Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

CHAPTER 6 – Obesity and Nutritional Disorders

Lars E. Helgeson, MD









Perioperative Concerns



Protein-Energy Malnutrition Disorders



Childhood Disorders



Adult Disorders



Micronutrient Disorders





Obesity is not an uncommon disease. According to statistics from the Centers for Disease Control and Prevention (CDC), in the United States the incidence of overweight/obesity in adults is rising to alarming levels and is, in fact, becoming the norm. In 1994, 56% of the population was classified as overweight and 23% was classified as obese. In 2002 the overweight figure was 65% and the obese figure was 31% ( Fig. 6-1 ).[1] A significantly higher percentage of minorities than whites are classified as obese ( Table 6-1 ).[2] Most alarming is the rise in childhood obesity. In 1963, 4% of children 6 to 17 years of age were overweight. In 1994, 11% were overweight; and in 2004 the figure was 15% ( Table 6-2 ). This trend shows no sign of abating. Long-term consequences for these children are substantial. They have a significantly greater chance of developing associated medical problems, such as diabetes, hypertension, and heart disease, at a much earlier age. They are also much more likely to suffer from depression and social isolation.


FIGURE 6-1  Age-adjusted prevalence of overweight and obesity among U.S. adults, age 20-74 years. (Age-adjusted by direct method to the year 2000 Bureau of the Census estimates using the age groups 20-39, 40-59, and 60-74 years.)



TABLE 6-1   -- Overweight and Obesity Prevalence by Ethnicity

Population Group

Prevalence of Overweight and Obesity in Adults BMI ≥ 25

Prevalence of Obesity in Adults BMI ≥ 30

Prevalence of Overweight in Children Ages 6–11

Prevalence of Overweight in Adolescents Ages 12–19

Total population





 Total males





 Total females
















Mexican American


























Modified from American Heart Association: Heart Disease and Stroke Statistics—2003, American Heart Association, Dallas.

BMI, body mass index.





TABLE 6-2   -- Prevalence (%) of Overweight Among Children and Adolescents Ages 6–19 Years for Selected Years 1963–1965 Through 1999–2000

Age (Yr)[*]

1963–1965 1966–1970[†]

















Adapted from Centers for Disease Control and Prevention National Center for Health Services: Prevalence of Overweight. Among Children and Adolescents: United States, 1999/2000. Available athttp://cdc.gov/nchs/products/pubs/pubd/hestats/overweight99.htm


Excludes pregnant women starting with 1971–1974. Pregnancy status not available for 1963–1965 and 1966–1970.

Data for 1963–1965 are for children 6–11 years of age; data for 1966–1970 are for adolescents 12–17 years of age, not 12–19 years.



The United States is not alone with this epidemic. Currently, half the populations of Russia and the United Kingdom are classified as overweight or obese. Developing countries are “catching up” in this regard; 15% of China is classified as overweight, and the number is growing.[3] In parts of Africa, overweight children outnumber underweight children by a ratio of 3:1.

According to the World Health Organization, “overweight and obesity are now so common that they are replacing the more traditional public health concerns such as under-nutrition and infectious diseases.”[4] Globally, there are now as many overnourished people as undernourished people. Obesity causes greater morbidity and mortality then tobacco and alcohol combined.[5]


The degree of obesity is most commonly and easily measured by the body mass index (BMI) which is calculated as mass (in kilograms) per height (in meters) ( Box 6-1 ).[2] Using the BMI as a diagnostic tool is very useful, with certain limitations.[6]

BOX 6-1 

Calculation of Body Mass Index

Body Mass Index (BMI) = Mass in kilograms divided by height in meters[2] (BMI = kg/m2)

Simplistically, obesity is caused by caloric intake above metabolic needs. Realistically, the causes of obesity are multiple, complex, and interconnected to varying degrees. Several causes are outlined in Box 6-2 .

BOX 6-2 

Etiology of Obesity

Sedentary lifestyle

Dietary norms

Familial/genetic tendencies

Intrinsic physiologic tendency


Disease states (e.g., diabetes, hypothyroidism, Cushing's syndrome, hypothalamic lesions, Prader-Willi syndrome)


Most cases of obesity appear to be related to a lack of a sense of satiety. How is it that one individual would be satisfied with a 2100 kcal/day diet whereas another would feel unsatisfied with twice that? Obesity is not a choice or a sign of “weakness.” It should be considered both a behavioral and medical condition that needs to be dealt with like any other disease state. Clearly, there are very strong biologically driven underpinnings. Metabolically, satiety has multiple feedback loops with complex interactions involving hormones, neural peptides, and proteins that are further complicated by social, genetic, and environmental factors.

The role played by societal dietary norms is clear. In many developed and developing countries, traditional dietary norms are such that overweight/obesity is uncommon. As these norms become displaced by high-fat fast food and other refined food products, the incidence of overweight and obesity rises. It is hard to miss the saturation advertising of snack food, fast food, and soft drinks (including “super-sizing”) in many societies. These factors combine with sedentary lifestyles to cause the vast majority of overweight and obesity.

Pharmacologic agents occasionally contribute to obesity. Table 6-3 outlines several implicated medications. Affected individuals represent a small minority.

TABLE 6-3   -- Drugs Contributing to the Etiology Of Obesity






Hypoglycemic agents



Insulin, sulfonylureas






Amitriptyline, imipramine, desipramine, fluvoxamine



Central nervous system agents



Valproic acid, methysergide, metergoline






Clonidine, prazosin, propranolol



Sex hormones









Phenothiazine, cyproheptadine, lithium

Adapted from Atkinson RL: A 33-year-old woman with morbid obesity. JAMA 2000;283:3236-3243.




Obesity can often be “diagnosed” simply by appearance. Obese individuals generally appear obese. However, it is important to evaluate the degree of obesity. Obesity is most commonly quantified by utilizing the BMI as outlined in Table 6-4 . This method does have its limitations. There are three subtypes of individual in which BMI is misleading: (1) A sarcopenic individual is defined as having a relative decrease in lean body mass and a relative increase in body fat yet will have a normal BMI. This can occur in elderly and bedridden patients. (2) Bodybuilders often have a mass of more then 100 kg and would certainly have a BMI of 30 or more kg/m2, suggesting obesity. These individuals have a very low body fat percentage and could never be mistaken as being obese on appearance. (3) Lastly, the hypermuscular and obese patient would have a misleadingly high BMI.

TABLE 6-4   -- Classification of Obesity and Malnutrition Using Body Mass Index


BMI (kg/m2)

Severely malnourished


Moderate malnutrition


Mild malnutrition








Morbid obesity


Super morbid




Alternative methods of assessing body fat include abdominal girth taping, standardized height-weight tables, bioelectric impedance analysis, hydrostatic weighing, and skinfold caliper measurements (anthropometry). Each of these techniques has its own set of limitations.


Even in “merely” overweight individuals (BMI of 28 kg/m2) there is undeniably an increased risk of poor health and premature death. [7] [8] [9] [10] Obesity is closely associated with several other disease states ( Box 6-3 ). It is true that certain disease states such as hypothyroidism, diabetes, and Cushing's syndrome can cause obesity. Most often it is the obesity that is the cause (not the effect) of many diseases. Table 6-5 outlines the increase in prevalence of several disease states directly attributable to obesity.

BOX 6-3 

Comorbidities of Obesity


Coronary artery disease

Deep venous thrombosis


Increased stroke risk

Insulin resistance

Diabetes mellitus type II

Orthopedic (knees, hips, spine)

Psychosocial (depression, anxiety, interpersonal difficulties)


Gastroesophageal reflux

Sleep apnea

Obesity hypoventilation syndrome (pickwickian syndrome)


Fatty liver

Cholecystitis and cholelithiasis

Cancer (breast, uterine, prostate, renal, colon, pancreatic, gastric)


Menstrual abnormalities

Complicated labor and childbirth

Poor surgical wound healing

Increased risk for postoperative thrombophlebitis and pneumonia

TABLE 6-5   -- Proportion of Disease Prevalence Attributable to Obesity

Type II diabetes




Coronary heart disease


Gallbladder disease




Breast cancer


Uterine cancer


Colon cancer


Adapted from Bessesen DH, Kushner R (eds): Evaluation and Management of Obesity. Philadelphia, Hanley & Belfus, 2002, p 2.




