Crohn’s Disease: Complications

The following are the most important diseases or complications that may be contributed to by Crohn’s disease:

Respiratory system (J00-J99)

  • Fibrosing alveolitis – disease of the lung tissue and alveoli (air sacs).

Eyes and eye appendages (H00-H59).

Blood, blood-forming organs – immune system (D50-D90).

Endocrine, nutritional and metabolic diseases (E00-E90).

  • Amyloidosis – extracellular (“outside the cell”) deposits of amyloids (degradation-resistant proteins) that can lead to cardiomyopathy (heart muscle disease), neuropathy (peripheral nervous system disease), and hepatomegaly (liver enlargement), among other conditions.
  • Hyperoxaluria – too high blood oxalate levels with the possible consequence of urinary stones.
  • Cachexia – extreme emaciation

Skin and subcutaneous (L00-L99)

  • Erythema nodosum (synonyms: nodular erythema, dermatitis contusiformis, erythema contusiforme; plural: erythemata nodosa) – granulomatous inflammation of the subcutis (subcutaneous fat), also known as panniculitis, and painful nodulation (red to blue-red color; later brownish). The overlying skin is reddened. Localization: both lower leg extensor sides, on the knee and ankle joints; less frequently on the arms or buttocks.
  • Psoriasisform phenomena (therapy-induced).
  • Pyoderma gangraenosum – painful disease of the skin in which there is ulceration or ulceration (ulceration or ulcer) and gangrene (tissue death due to reduced blood flow or other damage) over a large area, usually in one place.
  • Zinc deficiency dermatitis

Cardiovascular system (I00-I99)

  • Perimyocarditis (inflammation of the heart muscle).
  • Thrombosis
  • Deep vein thrombosis (DVT; patients < 40 years of age have a two-and-a-half times increased risk) → Pulmonary embolism

Liver, gallbladder, and bile ducts-pancreas (pancreas) (K70-K77; K80-K87).

  • Cholangitis (bile duct inflammation).
  • Cholelithiasis (gallstones)
  • Chologenic diarrhea (bile acid-induced diarrhea) (caused by bile acids that are no longer reabsorbed due to omission of the ileum; these lead to increased motility in the colon (large intestine) and at the same time inhibit fluid and electrolyte absorption) [in condition after ileum resection/surgical removal of parts of the small intestine].
  • Bile acid loss syndrome (disease in which there is a functionally relevant deficiency of bile acids leading symptoms: chologene diarrhea (bile acid-related diarrhea), steatorrhea (fatty stools); secondary diseases; maldigestion (insufficient splitting of food components), possibly also cholesterol gallstones and oxalate kidney stones) [in condition after ileum resection / surgical removal of parts of the small intestine]
  • Pancreatitis (inflammation of the pancreas).
  • Steatosis hepatis (fatty liver)

Mouth, esophagus (esophagus), stomach, and intestines (K00-K67; K90-K93).

  • Anorectal fistulas – tubular ducts originating from the anus that generally do not heal spontaneously.
  • Abscess formation
  • Dysbiosis (imbalance of the intestinal flora)
  • Fistulas (tubular connecting ducts between organs) – to other intestinal loops (enteroenteral; enterocolic), vagina (rectovaginal), bladder (rectovesical) and to the skin (enterocutaneous) and perianal (“around the anus“).
  • Intestinal bleeding (intestinal bleeding).
  • Intestinal stenosis (intestinal narrowing) → subileus or ileus (intestinal obstruction).
  • Short bowel syndrome (see below small bowel resection/small bowel resection).
  • Malabsorption syndrome (see below “Insufficient coverage of energy and vital substance requirements (micronutrients)”).
  • Mechanical ileus (intestinal obstruction due to intestinal stenosis).
  • Perforation of the intestine
  • Perianal fistula/fistulas (perianal = “around the anus“; fistula = non-natural connection between a hollow organ and other organs or the surface of the skin) (cumulatively 20% of patients with Crohn’s disease after 10 years of disease; after 20 years, approximately 30%) – Gold standard of diagnosis of perianal fistulas in Crohn’s disease is magnetic resonance imaging of the small pelvis (fistula MRI of the small pelvis).
  • Toxic megacolon – toxin-induced paralysis and massive dilatation of the colon (widening of the large intestine; > 6 cm), which is accompanied by acute abdomen (most severe abdominal pain), vomiting, clinical signs of shock and sepsis (blood poisoning); lethality (mortality related to the total number of people suffering from the disease) is about 30%.

Musculoskeletal system and connective tissue (M00-M99).

Neoplasms – tumor diseases (C00-D48).

  • Colon carcinoma (colorectal cancer)
    • Less common than ulcerative colitis; risk of carcinoma increased 1.9-fold)
    • Colon carcinoma risk is increased by 40% compared with patients without inflammatory bowel disease (IBD); risk of colon carcinoma-related death is increased by approximately 70%
  • Prostate cancer (men with inflammatory bowel disease (IBD) have a 4.84-fold increased risk after 10 years).

