Nutritional Disease

Nutritional Disease

Lindsey B. C. Snyder

Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin–Madison, Madison, WI, 53706, USA


The World Health Organization defines obesity is an abnormal or excessive fat accumulation in adipose tissue to the extent that health is impaired [13]. Excess adipose tissue occurs when the caloric intake surpasses the caloric expenditure [4, 5]. Owing to the prevalence of obesity in the human population, the World Health Organization has classified obesity into simple obesity (body mass index [BMI] 30–34.9 kg m−2), severe obesity (BMI 35–39.9 kg m−2), morbid obesity (BMI 40–49.9 kg m−2), and super morbid obesity (BMI ≥40 kg m−2) [6]. Although it is unknown what the actual increase in anesthetic risk is due to excessive body weight, it is generally believed that the likelihood of anesthetic complications will be greater in the overweight animal.


Obesity is the most common medical condition in companion animals and is associated with several comorbidities [2]. Approximately 55% of dogs and 53% of cats in the USA are overweight or obese [7]. Worldwide, 22–40% of dogs are obese [2, 5, 8, 9]. Even higher percentages are observed in dogs and cats between 5 and 10 years of age [5]. Coincidently, with obesity in humans comes an increase in morbidity, such as diabetes and musculoskeletal conditions [7]. The criteria for obesity are not as clear‐cut in veterinary patients as with human patients, as optimal body weights have not been established for our species and varying breeds. However, it is still concluded that when a patient’s weight is 15% above normal for its breed, it is “overweight,” and when a patient’s weight is 30% above normal, it is “obese” [2]. Body condition scoring (BCS) has been established as a validated method to assess body composition (see the section titled “Ideal Body Weight”) [10].

Risk factors for the development of obesity in veterinary patients have been identified. There is a link between certain breeds and their genetic predisposition for obesity. Cairn Terriers, West Highland White Terriers, Scottish Terriers, Shetland Sheepdogs, Basset Hounds, Cavalier King Charles Spaniels, Dachshunds, Beagles, Cocker Spaniels, and Labrador Retrievers are genetically predisposed to obesity. Likewise, particular breeds appear to be resistant to obesity, such as the Sighthound group [2]. Aging is associated with an increase in the likelihood of obesity. With aging, the lean body mass decreases, resulting in a decrease in the total daily energy needs of the animal. In conjunction with a decrease in total daily energy needs, the animal’s voluntary activity is typically decreased, possibly because of comorbidities of aging, such as osteoarthritis. The decrease in total daily energy needs combined with a decrease in activity can lead to weight gain if caloric intake is not decreased as well [2].

Excessive weight can have a major impact on the overall health of the animal. In humans, morbid obesity (BMI of ≥40–44.9 kg m−2) is associated with an increased likelihood of diabetes mellitus [11], respiratory failure, hypertension, left ventricular hypertrophy, atherosclerosis, myocardial ischemia, and some forms of cancer compared to nonobese patients [4]. Mild to moderate hypertension is described in up to 60% of obese human patients, whereas 5–10% of obese human patients have severe hypertension. With time, hypertension can lead to left ventricular dilation, increased left ventricular wall stress, compensatory left ventricular hypertrophy, and left ventricular diastolic dysfunction [4]. Overweight animals are expected to have a shorter life span and increased incidence of osteoarthritis, diabetes mellitus, cardiovascular disease, pancreatitis, mammary tumors, and renal disease [5, 8]. Studies suggest that 31% of diabetes mellitus and 34% of lameness could be abolished if overweight and obese cats were at an ideal body weight [5].

An increase in body adipose tissue alters cardiopulmonary physiology, leading to an increase in cardiac output (CO), oxygen consumption, and closing capacity, and a decrease in functional residual capacity (FRC). In humans, these alterations can cause the associated pathologies of hypertension, coronary artery disease [1], and obstructive sleep apnea [11]. With morbid obesity in humans, the excessive body tissue decreases the FRC, expiratory reserve volume, and total lung capacity. The FRC decreases exponentially with increasing BMI in humans. When the FRC decreases to the range of the closing capacity, small airway closure takes place, leading to ventilation–perfusion mismatch, right to left shunting, and arterial hypoxemia [3]. Finally, with increasing body weight, there is an increase in blood volume proportional to the body surface area (BSA). This increase in blood volume contributes to an increase in preload and an increase in resting CO. Ultimately, increased left heart diastolic filling and left ventricular hypertrophy can occur (Table 10.1) [1].