There are several pathophysiologic implications, depending on the distribution of fat. Android (truncal) distribution, more commonly seen in males, is associated with an increased incidence of cardiovascular disease and increased oxygen consumption (Vo2). Gynecoid distribution is usually seen in females; it is found predominantly on the buttocks and thighs and is less distinctly associated with cardiovascular disease. It is also less metabolically active than android distribution.[11] Intra-abdominal fat is particularly associated with increased cardiovascular risk.[12]

The degree of expression of these comorbidities is highly variable, which must be taken into account whenever providing care to an obese patient.


A typical obese patient's bone structure is no different then that of a typical lean patient. Traditional parameters such as thyromental distance, narrow palate, receding chin, and overbite are equally applicable in the obese and lean patient. For most overweight/obese individuals, the excess fat has no significant impact on airway management. [13] [14] There is a subset of individuals whose airways are narrowed by redundant pharyngeal tissue. Obstruction is most often seen at the retropalatal level, but other sites may be involved. [15] [16] Even modestly overweight people can be affected by obstructive sleep apnea (OSA).[17] This symptom suggests that mechanical obstruction is likely, as the patient's level of consciousness diminishes. Except in super morbidly obese patients, the degree of pharyngeal tissue redundancy is not reliably predicted by external appearance. Neck flexion/extension is more commonly impaired in patients with a BMI greater than 40, owing to prominent fat stores on the anteroposterior neck, submental area, and anteroposterior chest wall.


Basal metabolic rate is related to body surface area and is usually normal. However, obese individuals have increased production of carbon dioxide (Vco2) and increased oxygen consumption (Vo2).[18] It was previously thought that adipose cellular metabolism was responsible for this increase. It has now been shown that this increased metabolism is primarily due to increased effort for movement and work of breathing due to “mass loading” of the chest wall. The work of breathing in the morbidly obese is increased by up to 70%, compared with the nonobese.[19] These increases are much more pronounced during exertion compared to lean individuals.


Obtaining preoperative pulmonary function tests (PFTs) is usually not indicated for obesity per se, because the results will not alter management. There does not seem to be any correlation between the abnormalities seen in the PFT results in obese patients and pulmonary complications,[20] although there is a correlation with airway, ventilator, and pulmonary management. Obese individuals have greater amounts of chest wall adipose tissue, including breasts in men and women. This “mass loading” has the net affect of increasing the intrathoracic pressure, which will increase the amount of alveolar compression and closure. This results in significant intrapulmonary shunting as deoxygenated pulmonary artery blood passes through nonventilated alveoli to mix with oxygenated blood in the pulmonary vein.[21] Some individuals have alveolar closure during normal, upright spontaneous breathing. [22] [23] This decrease in functional residual capacity is exacerbated by mass shifting from the abdomen as the patient lies supine and further worsened by the Trendelenburg position. Figures 6-2 and 6-3 [2] [3] illustrate this concept. The decrease in functional residual capacity can be so significant as to drop well below closing capacity. Clinically, this means that apnea for as short as 5 seconds can result in hypoxemia.[24] A conscious patient may have difficulty remaining supine for even short periods of time and in more severe cases may become hypoxic when supine for only a few moments. This may necessitate intubation, induction, and maintenance of general anesthesia in a semi-seated position. If possible, other techniques of “off-loading” can be employed ( Fig. 6-4 ).[25]


FIGURE 6-2  Comparison of lung volumes between lean and obese subjects. In some morbidly obese patients, lying supine, tidal volume (TV) can be at or below closing volume (CV). VC, vital capacity; IC, inspiratory capacity; FRC, functional residual capacity; IRV, inspiratory reserve volume; ERV, expiratory reserve volume; RV, residual volume.




FIGURE 6-3  Effect of position change in various lung volumes in nonobese subject compared with markedly obese subject. FRC, functional residual capacity; RV, residual volume; CC, closing capacity.  (From Brown BR [ed]: Anesthesia and the Obese Patient. Contemporary Anesthesia Practice Series. Philadelphia, FA Davis, 1982, p 26.)





FIGURE 6-4  Patient's abdominal panniculus mechanically lifted followed by markedly improved arterial oxygenation.  (From Wyner J, Brodsky JB, Merrell RC: Massive obesity and arterial oxygenation. Anesth Analg 1981;60:691-693.)




Postoperatively, obese patients are at increased risk of hypoxia, pulmonary atelectasis, and pneumonia.[26]


Many overweight patients have no significant cardiovascular disease, but incidental eccentric left ventricular hypertrophy is frequently found.[27] Normal left ventricular function is usually present, but diminished left ventricular compliance is common.[28] In some individuals, left ventricular diastolic dysfunction can develop, which results in greater sensitivity to changes in preload and afterload. As the duration and degree of obesity increases, so can the degree of ventricular dysfunction and, ultimately, pulmonary hypertension. [29] [30] [31] [32]

Guidelines for assessing the cardiovascular risk[33] are applicable to both the obese and lean patient ( Fig. 6-5 ). This includes the use of β blockers. Because of the diminished physical activity and increased incidence of hypertension, hyperlipidemia, and diabetes, there is an increased risk of cardiovascular disease compared with the general population. Cardiovascular disease must always be suspected, and the threshold is lower for a comprehensive cardiac evaluation.


FIGURE 6-5  Pathway for assessing preoperative cardiovascular risk in patients scheduled to undergo noncardiac surgery. The decision whether to perform noninvasive testing is based on the presence of clinical risk factors, the patient's functional status, and the type of surgery scheduled. If the result of a noninvasive test is abnormal, the decision whether to perform cardiac catheterization is based on several features. The likelihood of left main coronary artery disease or severe three-vessel disease is much higher, and cardiac catheterization should be considered more strongly if ischemia is provoked at a low level of stress or persists during stress testing, if there is severe ST-segment depression, if large areas of the myocardium appear to be at risk, or if ischemia is demonstrated in a patient known to have left ventricular dysfunction at rest. Coronary artery bypass grafting (CABG) and percutaneous coronary revascularization should be performed only if justified independently of the need for noncardiac surgery.[33]  (Modified from Fleisher LA, Eagle KA: Clinical practice: Lowering cardiac risk in noncardiac surgery. N Engl J Med 2001;45:1677-1682.)




Circulating blood volume is increased with increasing body weight. Cardiac output is increased, usually owing to increased stroke volume and an essentially unchanged heart rate.[34] This limits any increase in cardiac output that may otherwise be required.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

Perioperative Concerns

Evaluating every patient's baseline medical status is the starting point for any anesthetic. One has to know what medical conditions exist and how they can affect the patient's well being and our anesthetic management. Assuming that a patient has been properly treated for any preexisting medical conditions, maintenance of the patient's baseline medical status is the ideal preoperative situation. For example, continuing antiseizure or antihypertensive medications and tight control of diabetes through the day of surgery are well-established protocols.

If a patient's medical conditions are not properly treated, the case needs to be delayed until the medical status is stable. If the procedure cannot be delayed, then we must manage the patient as conditions present. In this context, management of the obese patient is no different than for any other patient. Obesity does present several unique issues that warrant special attention.

Emotional Issues

Obese individuals undergo a daily routine of subtle and not-so-subtle social slights, insults, and discrimination. They have had a lifetime of negative self-image, which is reinforced by almost all aspects of society. Advertising emphasizes “thin is good and fat is bad.” There are embarrassing difficulties in finding clothes that fit or having difficulty fitting in a movie theater or airline seat. Consequently, an obese patient will often bring varied emotional baggage with which we must deal. There are two principles to which we must adhere when dealing with an obese patient. First, we discuss with the patient the issues that are specifically relevant to our anesthetic care which are a consequence of the patient's weight. Discussions should be “matter of fact” and should avoid glossing over issues or using euphemisms. The patient knows that he or she is obese and that there are issues related to that fact. However, we should not bring undue attention to the patient's obesity or in any way come across as judgmental or patronizing. Second, we should act compassionately and treat the obese patient with simple kindness, humanity, and respect. We should avoid any condescension, innuendo, or comments about the patient's size and avoid any “talk” with other people anywhere near the patient.