Psyche – nervous system (F00-F99; G00-G99).

  • Depression
  • Fatigue – fatigue or increased need for rest and limitation of performance.

Symptoms and abnormal clinical and laboratory parameters not elsewhere classified (R00-R99).

  • Cachexia (emaciation; very severe emaciation).

Genitourinary system (kidneys, urinary tract – reproductive organs) (N00-N99).

Other consequences

Enteral protein loss syndrome

Impairment of the intestinal mucosa results in increased intestinal protein loss (protein loss), as leakage of plasma proteins through the intestinal mucosa into the bowel exceeds the rate of protein synthesis. The decrease in circulating plasma proteins is usually accompanied by a severe protein deficiency.Pathological protein loss may be promoted by a concomitant high dietary fat intake. When long-chain fatty acids are absorbed, lymphatic pressure is increased and high amounts of lymphatic fluid enter the intestine. As a result of increased lymph concentrations, there is a high enteral protein loss and ultimately a decrease in plasma proteins.The increased intestinal protein loss ultimately leads to a decrease in oncotic pressure and thus, depending on the extent of the decreased concentration of plasma proteins-hypoproteinemia-the formation of edema.

Inadequate coverage of energy and vital substance requirements (micronutrients)

Individuals who develop Crohn’s disease are often undersupplied with energy and essential nutrients and vital substances (macro- and micronutrients) due to impaired absorptive function and high losses of water and vital substances (micronutrients) through the stool. In particular, affected individuals with infectious complications and abscess formation have increased energy requirements. The deficiency of energy and essential nutrients and vital substances (macro- and micronutrients) in Crohn’s disease patients is often the result of:

  • An increased excretion with the stool – chologenic diarrhea, chologenic fatty stool – leading to high losses of macro- and micronutrients (vital substances).
  • A disturbed absorption or a reduced absorption surface – in addition to extensive bacterial infestation inside the intestine also after resection of parts of the small intestine.
  • Of an increased energy requirement during surgery as well as sepsis.
  • Of a loss of bile acid
  • Of an increased intestinal protein loss – enteral protein loss syndrome.
  • Restricted dietary recommendations
  • Unbalanced diet – increased use of refined carbohydrates, such as white sugar (sucrose), white flour products; low
  • Fiber consumption; high consumption of chemically processed edible fats.
  • Enteral fistulas, abscesses, fissures as well as stenoses.
  • Serious disorders in protein metabolism with a decrease in total protein in the blood (hypalbuminemia) – if the normal value of albumin in the blood of 3.6-5.0 g/dl is not reached, the oncotic pressure decreases and edema formation occurs; in addition, the transport capacity of the blood is reduced due to the lack of transport plasma proteins, such as transferrin, which means that the organism can be supplied only insufficiently with vital vital substances (eg iron)
  • Food intolerances associated with disorders of macro- and micronutrient absorption.
  • Side effects of medications
  • Negative nitrogen balance as a result of protein deficiency in the body – the body’s own protein-rich tissue, such as muscle tissue, is broken down more and the resulting nitrogen is excreted, so that more nitrogen is excreted than is absorbed
  • Insufficient supply with food – lack of appetite.
  • Little varied diet with deficiencies in energy, nutrients and vital substances – for fear of intolerances with subsequent symptomatology – including pain, vomiting, diarrhea.

Crohn’s patients often have an increased need for:

  • Vitamin A, D, E, K
  • Beta-carotene
  • Vitamin C
  • Vitamin B2, B3, B6, B9, B12
  • Calcium
  • Magnesium
  • Phosphorus
  • Potassium
  • Sodium chloride
  • Iron
  • Zinc
  • Selenium
  • Copper
  • Manganese
  • Molybdenum
  • Secondary plant compounds, such as carotenoids, saponins, sulfides and polyphenols.
  • Essential fatty acids, such as omega-3 and -6 fatty acids.
  • Protein and important amino acids
  • Fiber
  • Water

In active Crohn’s disease, serum concentrations of zinc, selenium and vitamin D, among others, are often observed to be below normal [5.1. ].Because vitamin D is often consumed in dietary amounts that are too low – low consumption of fish, such as eel and herring – and sunlight exposure is low, especially during the winter months, vitamin D supplementation is recommended.In addition, constant watery diarrhea contributes to vital substance (micronutrient) deficiencies. The increased loss with stool increases the need for water-soluble vitamins – vitamin C, B vitamins – and electrolytes, such as calcium, magnesium, potassium, as well as sodium.

Prognostic factors

  • Smoking has an unfavorable effect on the course of Crohn’s disease.
  • Obesity – marker for a less severe course of the disease.