Short bowel syndrome.

Short-bowel syndrome. 

It is a disorder clinically defined by diarrhea, malabsorption, steatorrhea, fluid and electrolyte disturbances and malnutrition. Among all the causes, the final common etiologic factor in short-bowel syndrome is the anatomic or the functional loss of extensive segments of small gut so that absorptive capacity of intestine is severely compromised. The resection of the colon alone typically does not result in short-bowel syndrome. The presence of short-bowel syndrome can be a critical factor in the management of patients who lose significant amounts of small intestine.

The average length of small intestine of human is approximately 600 cm as calculated on cadavers. Any disease, vascular accident, traumatic injury, or any other pathology that results in a loss of 50% or more of the small gut or less than 200 cm of viable small intestine places the patient at risk for developing short-bowel syndrome.

What are the causes of short-bowel syndrome? 

Patients having short bowel syndrome mostly present with a history of, 

1. Several gut resections, as occurs e.g. In Crohn disease, 

2. Major abdominal vascular accident or other catastrophe such as midgut volvulus. 

3. Embolus to the superior mesenteric vessels

There may be a significant weight loss in patients with short-bowel syndrome because of protein imbalance. Other notable features include malaise, fatigue and lethargy. These symptoms are due to protean deficiency but consistent with the diarrheic diathesis and resultant dehydration, electrolyte imbalance, protein-calorie malnutrition, and loss of minerals and critical vitamins. 

Signs and symptoms in patients with short-bowel syndrome. 

Short bowel syndrome can lead to some specific symptoms due to deficiencies of Vitamin and mineral which are as follows:

vitamin A deficiencies may lead to xerophthalmia and night blindness.

vitamin E deficiency can cause ataxic gait, paresthesias and visual disturbances due to retinopathy.

Depletion of vitamin D can be associated with tetany and paresthesias.

Vitamin K depletion may lead to prolonged bleeding or easy bruisability.

Folic acid, vitamin B12 or iron deficiency  can cause lethargy or dyspnea on exertion. 

Magnesium and Calcium depletion can cause tetany and paresthesias. 

Critically low levels of zinc in patients with short-bowel may describe anorexia, diarrhea, poor wound healing, angular stomatitis and alopecia.

The essential fatty acids are . Patients with short-bowel having deficiency of essential fatty acid (e.g linoleic and linolenic acids) may experience growth retardation, alopecia and dermatitis

Physical examination of patients with short-bowel. 

Temporal wasting, loss of digital muscle mass and peripheral edema.

Due to severely protein and energy-malnourished

Growth retardation due to deficiencies of essential fatty acids like linoleic and linolenic acids. 

Dermatitis and alopecia due Zn and essential fatty acids deficiency.

Corneal ulcerations due to vitamin A deficiency.

Stomatitis, glossitis and cheilosis due to low levels vitamin B complex.

Poor growth and bowed extremities due to depletion of vitamin D.

Petechiae, purpura, ecchymoses and outright bleeding diatheses are the hallmark of vitamin K Deficiency.

Workup

complete blood count (CBC) with peripheral films to determine if the patient is anemic. Peripheral film further help to identify if the anemia is hypochromic microcytic anemia as seen in Iron depletion or megaloblastic anemia associated with vitamin B12 deficiency.

Plasma albumin. This is a good indicator of overall nutritional status. The half-life of albumin is approximately 21 days. Severely decreased levels of albumin (below 2.5 g/dL) are associated with increased rates of major morbidity and mortality in surgical patients.

If there abnormally elevated albumin level than it may be due to dehydration.

Prealbumin

Being short half-life of approximately 3-5 days, it is good indicator of acute nutritional status.

Hepatocellular enzymes. 

Many patients who are on long-term total parenteral nutritional support have transient elevations of hepatocellular enzyme(eg, aspartate aminotransferase [AST], alanine aminotransferase [ALT]). So it is important to monitor, especially in those receiving long-term parenteral nutritional support.

Serum Electrolytes specially including sodium, potassium, chloride, and carbon dioxide levels.

Blood urea nitrogen (BUN) to determine  renal reserve or function.

Vitamins and serum levels of zinc, selenium, chromium and some other important trace elements and minerals. This is done when a specific abnormality can be attributed to a vitamin/mineral deficiency is suspected on clinical grounds.

Management of Short-bowel syndrome 

Management of Short bowel syndrome 

Medical Therapy 

Active resuscitation. 

Management of primary  precipitating condition leading to intestinal resection. 

Repletion of fluid and electrolytes lost in the severe diarrhea that mostly occurs in patients with short-bowel.

High dose  histamine-2 receptor antagonists or proton pump inhibitors (PPI). These reduce gastric acid secretion. 

Most of the patients with short-bowel require long term total parental nutrition (TPN).

Modified and supplemented diets (eg, glutamine, growth hormone high carbohydrate and low fat). 

Nontransplant Surgical Therapy.

The goal of  surgery is to increase nutrient and fluid absorption. This is done by either slowing intestinal transit or increasing intestinal length. Nontransplant Surgical options include, 

1. Stoma reversal in patients having stoma

2. (LILT) Longitudinal intestinal lengthening and tailoring  procedure.

3. (STEP) Serial transverse enteroplasty procedure (STEP).

Serial transverse enteroplasty procedure (STEP)

Intestinal Transplantation.

Intestinal Transplantation can be done alone or in combination with liver and pancreas.