Our goal is to provide a safe anesthetic, and gaining control of the patient's airway is central to this. It is wise to optimize all factors to safely gain control of the patient's airway. Because of fat distribution on the obese patient's back and shoulders, it is necessary to build a custom ramp out of blankets to properly align the oral, laryngeal, and pharyngeal axes ( Fig. 6-6 ). A useful reference point is an imaginary horizontal line drawn between the earlobe and sternum, as noted in Figure 6-7 .


FIGURE 6-6  Schematic diagram demonstrating head position for endotracheal intubation. A, Successful direct laryngoscopy for exposure of the glottic opening requires alignment of the oral, pharyngeal, and laryngeal axes. B, Subsequent head extension at the atlanto-occipital joint serves to align the three axes, resulting in the shortest distance and most nearly straight line from the incisor teeth to glottic opening.  (Adapted from Nichol HC, Zuck D: Difficult laryngoscopy: The “anterior” larynx and the atlanto-occipital gap. Br J Anaesth 1983;55:141.)





FIGURE 6-7  This figure illustrates proper positioning (“ramping”) allowing optimal airway alignment in an obese patient. A useful reference point is an imaginary horizontal line drawn between the earlobe and sternum (dashed line). Upper arm distortion (solid lines)precludes standard placement of noninvasive blood pressure cuff.



The American Society of Anesthesiologists (ASA) difficult airway algorithm, noted in Figure 6-8 ,[35] is a well-known and proven guideline. This algorithm is applicable to both the obese and lean patient. As noted earlier, most overweight/obese patients do not present with a difficult airway, although they do have a greater likelihood of it occurring compared with the general population.


FIGURE 6-8  ASA difficult airway algorithm.  (From Practice guidelines for management of the difficult airway: A report by the American Society of Anesthesiologists task force on management of the difficult airway. Anesthesiology 1993;78: 597-602.)




A recent history of previous difficult or uneventful intubations should be obtained. This is the best predictor for an uneventful laryngoscopy/intubation. A thorough evaluation should be done, including the Mallampati score, atlanto-occipital mobility (neck extension), mouth opening, mandible width, neck circumference, thyromental distance, and dentition. The degree of any limitations in range of motion must be identified. One critical bit of usually missing information is the amount of fatty redundant tissue in the pharynx. This is very difficult to assess. A history of significant OSA is suggestive (but not reliably predictive), as is a large-circumference neck and lateral neck radiographs, ultrasound, or computed tomographic scan.[36] A preoperative otolaryngologic evaluation may be helpful.[37] Anecdotally, another suggestive parameter is a BMI greater than 50 kg/m2.

With excessive tissue redundancy, the only reason the airway is patent may be due to the patient's muscle tone, which will stent open the pharynx. This redundant soft tissue is likely to collapse and obstruct the pharynx after the patient loses consciousness. When induced, it may not be possible to ventilate or intubate the patient. It is these patients who have the severest form of OSA and who may later develop pickwickian syndrome.

There are many routines in the approach to management of a suspected difficult airway. Box 6-4 illustrates one approach for preparing a patient's airway for awake manipulation. One deviation from the ASA algorithm that can be very useful is performing a “direct look.” A patient who is suspected of having a difficult airway is prepared as for an awake fiberoptic intubation with an antisialagogue, optimum positioning, judicious sedation, and thorough topicalization with local anesthetic. Incremental, direct laryngoscopy is performed with additional topicalization. A laryngoscopic view is obtained, not only of the vocal cord grade but with special attention paid to the amount of redundant pharyngeal tissue. If there is good visualization of the vocal cords with minimal redundancy, a standard rapid-sequence induction is indicated. If the vocal cord view is poor or there is tissue redundancy, the trachea should then be intubated with the patient awake. Induction should occur only after confirmation of proper placement. An advantage of the “direct look” is that the oropharynx is well anesthetized, should awake fiber optic intubation be necessary.

BOX 6-4 

Airway Preparation for Awake Airway Manipulation




H2 blocker

(Non-particulate antacids)

Judicious sedation

Airway topical anesthesia options



Lidocaine 4% nebulizer



Viscous lidocaine gargle



Direct spraying



Transtracheal block



Superior laryngeal nerve block



Glossopharyngeal nerve block

Optimize airway alignment

Gastrointestinal Issues

Obese patients are at significantly greater risk for aspiration ( Box 6-5 ). As with any patient, anxiety, pain, trauma, and certain drugs all decrease gastric emptying.[38] It is well established that fasting obese preoperative patients have a gastric volume greater than 25 mL and a pH less than 2.5. [39] [40] If aspirated, this volume and pH can lead to significant pulmonary parenchymal injury. Steps to minimize this risk are outlined in Box 6-6 . The efficacy of cricoid pressure has been brought into question. [41] [42] Whereas most sources advocate some variant of aspiration prophylaxis, aside from keeping the patient NPO, there is no real evidence to support this widespread practice. However, it is prudent to continue this standard, because it is a relatively benign treatment and the consequences of aspiration are severe.

BOX 6-5 

Factors that Contribute to Increased Risk of Aspiration in the Obese Patient

Greater incidence of hiatal hernia

Altered geometry of gastroesophageal junction

Increased intra-abdominal pressure

Increased fasting gastric fluid volume

Decreased fasting gastric pH

Possible delayed intubation due to “difficult airway”

Possible gastric distention due to attempted mask ventilation

BOX 6-6 

Steps to Minimize Risk of Aspiration


H2 blocker or proton pump inhibitors the night before and morning of surgery (PO or IV)




PO: 2 hours preinduction or



IV: 30-45 minutes preinduction

Nonparticulate antacids, if unable to utilize H2 blockers

“Ramping,” with optimal airway alignment

Awake intubation, or rapid-sequence induction using cricoid pressure

Pulmonary Issues

As mentioned earlier, obese patients have a decreased functional residual capacity owing to mass loading of the chest wall, as well as transdiaphragmatic distention from the abdomen. The extent of this diminished functional residual capacity depends on the degree of obesity. Positioning of the patient for surgical needs may further diminish the functional residual capacity. Ventilator management under these conditions is challenging, to say the least. Trendelenburg positioning should be avoided, preferably using the reverse Trendelenburg position to offload the lungs, thereby improving the functional residual capacity. In select circumstances it is possible to maintain traction on the pannus, also offloading the lungs (see Fig. 6-7 ). Coordination with the surgeon is necessary to lessen the impact of abdominal packing and retractors. Proper prone positioning is actually less problematic then supine positioning, provided that the hanging abdomen is minimally supported.[43]

Use of positive end-expiratory pressure is often helpful because it maintains the patency of alveoli that would otherwise collapse. Careful attention must be paid to peak airway pressures to avoid barotrauma.[44] The ventilator “pressure control” setting versus “volume control” setting may be helpful in this regard. Alternatively, increasing respiratory rate and decreasing tidal volumes may be the only option. Hyperventilation resulting in hypocarbia should be avoided because of the rise in shunt fraction.[21] Ordinarily, hypoxia triggers the pulmonary hypoxic vasoconstriction response to lessen the intrapulmonary shunting. Volatile anesthetics generally blunt this response, which can result in even greater hypoxia. Initially, the obese patient's Fio2 should begin at 1.0 and then be titrated down, using pulse oximetry as a guide.


Even though the bone structure of obese individuals is essentially normal, the alignment is often distorted by the overlying tissue when supine. Proper “ramping” is often required for optimal airway alignment. The head must be properly supported in a neutral or slightly flexed position. One area not often considered is the lumbar spine. The buttocks can act as a fulcrum for the legs, which will extend the lumbar spine. A remedy for this is to support the knees, which will flex the hips, relieving the spine extension. Another area often ignored is the arms. With the patient lying on a ramp, the shoulders tend to extend downward (posteriorly), putting significant stress on the brachial plexus and shoulder joint. Because of the excess tissue on the upper arm, the lower arm also extends, putting excess stress on the elbow joint. It is vital to position the joints with slight flexion and to provide proper padding and support ( Fig. 6-9 ). Abduction of the shoulder to less than 90 degrees may likewise be necessary. One solution is to simply ask the patient if there is any discomfort or if there are any stress points and to then correct this before induction of anesthesia.


FIGURE 6-9  Illustration of proper (A) and improper (B) arm positioning. Proper positioning minimizes risk of joint, brachial plexus, and nerve compression injuries.




