Consequences of Starvation in Critically Ill Cats

2. Consequences of Starvation in Critically Ill Cats

General Consequences of "Stressed Starvation"

Critical illness induces unique metabolic changes in cats that predispose them to malnutrition and its deleterious effects. An important distinction in the body’s response to inadequate nutritional intake occurs in disease or stressed starvation compared with healthy starvation (Michel, 2004; 2006; Chan & Freeman 2006) (Table 2).

During a critical pathological process, the nutritional hormones are no longer substrate controlled. To maintain hemodynamic homeostasis during acute injury, an increase in sympathetic tone and catecholamine (e.g., epinephrine and norepinephrine) secretion occurs. The catecholamines stimulate glycogenolysis and sensitive hormone protein lipase to increase the plasma levels of FFAs, glucose and insulin. Insulin inhibits ketogenesis. The increase in sympathetic tone increases the resistance of the peripheral tissues to insulin. In septic patients the stress response is exacerbated by the release of polypeptide mediators including tumor necrosis factor (TNF-α) and interleukin- 1 that cause functional hepatic abnormalities, increase glucose intolerance and increase skeletal muscle protein catabolism (via the ubiquitin-conjugation proteasome pathway) (Atkinson & Worthley, 2003). The inflammatory response also triggers alterations in cytokines and hormone concentrations and shifts metabolism toward a catabolic state with accelerated proteolysis that typically results in significant negative nitrogen balance (Figure 1). Paradoxically, these patients may preserve fat deposits in the face of lean muscle tissue loss (Chan & Freeman, 2006). The consequences of lean body mass loss include delayed wound healing, immunosuppression, reduced muscle strength (both skeletal and respiratory), and ultimately increased morbidity and mortality (Marik & Zaloga, 2001; Atkinson & Worthley, 2003) (Figure 2).

Figure 2. General consequences of starvation in critically ill cats.

Specific Topics in Critically Ill Cats

Alterations in Carbohydrate Metabolism in Critically Ill Cats

Similar to critically ill humans, alterations in carbohydrate metabolism are present in critically ill cats and likely contribute to the hyperglycemia commonly observed in this population. Alterations in carbohydrate metabolism in critical illness include increased glucose production (gluconeogenesis), depressed glycogenesis, glucose intolerance, and peripheral insulin resistance. Concentrations of counter-regulatory hormones, such as glucagon, cortisol, and epinephrine are increased and these hormones play a role in up-regulating gluconeogenesis. In addition, hepatic gluconeogenesis appears to become resistant to the regulatory effects of insulin and blood glucose, further contributing to hyperglycemia.

Activation of inflammatory cytokines and neuroendocrine pathways are believed to play a key role in lipid, protein and carbohydrate metabolism. Interactions between the various metabolic pathways are also believed to contribute to hyperglycemia. Glucose intolerance has also been found to parallel the severity of illness. Hyperglycemia has been associated with poorer outcome in critical human patients (Van den Berghe, 2004), and studies have demonstrated the benefits of insulin administration in the critically ill population (Van den Bergh, 2004).

The impact of hyperglycemia on outcome in critically ill cats has not been as well characterized. In a retrospective study, Chan et al.(2006) reported that cats presented to the emergency service with hyperglycemia were significantly more likely to die or be euthanized than those without hyperglycemia. However, in this study, the degree of hyperglycemia did not appear to impact outcome. Critically ill cats have also been reported to be at risk for developing hyperglycemia associated with parenteral nutrition (PN). Hyperglycemia was documented to occur in 75% (Lippert et al., 1993; Syring et al., 2001) and 20% (Crabb et al., 2006), respectively of cats receiving PN. More importantly, the development of hyperglycemia in cats receiving PN was shown to negatively impact survival (Pyle et al., 2004). Chan et al. (2006) reported that critically ill cats had higher circulating concentrations of glucose, lactate, glucagon, non-esterified fatty acids, and cortisol compared with healthy controls. Critically ill cats also had lower insulin and insulin:glucagon ratios compared with healthy controls. The phenomenon of hyperglycemia in critically ill cats is complex, remains incompletely understood and likely involves multiple pathophysiological mechanisms.

Gastro-intestinal Motility and Mucosal Integrity

Cats that are post-anesthetic, postoperative (especially abdominal surgery), hypokalemic, suffering from gastrointestinal, reticuloendothelial, or neuromuscular diseases, or on narcotic analgesics have a strong likelihood of gastrointestinal paresis. Several aspects of digestive physiologic and intestinal microbiologic characteristics of cats suggest a possible role of bacteria in these abnormalities. It has been suggested that increased numbers of bacteria in the feline intestine serve to enhance digestion of protein and fat (Zoran, 2002). Ileus predisposes the patient to bacterial and endotoxin translocation, poor intestinal nutrient digestion and absorption, gastrointestinal ulceration and vomiting. The patient should be auscultated at least three times daily for bowel sounds (Kirby, 2004). In addition, critically ill cats receive numerous medications that can cause anorexia, nausea and vomiting (Table 3). These clinical symptoms contribute to the inappetance characteristic of critically ill cats.

Feline Hepatic Lipidosis

Feline hepatic lipidosis (FHL) is the most common metabolic hepatic disease for cats; especially cats that are obese or stressed (Zoran, 2002; Center, 2005). Although the etiopathogenesis of FHL is still incompletely understood, it is now clear that most cats (over 95%) have an illness or circumstance directly causing a catabolic state (Center, 2005). Nutrients including taurine, arginine, non esterified FFAs and B-vitamins have been suggested, but not proven, to be involved in the pathogenesis of FHL (Zoran, 2002).

Successful treatment of FHL is based on early intervention and adequate nutritional support. In cats that receive early aggressive nutritional support, the prognosis for survival approaches 90%, but in cats not receiving such treatment, the chance of survival is only 10 to 15%. The best diet for treatment of cats with FHL is unknown, but evidence clearly suggests that dietary protein reduces hepatic lipid accumulation and maintains nitrogen and energy balance in cats with FHL (Biourge et al., 1994; Center, 2005) (see Chapter 4).

Obesity is a form of malnutrition often responsible for complications in the event of intensive care. (© ENVL-SIAMU).

Goal of Nutritional Support in Critically Ill Cats

The immediate goal of providing nutritional support to hospitalized cats is not to achieve weight gain, which mostly likely reflects a shift in water balance, but rather to minimize further loss of lean body mass. Nutritional support will not reverse the factors causing proteolysis, gluconeogenesis or lipolysis associated with sepsis or stress. Therapy should therefore focus upon decreasing catecholamine secretion by correcting hypotension, hypoxia and pain, and decreasing the levels of catabolic polypeptide mediators by treating sepsis (e.g., antibiotics, fluid therapy). Nevertheless, while nutrition may not reverse the catabolic response, it enhances protein synthesis and may retard protein catabolism, and therefore may reduce the total burden of body protein loss if introduced early in the management of the acutely ill patient (Atkinson & Worthley, 2003; Kirby, 2004; Chan & Freeman, 2006).