Simple starvation differs from the metabolism of the critically ill, because long periods of food deprivation can be tolerated by the body’s coping mechanisms, using hepatic glycogen, triglycerides within adipocytes and amino acids (skeletal muscle, visceral protein). Hepatic glycogen stores are depleted within 12 hours and glucose and insulin decrease initially. There is increased glucagon to stimulate glycogenolysis, and gluconeogenesis is also increased. As glucagon increases, lipolysis increases. This leads to increased glycerol, ketones and free fatty acids (FFAs). The basal metabolic rate (BMR) is downregulated to protect lean body mass. When glycogen sources are gone, amino acids are used for gluconeogenesis. Fat-derived fuels are used instead of glucose in tissues where this is metabolically possible (Mauldin & Davidson 2003).

Stressed starvation occurs when the body is in a hypermetabolic state as a result of a traumatic or inflammatory insult. Hypermetabolism compromises the normal metabolic adaptations to starvation that occur in simple starvation. Hormonal changes (increased catecholamine, cortisol, ACTH, glucagon, growth hormone) occur which lead to an increased BMR. An increased BMR, along with an increased need for clotting factors, acute phase proteins, white blood cells and other inflammatory components all increase the demand for glucose and amino acids to such a degree that lean body mass cannot be spared from catabolism, as it would be in simple starvation (Mauldin & Davidson 2003).

Nutritional support is required to prevent malnutrition and a compromised immune function, decreased wound healing, catabolism of lean body mass and likely a negative impact on overall survival (Chan & Freeman 2006). Often energy demands are not met without nutritional intervention, due to anorexia, decreased absorption, vomiting, etc. A high protein intake (up to 50%) is needed to provide the critically ill dog or cat with enough amino acids to stop catabolism of body protein (Donoghue 1989). This may be especially important in the cat, where a lack of amino acids may be responsible for impaired hepatic lipid release, leading to hepatic lipidosis. Fat is the main energy source for most tissues during complicated starvation, whereas carbohydrate may not be used with maximal efficiency due to persistent glucose intolerance and hyperglycaemia (mostly due to peripheral insulin resistance) (Mauldin & Davidson 2003).

In humans, providing nutrition decreases urinary nitrogen loss, stimulates immune function, reverses hypometabolism and provides sustenance during hypermetabolism. This improves recovery, lowers mortality and improves response to trauma and stress. The goal of providing nutrition in animals is to prevent catabolism of tissue proteins (Donoghue 1992). Enteral nutrition (assisted or voluntary) supports the integrity of the gastrointestinal tract (GIT) (Armstrong et al 1990, Robben et al 1999).

Nutritional support should be pre-empted (e.g. anticipated anorexia of more than 3–5 days, trauma, sepsis, peritonitis, pancreatitis, burns, large wounds, major gastrointestinal (GI) surgery, protracted vomiting, diarrhoea). Late signs of malnutrition are weight loss (>10%), poor hair coat, muscle wasting, hypoalbuminaemia, lymphopenia, coagulopathy and inadequate wound healing. Intervention such as placement of a feeding tube or parenteral nutrition should be given prior to these signs (Chan & Freeman 2006). Animals with hypoalbuminaemia are better treated with earlier intervention, as hypoalbuminaemia reflects a prolonged period of malnutrition (Withrow & Vail 2007).

The benefits of dietary support in cancer patients include increased tolerance to surgery, chemotherapy and radiation therapy, improved immune function, immunoglobulin and complement levels, and phagocytic function of white blood cells (Ogilvie & Vail 1990).

In the authors’ experience, these dogs form the majority of patients seen in referral veterinary oncology practice, perhaps because many die of their cancer before they become cachectic. Dogs with cancer and no weight loss still show the alterations in protein, carbohydrate and fat metabolism as described above, without any evidence of clinical signs (Ogilvie 2001). Several studies have found no significant differences in resting energy expenditure (and presumably caloric requirements) in dogs with a wide range of malignancies when compared with healthy, client-owned dogs. This finding suggests that, in general, dogs with cancer and no evidence of weight loss do not have energy requirements higher than those of apparently healthy dogs without cancer (Ogilvie 2001). However, the source of their dietary energy may be more critical than their net energy requirements.

The first clinical signs of these metabolic alterations are anorexia, mild weight loss, lethargy and an increased susceptibility to side effects of chemotherapy, radiation therapy, surgery, etc. (Ogilvie 2001). A prolonged state of metabolic derangement resulting in accelerated starvation and profound malnourishment is termed ‘cancer cachexia’. Decreased nutritional intake/assimilation, abnormal nutrient losses, treatment-related factors, abnormal metabolic pathways and competition with the tumour for nutrients all contribute. End-stage cancer cachexia is characterized by marked muscle wasting, weight loss, debilitation, weakness, loss of body fat stores and lethargy (Ogilvie & Marks 2000) (Figure 12.1).

In the authors’ experience, advanced cancer cachexia is not seen commonly. When it has been seen, it has tended to affect dogs with a significant ongoing, progressive, uncontrolled and often end-stage tumour burden. Overt cancer cachexia is a poor prognostic sign, as patients have a decreased quality of life, decreased response to therapy and shortened survival time compared to those with similar diseases without cachexia (Ogilvie 2001). Dogs with cancer may develop cachexia despite a nutritional intake considered adequate for a normal dog (Ogilvie & Vail 1990).

The finding that tumour cells tend to use carbohydrate and protein preferentially to lipid for fuel has led to the hypothesis that feeding foods relatively high in fat may be more beneficial than feeding carbohydrate-rich foods. This diet is then designed to ‘feed the dog and starve the tumour’. Foods containing less than 30% protein calories and more than 40% carbohydrate calories should be avoided in cancer patients (most commercial foods are suboptimal in this regard) (Ogilvie & Marks 2000).