Electrocardiography and pulse oximetry do not present any differences compared with those in the lean patient. Central venous pressure or pulmonary artery catheter monitoring should be performed only when clinically indicated and not based on obesity alone. Frequently, the upper arms of obese patients have a pronounced cone shape (see Fig. 6-7 ). A noninvasive blood pressure (NIBP) cuff is designed to work on a cylindrically shaped arm. A larger NIBP cuff may reach around the arm, but the arm shape remains problematic and will often give erroneous readings, as noted in Table 6-6 . There are alternatives ( Fig. 6-10 ), which are further outlined in Table 6-7 .

TABLE 6-6   -- Blood Pressure Reading Discrepancies by Varied Arm Circumferences

Bladder width (cm)




Ideal arm circumference (cm)




Arm circumference range (cm)




Arm circumference (cm)


































































































Modified from Graves JW, Bailey KR, Sheps SG: The changing distribution of arm circumferences in NHANES III and NHANES 2000 and its impact on the utility of the “standard adult” blood pressure cuff. Blood Press Monit 2003;8:223–227.





FIGURE 6-10  Alternative noninvasive blood pressure monitoring devices. A, T-Line by Tensys Medical. B, Vasotrac by Medwave.



TABLE 6-7   -- Alternatives for Blood Pressure Monitoring



Arterial line

Time consuming


Technical problems with placement


Technical problems with monitoring


Some risk to patient

NIBP cuff placement on forearm

Usually reliable


Simple to use


Pulse pressure slightly wider than proximal placement

Vasotrac by Medwave

Relatively newer technologies

T-Line by Tensys Medical (see Fig. 6-10 )

Near continuous NIBP monitoring at the radial artery


Usually but does not always correlate with NIBP cuff or arterial line


Some technical problems with use. Precise placement over radial artery required.

NIBP, Noninvasive blood pressure.




When providing any anesthetic, our drug dosages are calculated based on well-established protocols, as well as “titration to effect.” In the obese patient, there is usually much more “titration” involved than in the lean patient. This variability in recommendations for drugs is not clarified by the lack of consensus in the literature concerning anesthetic drugs and their pharmacokinetics and pharmacodynamics. [45] [46] [47] [48] [49] [50] [51] [52] [53] Table 6-8 outlines several anesthetic drugs and their suggested dosing guidelines for obese patients.

TABLE 6-8   -- Dosage of Anesthesia Drugs


Dosage Based on:








Increase induction dose somewhat due to increased blood volume



Increase dose ∼10% relative to IBM. Larger volume of distribution

Volatile agents


No change in minimal alveolar concentration



Increased dosage expected, relative to IBM.




Titrate to effect



Titrate to effect (see text)



Increase dosage based on IBM due to ↑ plasma cholinesterase



Minimal data




Increase somewhat relative to IBM






Based on ABM or IBM






Increase dosage ∼10% relative to IBM

ABM, actual body mass; IBM, ideal body mass, LBM, lean body mass.




The following discussion of reference dosages is based on ideal body weight (IBW) in the obese patient. Because of the increased circulating blood volume, the volume of distribution is somewhat increased for the water-soluble drugs. Clearly, the volume of distribution for fat-soluble agents is significantly increased. However, the termination of effect and clearance is similar between the obese and lean populations. Owing to the higher levels of pseudocholinesterase in obese patients, the dosage of succinylcholine should be increased. Most nondepolarizing neuromuscular blockers should be dosed based on IBW. Mivacurium should be dosed based on IBW, but the dosage of pancuronium should be slightly increased. Interestingly, atracurium has a similar duration of action when dosed on either IBW or actual body weight.[54] Inhalation agents show no difference in minimal alveolar concentration (MAC). Because of the very low fat solubility of currently used agents, equilibrium is rapidly reached. Washout and emergence is not significantly different in the obese. Propofol dosing should be based on IBW with additional small dose titration. Recovery is similar to that in nonobese patients.[55]Thiopental induction dose should be increased somewhat.

Narcotic dosages are not well defined in obese patients, and administration should be altered judiciously, compared with a lean patient. Further clouding the situation, narcotics have significant interpatient variability. All narcotics should be titrated to effect.

Morphine is generally dosed based on IBM. Fentanyl dosage should be based on actual body mass.[51] Alfentanil has a reduced clearance and therefore a more prolonged half-life and should be dosed based on IBM, as should remifentanyl.[56]

The primary concern with narcotic use in the obese patient is postoperative respiratory depression. This concern, along with dosing uncertainty, often leads to poorly treated postoperative pain. This can lead to decreased mobility and deep breathing, which results in greater risk for deep vein thrombosis, atelectasis, and pneumonia. There must be a balance struck between the concern for respiratory depression and adequate postoperative pain control.

This degree of dosing uncertainty clearly illustrates the fact that there are multiple variable physiologic influences on anesthetic pharmacokinetics and pharmacodynamics. The suggested dosage adjustments in Table 6-8 are a reasonable starting point, but judgment and “titration” play a significant role in proper anesthetic drug administration.

Pickwickian Syndrome

This term was classically described as the combination of morbid obesity, hypersomnolence, plethora, and edema[57] and originated from a prominent literary character in Charles Dickens Oliver Twist. This condition is commonly referred to as “obesity hypoventilation syndrome” (OHS). Owing to the mass loading of their chest walls, these individuals have difficulty adequately ventilating their lungs, resulting in poor gas exchange. They are often hypoxic and hypercapnic when awake at rest and have secondary polycythemia. They often develop pulmonary hypertension and are more prone to right-sided heart failure in advanced stages. Some reserve the term pickwickian for OHS patients with signs of cor pulmonale.[19] The etiology for OHS is not well understood but is related to the combination of an alteration in the brain's control of ventilation and mechanical effects on the chest wall. Patients with OHS may also have concurrent OSA, but many do not. It does not appear that OSA is the direct cause for OHS, but it may contribute in some cases. [58] [59] Anesthetic implications are similar to those for the “ordinary” obese patient. These patients are more sensitive to the respiratory depression caused by narcotics and hypnotics. [60] [61] The added concern of hypoxia, hypercarbia, and potential pulmonary hypertension and right-sided heart failure warrants special attention. At a minimum, baseline arterial blood gas values are appropriate as reference points for later management. These patients are more likely to have perioperative cardiopulmonary problems, so invasive monitoring should be considered, not only for intraoperative management but also for postoperative care. Management of perioperative OHS patients should reference their baseline values and not the “normal” reference parameters.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier


This relatively recent term refers to several different undernourished states. As the name implies, there is a dietary deficiency in protein and/or caloric intake. There is a wide range of clinical presentations, depending on patient age, acuity, severity, duration, and concurrent diseases. There is significant overlap (especially with marasmus and kwashiorkor) regarding causes, presentation, treatment, and anesthetic implications.

Protein-energy malnutrition (PEM) can be “primary,” resulting from inadequate dietary intake, and is noted in developing countries and has multiple socioeconomic, political, and environmental causes. Secondary PEM is a result of decreased absorption or increased nutritional needs (as from acute or chronic illness) and is mainly seen in developed countries ( Table 6-9 ).[62]

TABLE 6-9   -- Representative Causes of Secondary Protein-Energy Malnutrition






Pancreatic insufficiency






Bacterial overgrowth



Gluten-sensitive enteropathy



Radiation enteritis



Intestinal ischemia



Assorted surgical alterations



Motility diseases



Increased needs









Altered appetite






Chronic illness












This discussion includes an overview of each of the various PEM syndromes. Deficiencies of specific amino acids are not discussed. For further details, the reader is referred to more in-depth sources. [62] [63] [64] [65] [66] [67]

Childhood Disorders


The term kwashiorkor originated from the GA language in western Africa and refers to the child who is weaned from breast feeding when another child is born. The result is the loss of often the only source of high-quality dietary protein. It is sometimes referred to as edematous PEM. Typically, kwashiorkor occurs when weaning or shortly thereafter. It occurs most often in tropical societies where the main dietary staple is carbohydrates with low protein content (cassava, yams). This is in contrast to that in temperate countries, where the staples are grains relatively rich in proteins. Very rarely, it has occurred in developed countries in cases of child neglect or misdirected dietary restrictions. At first glance, these children appear nourished, but they have a severe protein deficiency. They are colloquially referred to as “sugar babies” ( Fig. 6-11 ). These children's abdomens are distended not due to ascites but from edematous and distended intestine and an enlarged, fatty liver.


