harris-Benedict equation utilizes age, sex, weight, height to estimate resting energy requirements.

For critically ill patients in the ICU energy goal is equivalent to resting energy expenditure multiplied by 1.0-1.2 (Singer P).

20-25 kcal per kg of body weight is total caloric target range for most adult patients in the ICU.

Controlled studies comparing higher enteral nutritional delivery with usual care in critically ill patients showed no reduction in mortality with the higher enteral nutrition.

Studies augmenting energy intake with parenteral nutrition have resulted in no change in mortality and increased time to discharge from ICUs.

Among critically ill patients receiving parenteral nutrition lower mortality was observed with hypocaloric nutrition than with standard nutritional support.

Randomized trials with patients with acute lung injury or acute respiratory failure evaluated minimal enteral feedings of 15-25% of estimated caloric requirements with no protein supplementation for up to six days and showed outcomes randomized trials with patients with acute lung injury or acute respiratory failure evaluated minimal enteral feedings of 15-25% of estimated caloric requirements with no protein supplementation for up to six days and showed outcomes were similar to standard enteral feedings.

Survivors of critical illness often have reduced physical function, psychological symptoms and impaired quality of life.

An association between critical illness and long-term cognitive impairment exist.

Impairment in executive function and memory are most cognitive factors altered by critical illness.

Critical illness can result in multiple acquired or exacerbated conditions that may persist for years after the critical illness, and may not be wholly reversible.

Survivors of critical illness recently we have come to dysfunction, characterized by new deficits in global cognition or executive function.

The critical illness polyneuropathy is characterized by primary axonal degeneration, without demyelination, that affects motor nerves more than sensory nerves.

The critical illness polyneuropathy predominant spinal cord finding is loss of anterior horn cells due to axonal degeneration.

In the critical illness polyneuropathy, electrophysiology studies shoe nerve conduction velocity is preserved, but there is reduced amplitude in the compound muscle action potentials (CAMPs) and sensory nerve-action potentials.

The critical illness polyneuropathy affects extremities, particularly the lower extremities,

Delirium is common during critical illness and is this is associated with long-term cognitive impairment.

Longer duration of delirium in critically ill patients is associated with worse cognition and executive function at three and 12 months (Brain-ICU study Investigators).

Bowel dysfunction in critically ill patients associated with adverse outcomes such as delayed gastric emptying with gastroesophageal reflux, aspiration, decreased enteral feeding and delayed ICU discharge.

Most critically ill patients on mechanical ventilation will develop endoscopic evidence of stress ulceration in the upper G.I. tract, and 10 to 25% of these patients will manifest overt signs and symptoms of G.I. bleeding, and another 5% will progress clinically significant hemorrhage.

Critical illness can disrupt local and systemic mechanisms that protect upper G.I. bleeding, a process that may be associated with increased mortality, particularly among patients receiving extra corporeal life-support.

Approximately 1 million hospitalizations in United States annually require mechanical ventilation and are risk for stress-related G.I. hemorrhage.

Gastric acid suppression is recommended for critically ill patients, particularly for patients who are being ventilated.

Stress ulcer bleeding is less prevalent than it was in the past, as a result of improved care in the ICU.

PEPTIC Investigation of 26,828 patients in ICU is assigned to histamine-2 receptor blockers or proton pump inhibitors for stress ulcer prevention:   Patients assigned the proton pump inhibitor experienced clinically important UGI bleeding IN 1.3% versus 1.8% in histamine-2 receptor blocker group.
The study showed an absolute increase in mortality of 0.8% with a decrease incidence of G.I. bleeding with 0.5%in patients with PPI treated patients.
In the above study newly acquired C. difficile infections did not differ between the two drug regimens, nor did the duration of the mechanical ventilation or hospital length of stay.

Suppression of gastric acidity is associated with higher rates of pneumonia and C. difficile infection.

The overall benefit of PPIs may be reduced by adverse events associated with these agents, including nosocomial pneumonia, clostridium difficile enteritis, and myocardial ischemia.

Administration of enteral feedings in parallel with bleeding prophylaxis may reduce the risk of G.I. bleeding, possibly obscuring the benefits of PPIs, but conversely the combination may increase the risk of nosocomial pneumonia.

The use of glutamine and antioxidants in critically ill patients did not improve clinical outcomes, and glutamine increased mortality in patients with multiorgan failure (Heyland D et al).

Of patients surviving critical illness there is a high level of fatigue, muscle weakness and other symptoms that contribute to delayed recovery.

ICU acquired weakness is prevalent among survivors of ICU hospitalizations and encompasses a critical illness myopathy with myosin-depletion, polyneuropathy, or a combination of these disorders.

ICU acquired weakness, accounts for increased number of days on mechanical ventilation, prolonged ICU stays, complex post ICU transition, care, and increased number of emergency department visits or hospital and ICU readmissions, and increased long-term disposition and healthcare costs: the condition may be permanent.

Cognitive impairment, posttraumatic disstress, anxiety, and depression are common in patients who survived critical illness.

Following critical illness rehabilitation programs including physical and nutritional therapy does not improve physical recovery or health-related quality-of-life (Walsh TS et al).

When frailty occurs or worsens after ICU admission it is associated with increased in-hospital and long-term mortality, increased functional dependency, reduced health related quality of life, a lower likelihood of return to community-based living, and a greater likelihood of hospital readmission.

The one year cognitive outcome among ICU survivors is independent of age, similar to severity to mild Alzheimer’s type dementia, or moderate traumatic brain injury and related to cortical loss, white matter injury, or both diring critical illness.

The duration of ICU delirium is the most potent risk factor for a one year, global cognitive dysfunction and impaired executive function.

Most children treated in the pediatric ICU survive to discharge and has caused a shift from mortality to long-term morbidity is the outcome of interest in pediatric critical illness.

The pediatric post intensive care syndrome, the physical, emotional, and social, cognitive sequelae of critical illness can adversely affect surviving children and their families beyond hospitalization.

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