Obesity results in restrictive lung disease due to the presence of excessive visceral fat, adding pressure to abdominal organs and increasing the inhalational efforts of the animal. Ventilation is subsequently limited by the adipose tissue and breathing is easily compromised by placing the animal in a recumbent position. Dorsal recumbency is the worst position, as it puts the largest portion of the lung in a dependent position [8]. Ventilation should be supported in all obese patients. This can be accomplished with manual ventilation or with a mechanical ventilator. Monitoring of the patient’s arterial CO2 and O2 levels is used to determine the rate and volume of ventilation needed by the animal.

Adipose tissue is a major source of inflammatory mediators, and obesity is, therefore, linked to chronic low‐grade inflammation [12]. Research suggests a mechanism for the link between excess body weight and many diseases. Adipose tissue, once thought to be physiologically inert, is an active producer of hormones such as leptin and resistin, and numerous cytokines [5]. The chronic inflammation observed in obese humans is thought to be one of the significant links between obesity and cardiovascular disease [12]. Additional physiologic alterations associated with obesity include increases in tubular reabsorption, which initiates volume expansion of the extracellular volume. In humans, the total extracellular volume is increased; however, the circulating blood volume on a volume/weight basis is decreased [4]. Finally, splanchnic blood flow is approximately 20% higher in obese as compared to lean individuals. Cerebral and renal blood flows are near normal in the face of obesity [4].

Table 10.1 Physiologic changes associated with obesity.

Left ventricular hypertrophy
Restrictive pulmonary disease
Increased intraabdominal pressure
Decreased chest wall compliance
Decreased lung volumes
Exercise intolerance
Increased atelectasis
Increased ventilation/perfusion mismatching
Increased volume of distribution
Musculoskeletal conditions
Increased blood volume

Anesthetic Management of the Obese Patient


Anesthetic induction is a demanding period regardless of the patient’s BMI. With an obese patient, morbidity causes induction to be even more delicate. With induction and intubation, obese humans have a proportionately greater decrease in cardiac index (CI) than lean individuals. CI decreases 17–33% in obese patients compared to 4–11% in controls. This decrease in CI continues postoperatively in obese individuals, whereas it returns to baseline in nonobese control patients [1, 13].

The physiologic changes induced by obesity, such as the decrease in CI, can significantly affect the distribution, binding, and elimination of anesthetic drugs. The alterations in pharmacokinetics can lead to severe adverse events if dosing is based solely on the actual body weight [4]. However, systemic absorption of oral drugs does not seem to be significantly affected by obesity, although some studies report a delay in gastric emptying in the overweight patient [4].

When evaluating the alterations of pharmacokinetics on the drug propofol, obese children require significantly less propofol for loss of lash reflex than do lean children; obese children are given a lower dose of propofol on the basis of actual body weight than their nonobese peers [14]. Clearance of propofol appears to be linearly related to lean body weight rather than to total body weight [6]. It is recommended that the dose of propofol for both induction and maintenance of anesthesia should be based on actual body weight in obese individuals analogous to their lean counterparts [4]. In obese humans, both the volume of distribution and the clearance of propofol were significantly correlated to total body water. Therefore, there is a concurrent increase in the volume of distribution, as well as clearance, with the elimination half‐life being similar in obese and lean patients. There were no signs of propofol accumulation or prolonged duration of action when propofol was administered on actual body weight in obese humans [4].

In veterinary patients, overweight dogs were found to need a lower intravenous propofol dose per kilogram of total body weight for endotracheal intubation compared to normal body conditions dogs. This suggests that a dosing on lean body weight might be more beneficial in overweight dogs [15]. However, when obese dogs are dosed for propofol based on a lean body weight adjustment, the dose of propofol administered was higher than for ideal body condition score dogs. The differences in doses may conclude that fat interferes in the pharmacokinetics and pharmacodynamics of propofol and raises the question of whether it should be excluded or not when calculating the propofol dosage in induction of anesthesia in obese dogs (Table 10.2) [16].

Thiopental, however, has a significantly longer elimination half‐life when administered on actual body weight in obese individuals owing to the increased volume of distribution. The dose of thiopental for induction of anesthesia of obese patients can be based on lean body mass to avoid prolongation of effects [4].

Table 10.2 Drug dosing in the obese patient.

Propofol Actual or lean body weight
Thiopental Lean body weight
Midazolam Actual body weight
Diazepam Actual body weight
Opioids Dependent on lipophilic nature of drug
Highly lipophilic Lean body weight
Minimally lipophilic Actual body weight

Only gold members can continue reading. Log In or Register to continue

Oct 18, 2022 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Nutritional Disease
Premium Wordpress Themes by UFO Themes