FIGURE 6-11  Kwashiorkor. This patient has a typical “sugar baby” appearance with generalized edema. Note the periorbital and limb edema.  (From Zitelli BJ, Davis HW: Atlas of Pediatric Physical Diagnosis, 4th ed. Philadelphia, Mosby, 2002, p 339.)



This disorder refers to a dietary deficiency of both protein and calories and is sometimes referred to as nonedematous PEM. These children's progressively starved appearance is one of emaciation with generalized muscle wasting. Later stages show virtually no subcutaneous fat and a face that appears withdrawn or “wizened,” with sunken eyes and hollow cheeks. This occurs mostly in areas of famine but can occur in developed countries in cases of child abuse and neglect ( Fig. 6-12 ). There are less severe cases of marasmus that are related to commercial formula feeding[68] and in hospitalized children undergoing treatment for other conditions. [69] [70]


FIGURE 6-12  Marasmus. Note the profound wasting and sparse hair.  (From Zitelli BJ, Davis HW: Atlas of Pediatric Physical Diagnosis, 4th ed. Philadelphia, Mosby, 2002, p 338.)


Marasmic Kwashiorkor

This refers to children exhibiting variable characteristics of both marasmus and kwashiorkor. The presentation is seen in children with an inconsistent diet that varies in protein and calories.

Refeeding Syndrome

This problem was first described in post-World War II victims of starvation. The logical thought was to provide a high-calorie, high-protein diet to these victims. What was not understood is “reductive adaptation,” which is an energy and nutrient conserving adaptive response by severely undernourished individuals. Unfortunately, severe gastrointestinal and metabolic derangements occurred, with many patients dying as a result of the best intentions. This is an ongoing problem today. These misconceptions are common in afflicted areas, which is the reason that the mortality rate from PEM has remained virtually unchanged for the past 50 years. [71] [72] The proper protocols are clearly outlined by the World Health Organization[73] and shown in simplified form in Table 6-10 . These patients often have renal and electrolyte abnormalities, so intravenous hydration must be closely monitored. Gradual and progressive introduction of increasing amounts of carbohydrates, micronutrients, fats, and protein into the diet turned out to be the proper approach. The gastrointestinal mucosa is not able to process the sudden appearance of large amounts of food and must first be gradually stimulated back to normal functional levels. Additionally, the “machinery” of cellular metabolism and physiology needs to be corrected before advancing the diet to make up for the nutritional deficiencies.[74] This concept applies both to enteral and parenteral nutrition. Cardiac dysrhythmias, heart failure, respiratory failure, liver and kidney functional derangements, coma, convulsions, and death can all occur with a too aggressive nutritional or intravenous treatment. A key concern with the refeeding syndrome is hypophosphatemia (and hypokalemia) and their sequelae.[75]

TABLE 6-10   -- Initial Clinical Management of Severe Malnutrition



Resuscitate Acutely



Treat fluid and electrolyte imbalance and shock: administer oxygen and glucose, reduce heat loss, give antibiotics, maintain circulation, treat vitamin A deficiency.






Control energy and protein intake at maintenance: 400 kJ/kg/day (10 kcal/kg/day), 1 to 1.5 g protein/kg/day.



Small frequent meals: eight meals every 3 hours or six meals every 4 hours throughout 24 hours.



Correct deficiencies of specific nutrients by addition to food: potassium (4 mmol/kg/day), magnesium (0.4 mmol/kg/day), folic acid (1 mg/day), zinc (2 mg/kg/day), copper (0.3 mg/kg/day), multivitamin supplement.



Treat bacterial infection: broad-spectrum antibiotics, cotrimoxazole or ampicillin with gentamicin.



Treat small bowel overgrowth with metronidazole.



Treat helminth infections with mebendazole.



Transfuse for severe anemia.



Topical treatment and care for skin lesions.



Exclude tuberculosis.



Give sensory stimulation and emotional support.



Weight Gain (Rapid Catch-Up Growth)



Ad libitum intake to achieve at least 600 kJ/kg/day (15 kcal/kg/day), 4 g protein/kg/day.



Continue with micronutrient supplements.



Add supplemental iron.



Give sensory stimulation and emotional support.

Modified from Management of the Child with Severe Malnutrition: A Manual for Physicians and Senior Health Care Workers. Geneva, World Health Organization, 1999.




Clinical Implications

Table 6-11 outlines a comparison of kwashiorkor and marasmus to help differentiate the disorders. Kwashiorkor is considered by some to be a subtype of marasmus, where the child has an underlying infection or other stress leading to a metabolic cascade.[76] This idea explains only some of the clinical overlap. It is important to understand the physiologic alterations and how to deal with them.

TABLE 6-11   -- Comparative Diagnosis of Kwashiorkor and Marasmus

Clinical Finding



General appearance

Not cachectic

Severe generalized wasting


May appear well fed

Late in course, face has sunken or “wizened” appearance due to loss of temporal, buccal and orbital fat pads


Can have pitting edema of lower extremities

Absent edema


Advanced cases involve edema of the arms and face




Normal until advanced, becoming minimal


Apathetic, irritable when disturbed

Irritable behavior initially



Listless when advanced


Dermatosis such as dyspigmentation and hyperkeratosis due to desquamation

Dry, loose skin due to loss of subcutaneous fat.



Absent turgor



Thin, sparse, brittle


Straight, dry and brittle



Color changes to red or gray



“Flag sign”: cyclical periods of poor and good nutrition that result in alternating bands of normal and abnormal hair



Protuberant due to edematous intestine and hepatomegaly due to fatty infiltration

Flat with intestinal pattern easily seen


No ascites



Normal or stunted depending on severity and duration

Normal for age in acute cases



Stunted in chronic or recurrent cases


Weight for age ∼70%

Weight for age <60%


Often involves some muscle wasting, but edema can be misleading

Very low weight to height ratio


May have weight loss, but often maintain weight

Significant muscle wasting

Vital signs

Not generally affected

Adaptive metabolic regulation resulting in poor thermoregulation, hypotension and bradycardia


Higher than marasmus

Lower than kwashiorkor


Treatment dependent (see text)

Treatment dependent (see text)



Preoperatively, these children must be nutritionally improved and it is vital that the refeeding syndrome be avoided. Problems concerning drug metabolism and distribution, myocardial, renal, and hepatic function, and electrolyte derangements are all highly unpredictable and place the child at extreme risk. Any sort of surgical procedure must be delayed, except in the direst of circumstances. Ideally, the child should be fed so as to eventually approach a “normal” height/weight ratio. Certainly, this is usually not a realistic option. There would be an improvement in outcome if the procedure could be delayed even some days while following the guidelines of the World Health Organization of resuscitation and stabilization. This will at least begin to repair some of the cellular metabolic derangements to improve the patients' physiologic responses to the anesthetic and surgical stresses. It is difficult to give any specific anesthetic management suggestions concerning the PEM child in the acute phase of the disorder. The plan and management must be highly individualized (taking into account the physiologic changes noted in Box 6-7 ) and to proceed only with patience, great reluctance, and extreme care.

BOX 6-7 

Physiologic and Metabolic Effects of Protein-Energy Malnutrition with Anesthetic Implications




Altered metabolic pathways



Depressed albumen production



Depressed plasma cholinesterase production

Altered drug redistribution (fat soluble)

Altered neuromuscular junction activity

Altered sensitivity to narcotics

Renal function in advanced stages:



Impaired fluid-electrolyte balance



Impaired drug excretion

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

Adult Disorders

Refeeding Syndrome

This topic has been discussed previously in detail. This syndrome must be taken into account in all forms of adult starvation. The principles and practice are equally applicable for both adults and children and bear no further discussion here.

Anorexia Nervosa and Starvation

Anorexia nervosa is a subtype of adult starvation. It is a psychiatric/emotional disorder of primarily adolescent and young women in wealthy societies. It occurs uncommonly in males. There are societal pressures emphasizing the idea that one needs to be thin to be attractive or worthwhile. Combined with a distorted body image,[77] affected individuals diet to the point of starvation ( Figure 6-13 ).


