Complications

Malnutrition

Weight loss and malnutrition are the most prevalent nutritional disturbances in patients with IDB.103 Approximately 85% of children with Crohn's disease have a history of weight loss at initial diagnosis.127 Malnutrition is mainly due to decreased intake caused by either primary anorexia from proinflammatory cytokines, or intestinal inflammation. An active inflammatory process, especially associated with fever, may further increase the body's caloric consumption.

Estimates suggest that an increase in 1°C increases the metabolic rate by 7%. For this reason, children with Crohn's disease who experience recurrent febrile episodes often need to receive additional calories.

As the result of the location of chronic intestinal inflammation in Crohn's disease, a variety of micronutrient deficiencies may occur. These deficiencies include water-soluble vitamins (mainly folic acid and vitamin B12), fat-soluble vitamin D, and minerals (iron, copper and zinc).103 Deficiency of these micronutrients may be subclinical or associated with specific clinical signs and symptoms (Table 23.4). The following factors may create or potentiate specific nutrient deficiencies: inadequate intake, the inflammatory/immunological response, poor absorption, increased nutrient demand for tissue repair or concurrent usage of specific medications. The severity of nutrient deficiency is often associated with the duration of disease and the degree of Crohn's disease activity.

Hepatobiliary and pancreatic complications

Bile salts are absorbed in the distal ileum via an enterohepatic circulation. Malabsorption of bile salts caused by ileal inflammation or resection results in increased colonic bile salts and diarrhea. Bile salt malabsorption also may predispose towards gallstone formation. Agents that bind bile acids may be beneficial in these clinical situations.

Table 23.3 Extraintestinal manifestations of Crohn's disease

Presentations

Percentage

Reference

Joint

arthritis/arthralgia

2*, 15 (adult data)

126

Skin

erythema nodosum

1*, 8-15 (adult data)

18, 125

pyoderma gangrenosum

0.5*, 1.3 (adult data)

Eye

episcleritis

125, 126

uveitis

orbital myositis

Hepatobiliary involvement

3*

18

PSC

<1*

Pancreatitis

1*

18

* At time of diagnosis. PSC, primary sclerosing cholangitis

Table 23.4 Micronutrient deficiencies

Clinical

Micronutrient Prevalence

presentations

Laboratory test

RDA

Reference

Water-soluble vitamins

Vitamin B12 20-60%

macrocytic

plasma vitamin B12

1.5-3 |ig for

168

anemia,

level

children;

169

neuropathy

3 |ig for adults

170

Vitamin C *

scurvy (ecchymoses,

plasma vitamin C

40-45 mg for

171

gingival bleeding,

level

children

172

petechiae,

60-125 mg for

173

hyperkeratosis,

adults

174

arthralgia, poor

wound healing

Folate 34-54%

macrocytic anemia

plasma folate level

200-400 |lg for

127

children;

168

400 |ig for adults

175

Thiamine *

beriberi-like

erythrocyte thiamine

0.9-1.5 mg for

122

(vitamin B-|)

symptoms

transketolase (ETKA),

children;

169

(neuropathy,

or blood thiamine

1-1.4 mg for

cardiomyopathy,

concentration, or

adults

encephalopathy,

transketolase urinary

gastrointestinal

thiamine excretion

symptoms)

Nicotinic acid *

pellagra

? plasma nicotinic

12-20 mg for

122

(dermatitis,

acid level

children and

169

diarrhea and

adults

176

dementia)

177

Riboflavin (B2) *

photophobia,

plasma riboflavin

0.4 mg for infants;

122

angular

level

1.1-1.8 mg for

169

stomatitis,

children and adults

177

dermatitis

178

Pyridoxine *

neuropathy,

plasma pyrodoxal-5-

0.9-2 mg for

122

(vitamin B6)

glossitis,

phophate (PLP) level,

children;

169

dermatitis

or erythrocyte

2 mg for adults

178

transaminase activity,

or urinary 4-pyridoxic

acid excretion, or

urinary excretion of

xanthurenic acid

Fat-soluble vitamins

Vitamin A 11%

xerophthalmia

plasma retinol level

2500-4000IU

171

(dry eyes and skin,

for children;

172

blindness)

4000-5000IU

179

for adults

180

181

Vitamin D 75%

osteomalacia, rickets

plasma vitamin D level

400IU for

122

children and adults

182

Vitamin E *

neuromuscular

plasma vitamin E level

9-15 IU for

171

disorders, hemolysis

children and 30IU

172

and anemia

for adults

173

Vitamin K *

bleeding diathesis

20-80 |ig for

168

children; 65-80 |ig

for adults

continued

Table 23.4 continued Micronutrient deficiencies

Clinical

Micronutrient Prevalence

presentations

Laboratory test

RDA

Reference

Minerals

Calcium 13%

osteopenia, rickets

plasma calcium level

800-1200 mg

168

for children

173

and adults

Copper *

skin and hair

plasma copper level

0.4-0.6 mg for

183

abnormalities

infants; 1.5-3mg

for children and

adults

Iron 39-81%

microcytic anemia

plasma iron level

10-18mg for

168

children and adults

184

Magnesium 14-33%

myopathy

plasma magnesium

200-400 mg for

122

level

children;