FIGURE 6-13  Anorexia nervosa.  (From “Fathers for Life,” www.fathersforlife.org)


Adult victims of starvation can come from different situations. They may have been prisoners or hostages, be engaged in hunger strikes, or, most often, live in an area with environmental, political, or socioeconomic upheaval. Prognosis is dependant on several variables.[78] However, there are two groups of patients with underrecognized states of malnutrition. One group is the elderly, who may be living independently in the community or in a nursing home and may be undernourished for varied reasons. [79] [80] Another group is the hospitalized patients, especially the elderly, with chronic medical conditions. [81] [82] [83] [84] [85] These patients' nutritional status and requirements are often not adequately considered or monitored when treating their underlying medical conditions.

Clinical Implications

Starvation entails a progressive increased use of body fat for metabolic fuel. In the first 12 to 24 hours after a meal, glucose use by muscle diminishes and fatty acid production and utilization increases. Ketone body levels in the plasma gradually become elevated over the first week, which then provides 70% of the energy to the brain. Glucose production drops significantly as fatty acid delivery to the liver increases. The net effect is to spare protein (and muscle) loss. Nevertheless, there is still a net negative nitrogen balance.[86] The body is also able to diminish energy requirements. After 7 days, the resting metabolic rate drops by 15% and, after 14 days, by 25%.[87]

In general, an adult human can withstand up to approximately a 40% decline below ideal body mass, at which point the patient will begin to systemically collapse and gradually die.[88] When the BMI falls to approximately 13 kg/m2, death is virtually certain.[89] Virtually all organ systems are affected, with infection often being the final step to death. Often, these patients have emotional and psychiatric concerns with which we need to deal, particularly with anorexia nervosa, former prisoners and famine victims. As mentioned, whenever possible it is prudent to delay a surgical procedure until the patient's nutritional status can be improved. A severely malnourished patient undergoing an emergent surgical procedure has a significantly increased morbidity and mortality, related both to surgical and anesthetic concerns. It is vital to avoid the refeeding syndrome because such a patient is at even greater risk than in their malnourished state alone.

These surgical patients have virtually no metabolic reserve. The patient may survive the surgery but could die immediately postoperatively as a result of stress. Wound healing or a simple infection may metabolically demand more then can be delivered by the severely undernourished patient. [88] [90]

There is evidence that the heart is not “spared” protein loss. There may be unsuspected myocardial atrophy with concurrent risk for arrhythmia and heart failure, [91] [92] [93] particularly when fluids are not administered cautiously.

As with children, in adults suffering severe malnutrition with an immediate surgical need it is very difficult to give specific recommendations concerning an anesthetic. It is of paramount importance to take into account the physiologic changes inherent with starvation states.

Some general suggestions include assessing the situation on a case-by-case basis. One needs to evaluate the degree and duration of undernutrition and assess the degree of organ dysfunction, particularly cardiac. [91] [92] [93] Renal and liver function should be assessed by laboratory studies of albumen, liver enzymes, blood urea nitrogen, and creatinine. We also need to investigate the degree of electrolyte abnormalities, particularly potassium and phosphorus.

Serum protein and albumin levels are decreased, but albumin levels are a more reliable and sensitive indicator of protein nutritional status. In tropical and subtropical populations with known inadequate protein intake, individuals may have normal total serum protein levels.[94] It is generally accepted that a serum albumin level below 3 g/dL or a transferrin level below 200 mg/dL indicates severe protein malnutrition.

With therapeutic diets, specific serum transport proteins improve more rapidly than serum albumin. This is due to the shorter half-lives of these proteins. It is unclear if measurements of these proteins are superior to albumin for the detection of inadequate dietary protein. [95] [96]

Bulimia Nervosa

This condition has a similar etiology to anorexia nervosa but presents differently. These individuals (usually in young women, with a peak incidence at age 20 years) usually appear well nourished but alternate between binge eating and vomiting. They often have primarily a psychological disorder involving self-image, obsessive-compulsive behavior, and depression. They may abuse laxatives and diuretics. There are fewer physiologic concerns than with anorexia nervosa. There may be esophageal erosions from gastric acid and diminished gastroesophageal sphincter tone, which predisposes to pulmonary aspiration. There is a greater likelihood of having metabolic and electrolyte derangements from excessive vomiting and diuretic use when compared with anorexia nervosa.

Obese Starvation

Overweight and obese patients may go on an unsupervised starvation or semi-starvation diet with unexpected complications. This sort of diet can produce rapid weight loss, but numerous vital nutrients may not be ingested. This can result in an undernourished yet obese patient. Significant deficiencies of multiple vitamins and minerals can develop, with special attention to copper, potassium, and magnesium. A deficiency of these three minerals may play an especially important roll in promoting an electrically unstable heart, particularly in patients with prolonged QT intervals on an electrocardiogram. Stress from any source can create an autonomic imbalance, which can then lead to arrhythmias and potentially sudden death.[93] Properly supervised and supplemented diets of this type can result in significant and safe weight loss.[97]

Micronutrient Disorders

Vitamins and minerals are highly varied in biochemical and physiologic function. They are involved in complex interactive metabolic pathways, such as carbohydrate and protein metabolism, hormone production and regulation, as well as “routine” physiologic functioning, such as neural impulse propagation or oxygen utilization in the tissues. Because of the complexity of human biochemistry and physiology, only the primary clinical implications of essential micronutrient derangements are discussed here. More in-depth information can be found in the referenced sources.

The four fat-soluble vitamins (A, D, E, and K) can be stored in significant quantities, so a dietary deficiency may not manifest clinically for up to 1 year. The water-soluble vitamins have minimal body storage (except cyanocobalamin vitamin B12) and can manifest a deficiency in a matter of weeks. The water-soluble vitamins are absorbed directly into portal blood (compared to the fat-soluble vitamins) and are excreted in the urine when plasma levels rise.

It is unusual to have isolated micronutrient abnormalities. Deficiencies often happen in concert with other micronutrient deficiencies to varying degrees, along with macronutrient deficiencies of starvation syndromes. Virtually all micronutrients are ubiquitous in foodstuffs, the result being that clinically significant deficiencies are virtually nonexistent, except in specific circumstances. Deficiencies can occur in people on unusual or highly restrictive diets but more commonly in debilitated or hospitalized patients on prolonged inappropriate total parenteral nutrition (TPN). Certain malabsorption syndromes have been implicated ( Table 6-12 ), as well as drug-mediated deficiencies ( Table 6-13 ).

TABLE 6-12   -- Malabsorption Syndromes Associated with Micronutrient Deficiencies




Vitamin B12, vitamin D, iron, calcium

Short bowel syndrome

 Ileum resection

Iron, multiple water-soluble vitamins and minerals

 Jejunum resection including duodenum

No clinically relevant deficiencies


Vitamin B12 and folate


Impaired fluid and minerals especially electrolytes

Decreased bile production

All fat-soluble vitamins

Rapid transit/diarrhea

Often minimal sequelae

Ulcerative colitis

Severe disease results in electrolyte abnormalities

Crohn's disease


Sprue/gluten intolerance

Tropical sprue

Vitamin B12 and folate

Bacterial overgrowth

Vitamin B12 (normal folate)


Fat-soluble vitamins



TABLE 6-13   -- Drug-Mediated Effects on Micronutrients





Vitamin B12

Impairs absorption


Pyridoxine (B6)

Impairs utilization, not absorption


Vitamin D, folate

Binds in gut, impairing absorption



Increases renal excretion



Decrease absorption and blocks dependent enzymes



Micronutrient excess is virtually always the result of excessive nutritional supplementation. This presents no problem with most micronutrients, because excess amounts are readily excreted. Exceptions are iron, the fat-soluble vitamins (A, D, E, K), or patients with liver or renal insufficiency/failure.

For simplicity, the minerals calcium, magnesium, and phosphorus are included in the topic of “micronutrients,” even though they are often ingested in gram and multiple-gram amounts.

Fat-Soluble Vitamins

Vitamin A.