168

300-350mg for

169

adults

185

186

187

Selenium *

cardiomyopathy,

plasma selenium level

20-50 |ig for

173

encephalopathy,

children;

188

immune dysfunction

55-70 |lg for

189

adults

190

191

Zinc 40-50%

growth retardation,

plasma zinc level

10-15 |ig

122

alopecia, dysgeusia,

for children;

168

acrodermatitis,

15 mg for adults

192

impaired wound

193

healing

* Not specified

RDA, recommended daily allowance

Pancreatitis can occur as a result of inflammation in the duodenum or by medications such as azathioprine, 6-mercaptopurine or 5-aminosali-cylic acid.103 In some patients, the cause of pancreatitis is unknown and may be recurrent. Pancreatic insufficiency and carbohydrate intolerance are rare in Crohn's disease, but a trial of pancreatic enzyme supplementation may be beneficial in treating inflammation.

Nephrolithiasis

Patients with Crohn's disease have an increased risk of developing calcium oxalate and uric acid renal stones as a result of chronic steatorrhea and diarrhea. Under normal circumstances, free dietary calcium binds to oxalate in the intestinal lumen and is eliminated in the stool. In patients with steatorrhea, increased luminal fatty acids competitively bind free dietary calcium and leave oxalate free to be absorbed. The increased oxalate absorption results in hyperoxaluria. Dehydration and metabolic acidosis potentiate the formation of uric acid stones.

Thromboembolic events

Venous and arterial thromboembolism can result from hypercoaguability caused by thrombocytosis, hyperfibrinogenemia, elevated factor V and factor VII, and depression of antithrombin III.128,129 A retrospective study by Talbot et al in 7199 adult patients with either chronic ulcerative colitis or Crohn's disease demonstrated that thrombo-

embolic complications developed in 92 (1.3%) of these patients.130 An additional four patients had cutaneous vasculitis, and 17 had an arteritis-asso-ciated diagnosis. Of the thromboembolic complications, 61 were deep vein thromboses or pulmonary emboli.130 Peripheral arterial thrombosis, coronary thrombosis, and mesenteric and portal vein thrombosis were predominantly post-surgical complications, but 77% of peripheral venous thromboses occurred spontaneously.130,131 In isolated case reports, cerebrovascular accidents have occurred in children with Crohn's disease with seizures being the primary presenting symptom.132-134 Retinal vascular disease can also occur in patients with Crohn's disease.129,135,136 Children with clinical evidence of a hyperco-aguable state should be evaluated for underlying causes. Dehydration and indwelling catheters are the main risk factors that should be avoided.

Metabolic bone disease

Decreased bone density is an important and probably underdiagnosed complication in children with Crohn's disease. Multiple factors, including inflammatory cytokines that inhibit osteoclast activity, vitamin D deficiency and chronic systemic steroid therapy, may contribute to osteopenia or osteoporosis. Therefore, in children with Crohn's disease, it is crucial to assess bone density and decrease the risk factors for osteoporosis such as lack of physical exercise, chronic steroid use, lack of hormonal therapy of chronic secondary amenorrhea in adolescent girls, and deficient calcium and vitamin D supplementation.103 Bisphosphonates are synthetic analogs of inorganic pyrophosphate that inhibit bone resorption (Table 23.5). In a recent randomized study of 84 adult patients with Crohn's disease and osteopenia/osteoporosis, the efficacy of ibandronate and sodium fluoride as adjuncts to calcium and vitamin D treatment was evaluated.137 The results showed that both ibandronate and sodium fluoride were effective, safe and well tolerated in inducing an increase in lumbar bone density.137 Experience is very limited with bis-phosphonate therapy in children who have metabolic bone disease associated with Crohn's disease. Results from ongoing multicenter trials of bis-phosphonate in children with Crohn's disease will provide valuable information.

Local intestinal complications

Intestinal obstruction, severe hemorrhage, perforation, fistulae, intra-abdominal abscesses and toxic megacolon can occur as a result of chronic intestinal inflammation. Mucosal ulceration may result in bleeding and perforation depending on the site and size of the ulcer. Fibrosis, a complication of inflammation, may result in stricture formation that

Table 23.5 Bisphosphonate preparations

Preparations

Potency within generation

Potency across generation

First generation

low

Etidronate

Second generation

high

Pamidronate

Clodronate

Tiludronate

low

Third generation

high

Zolendronate

Ibandronate

Risedronate

Olpadronate

Alendronate

Neridronate

Incadronate

low

high

predisposes the patient to fistula, abscess, obstruction and perforation. In contrast to fibrosis, which usually accompanies Crohn's disease, perforation and toxic megacolon are unusual and most commonly associated with ulcerative colitis. These conditions may require surgical intervention.

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