Sources of this vitamin include animal (dairy, liver, fish) and plant (particularly red, orange, and yellow colored). This vitamin is involved in several functions, such as vision, epithelial differentiation, bone development and growth, immune functions, and reproduction. Vitamin A can be stored in the body for up to 1 year, but deficiencies can occur, especially in undernourished children younger than the age of 5 years. Children can develop poor visual dark adaptation, xerosis, and keratomalacia. Adults may have night blindness. Anorexia, skin erythema, and desquamation occurs, as can hepatomegaly and reproductive problems. [98] [99] [100] Toxicity can present as anorexia, desquamation, ataxia, conjunctivitis, and alopecia. Liver problems include hepatomegaly, portal hypertension due to venous sclerosis and congestion, and cirrhosis. There is also a link between maternal oversupplementation and teratogenicity. [101] [102] [103] [104] [105] Deficiency or toxicity is suggested by a thorough history. The presence of Bitot spots is suggestive of a deficiency. Plasma retinol levels can be performed, along with several other tests. [106] [107] [108] [109] [110]

Vitamin D.

This vitamin is produced with skin exposure to sunlight. People at risk for deficiency would include anyone with little exposure to sunlight (elderly, northern climates, sun sensitivities, and newborns) and in people with fat malabsorption syndromes. Vitamin D is involved in bone growth and development and is vital in the absorption of calcium and phosphorus from the intestine. A deficiency can result in hypocalcemia and in children can present as rickets. Adults can present with brittle bones and joint problems. [111] [112] [113] [114] [115] [116] [117] Toxicity due to excessive sun exposure does not occur due to cutaneous photochemical autoregulation.[118] In infants, toxicity presents with anorexia, failure to thrive, nausea and vomiting, hypertension, hypercalcemia, and renal insufficiency. Adults present additionally with soft tissue calcification of the kidney and heart, hyperphosphatemia, weakness, polyuria, polydipsia, and occasionally death. There is no readily available direct assay to assess vitamin D status. [119] [120] Clinical history is central, along with an index of suspicion. Elevated plasma alkaline phosphatase released from osteoclasts is suggestive of preclinical rickets. The plasma concentration of calcidiol is possibly an indirect indicator of vitamin D body levels. Individuals with low levels of vitamin D will typically have an elevated parathyroid hormone level. These tests are of limited reliability or specificity.

Vitamin E.

Sources of this vitamin include a wide variety of both plants and animals, with vegetable oils being the richest source. Deficiencies are therefore unusual. Vitamin E is an antioxidant. As such, it is centrally involved in cell membrane repair and maintenance, possibly adding mechanical stabilization. All membranes are susceptible to oxidation, particularly the mitochondria and endoplasmic reticulum. Tissues most susceptible include the erythrocytes, lung, and brain. Deficiencies are extraordinarily rare but can occur in certain fat malabsorption syndromes (e.g., cystic fibrosis), chronic cholestasis, premature infants, and the genetic disorder abetalipoproteinemia. Symptoms include ataxia, renal degeneration, hemolytic anemia, generalized weakness, retinal degeneration, ataxia, and other neurologic dysfunctions.[121] Toxicity is unusual, even with massive supplemental intake. [122] [123] There are reports of muscle weakness, diplopia, and gastrointestinal distress. [123] [124] [125] Toxicity can also present by interference with the function of other fat-soluble vitamins.[124] There is no accurate method to assess vitamin E levels in the body. There are several methodologies, which have little clinical application.

Vitamin K.

A significant amount of this vitamin is produced by colonic bacteria and is passively absorbed. Bacterial production was thought to be generally adequate for human needs, but this concept has been brought into doubt. [126] [127] Dietary sources include vegetable oils, green leafy vegetables, and some legumes. Animal sources provide a poor to fair source. Slight intestinal absorption is facilitated by bile and pancreatic enzymes. Vitamin K is required for the proper formation of vitamin K-dependent clotting factors II (prothrombin), VII, IX and X, which are produced in the liver. Vitamin K is central for blood coagulation and clotting. A deficiency interferes with the intrinsic and extrinsic pathways of fibrinogen activation into fibrin. There are four other vitamin K-dependent clotting proteins, whose roles are less clearly understood.[128]

Human deficiencies are rare but can occur in trauma, in patients in intensive care units, and in people on chronic antibiotic therapy (decreased bacterial flora). Newborns are particularly at risk because their colonic flora is not yet developed and their diet consists of milk, which is low in vitamin K. [128] [129] The primary clinical problems associated with vitamin K deficiency concerns impaired clotting and is suggested by a prolongation of prothrombin time. Coagulation and clotting times are prolonged with a risk of excessive surgical and trauma blood loss. There are unique issues with enclosed areas such as the epidural, intracranial, and pericardial spaces. There are also concerns with demineralization of bone.[130]

Toxicity from excessive supplementation of the natural form of vitamin K (phylloquinone) has not been described, owing to efficient metabolism. However, when infants have been given an excess of the synthetic form (menadione), hemolytic anemia, hyperbilirubinemia, and jaundice have been described.[123] Measurement of prothrombin time is nonspecific and merely suggestive of vitamin K status. More specific measurements are available but of limited practical use. [129] [131]

Water-Soluble Vitamins

Vitamin C (Ascorbic Acid, Ascorbate).

Primates, including humans, are some of the few animals not able to synthesize vitamin C. Nutritional sources include citrus and other assorted fruits and vegetables. Vitamin C is involved in the synthesis or metabolism of collagen, carnitine (fat metabolism), tyrosine (amino acid), and neurotransmitters (norepinephrine, serotonin), among other substances.[132] Additionally, it has a role as an antioxidant and is thought to be beneficial in assorted disease states, such as the common cold, cancer, cardiovascular disease, and others. [133] [134] [135] [136] [137] A deficiency can result in scurvy, which manifests as problems related to imperfect collagen metabolism. Common findings include bleeding gums, loose teeth, arthralgia, easy bruising, and poor wound and fracture healing. Rare in developed countries, it can occur in people with poor diets, such as alcoholics and the elderly. Toxicity can occur when dosages are well in excess of 1 g/day and can manifest as osmotic diarrhea and kidney stones. [138] [139]

Vitamin B1.

Thiamine is found in many different foods, but particularly rich sources include meat, legumes, yeast, and wheat germ. Thiamine is involved in energy transformation pathways, membrane maintenance, and nerve conduction. [140] [141] A deficiency can result in one of three forms of beriberi. Dry beriberi occurs in older adults with a chronic low intake and manifests with muscle weakness and wasting. Wet beriberi results in more extensive cardiovascular involvement, such as right-sided heart failure. Acute beriberi occurs primarily in infants. Thiamine deficiency is often associated with alcoholism and is due to poor diet, increased liver requirements due to liver damage, and decreased absorption. Alcoholics manifest Wernicke's encephalopathy characterized by ataxia, ophthalmoplegia, nystagmus, short-term memory loss, and confusion.[142] Massive intravenous or intramuscular doses can lead to headache, convulsions, and cardiac arrhythmias. [143] [144] [145]

Vitamin B2.

Riboflavin is widely found in different foods, particularly animal sources. It is involved in a wide variety of oxidation-reduction pathways, particularly the electron transport chain, pyruvate decarboxylation, fatty acid oxidation, monoamine oxidase synthesis, and others. There is no distinct disease associated with riboflavin deficiency. Some symptoms include photophobia, glossitis (magenta tongue), dermatitis, peripheral neuropathy, mouth edema, and perioral skin lesions. Toxicity has been described only under experimental conditions.[146]

Vitamin B3.

Niacin is found in many animal sources, as well as grains and legumes. There is a multitude of enzymes (mainly dehydrogenases) in which niacin is involved. Particularly, niacin is involved in the electron transport chain, fatty acid, cholesterol, and hormone metabolic pathways. A deficiency results in pellagra, classically described by the four Ds of dementia, dermatitis, diarrhea, and death. A deficiency can result from use of the antituberculosis drug isoniazid and from malabsorption syndromes. Toxicity is not well described. The nicotinic acid form of the vitamin is used in very large doses (over 3 g/day) to treat hypercholesterolemia. There are several side effects, including excessive histamine release, decreased bile flow, hepatic injury, dermatitis, and elevation of plasma glucose level. [138] [147]

Vitamin B6.

Vitamin B6 has several different forms. Pyridoxine is found primarily in plant foods, but the other forms are found in plant and/or animal sources. Vitamin B6 is involved in a large number of enzyme systems, primarily amino acid metabolism and glycogen catabolism. A deficiency can occur in select groups: the elderly with poor nutrition, alcoholics, hemodialysis patients, and patients taking certain medications (isoniazid, penicillamine, and corticosteroids). Findings of vitamin B6 deficiency include somnolence, fatigue, glossitis, stomatitis in adults, and seizures in infants. [148] [149] [150] Also seen is hypochromic, microcytic anemia due to deranged heme synthesis. Mega-dosing of vitamin B6 has been suggested for the treatment of several disorders, such as atherosclerosis, autism, and depression. While there has been some success, there are some toxic risks, such as neuropathy resulting in paresthesias, unsteady gait, and numb hands and feet. [123] [138] [151]

Vitamin B12.

All dietary cobalamin is produced by bacteria and obtained almost exclusively from animal sources. One exception is legumes, where the cobalamin is produced by nitrogen fixing bacteria.[152] Cobalamin is involved in amino acid metabolism and the Krebs cycle.

Nitrous oxide has been shown to interfere with cobalamin function. Patients who are cobalamin deficient and undergo a nitrous oxide anesthetic may manifest an acute deterioration of nervous system function. [152] [153] [154]

Cobalamin deficiency can result from a strict vegetarian (vegan) diet, but usually only after 1 and up to 20 or more years, owing to adequate body stores and minimal excretion.[155] Most cases occur from poor absorption rather then inadequate dietary intake. Megaloblastic macrocytic anemia can result with a gradual onset. The anemia can be abated by giving large doses of folate, but the neurologic impairment is caused by gradual demyelination and will not be improved by folate administration. The neurologic deficit is probably related to diminished vitamin B12-dependent production of methionine.[156] There is no direct clinical measure of an individual's cobalamin level.

Pantothenic Acid.

This vitamin is widely found in virtually all foodstuffs. In fact, the Greek term pantos translates as “everywhere.” Pantothenic acid is integral to the structure of coenzyme A, which is central for energy metabolism in the Krebs cycle and assorted other metabolic pathways. Deficiency occurs only in severely malnourished individuals and can present as vomiting, fatigue, weakness, and the “burning feet syndrome.” Toxicity has not been described.[157]


This vitamin was at one time known as vitamin H. Biotin is widely available in most foods and is also produced by colonic bacteria. Raw egg whites can bind to biotin and prevent its absorption. It is important in several metabolic pathways, such as the Krebs cycle, metabolism of fatty acids, and certain amino acids. Deficiency presents as several nonspecific features, such as anorexia, alopecia, dermatitis, hallucinations, and muscle pains. Toxicity has not been described.[158]

Folic Acid.

Folate is found in green vegetables, legumes, and liver. Fruits and meats are poor sources. Folate is a component of amino acid metabolism and is involved in purine and pyrimidine synthesis. There is a synergism between folate and vitamin B12 whereby the availability of vitamin B12 frees up the “trapped” metabolite of folate. A deficiency of folate can manifest as megaloblastic anemia after several months, and megaloblastic anemia due to vitamin B12 deficiency manifests after a much longer period. As mentioned in the discussion of vitamin B12, this sign can be masked by large doses of folate. Toxicity is difficult to accomplish[159] but can present as insomnia, malaise, irritability, and gastrointestinal symptoms.


The micro and macro minerals are outlined in Table 6-14 . Most minerals are found in all foods to varying degrees, and most diets result in adequate intake. In undernutrition states, most individuals have adequate body reserves for most circumstances. Under these conditions, low total body levels of any mineral are relatively unimportant compared with the issue of PEM. In other words, the consequences of PEM usually manifest prior to any mineral deficiency. Toxic levels of dietary minerals do not occur, except under conditions of renal dysfunction.

TABLE 6-14   -- Microminerals and Macrominerals



Primary Functions

Deficiency Findings



Dairy, sardines, dark green leafy vegetables, legumes

Bone and teeth structure


Acutely can result in hypercalcemia



Muscle contraction





Blood clotting





Multiple regulatory enzyme pathways






Chronic hypertension and colon cancer



Legumes, nuts, grains, soybeans, seafood

Bone physiology

Usually only seen in alcoholism or renal disease

Seen only in renal disease



Protein metabolism

Depression, tetany, muscle weakness, nausea, convulsions

Nausea, weakness, depression, double vision, slurred speech



Nerve impulses





Multiple enzymes




Meat, fish, eggs, dairy, legumes, nuts, grains

Bone physiology, especially energy cell utilization membranes







Seen only in infants taking phosphorus-fortified formulations









Neuromuscular abnormalities





Skeletal and hematologic abnormalities



Table salt, meat, seafood, dairy, most vegetables, grains

Cellular electrical activity, especially neural


Seen only in renal disease


Poor source: fruit

Muscle contraction











Muscle atrophy



Fresh and dried fruit, especially bananas, potatoes, beans, dairy

Cellular and electrical activity, especially neural

Does not happen from dietary deficiencies

Seen only in renal patients or iatrogenic




Occurs due to disturbance

Intractable cardiac arrhythmias




Muscle weakness, apathy, confusion, cardiac arrhythmias



Table salt, meat, seafood, dairy, most vegetables, grains

Primary anion: maintains electrical neutrality, pH balance

Anorexia, weakness, metabolic acidosis, lethargy



Poor source: fruit





Meats, dairy, legumes, nuts

Component of sulfur-containing amino acids and assorted metabolic pathways




Seafood, liver eggs, iodized salt

Thyroid hormone synthesis

Cretinism (children), myxedema, goiter

None known


Organ meats, shellfish, nuts, legumes, green leafy vegetables

Critical for formation of hemoglobin and myoglobin

Lethargy, fatigue, anemia, dysphagia angular stomatitis




Cytochrome function




Meats, whole grains, wheat germ

Enzymes in pathways involving energy metabolism, protein and collagen synthesis

Poor wound healing

Nausea/vomiting, abdominal cramps, bloody diarrhea




Diminished growth





Hair, nail, and skin changes



Organ meat, shellfish, whole grains, eggs, legumes

Synthesis of neurotransmitters, collagen, and lipid

Anemia, bone problems, hair and nail abnormalities




Facilitates iron utilization














Fish, meat, grain legumes

Bone and teeth maintenance

Dental caries





Bone fractures

Cardiac arrhythmia



Deficiencies can occur in long-term patients in intensive care units. These individuals are under immense physiologic stress, requiring large amounts of assorted minerals, particularly magnesium. Often, these hospitalized patients have poor or no enteral intake and are frequently receiving incomplete enteral or parenteral supplementation.

Of special note are the assorted nutritional supplements that are taken by increasing numbers of patients. Many of these mineral supplements have no direct impact on our care. However, other supplements are not purely “mineral supplements.” Herbal supplements often claim to help a variety of patient concerns, such as preventing osteoporosis in perimenopausal women. Some of the other ingredients in many “natural” supplements may pose an anesthetic risk. [160] [161] [162] [163]

The topic of “minerals” overlaps the topic of cellular physiology, electrolytes, and their homeostasis. Table 6-14 references primarily nutritional concerns. Discussions concerning electrolyte balance and physiology or causative disease states are more appropriately addressed in relevant internal medicine, biochemistry, and physiology texts.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier


Obesity presents a complex anesthetic challenge. The degree of obesity, comorbidities, and management issues are variable and interrelated. Associated medical and management concerns must always be considered, despite a negative history. Alternately, not all obese patients have coexisting diseases such as hypertension, diabetes, difficult airway, and so forth. Vigilance is particularly relevant in this population group.

A patient with severe PEM presents his or her own set of unique challenges. The “take-home” point is that the complexity and extraordinary degree of metabolic uncertainty are associated with profound management challenges. Due to the highly variable and unpredictable nature of these derangements, management must be highly individualized, with flexibility and vigilance being the cornerstone. Micronutrient abnormalities seldom present as isolated entities, due to the fact that most micronutrients are found in a wide variety of foods. Occasionally, isolated deficiencies occur under specific circumstances, such as with unusual and restricted diets. In developed societies, micronutrient deficiencies occur most frequently in elderly, debilitated patients with prolonged hospitalizations. In less developed societies, micronutrient deficiencies occur most commonly as a result of PEM, but they are often not recognized owing to the overriding issues of PEM. Micronutrient toxicity may present in cases of renal insufficiency or when consuming very large amounts of a particular food, but generally it occurs only with excessive supplementation.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier


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