Pantoprazole infusion

For actively bleeding ulcers give pantoprazole bolus followed by infusion.

• LOading dose: Pantoprazole 80mg IV in 100ml of NaCl 0.9% or 5% glucose over 20 - 30 minutes
  
• Infusion:
  
• Pantoprazole 200mg in Dextrose 5% 500mL at 20mL/hr (each mL is 0.4mg , 20mL/hr = 8mg/hr, 1mg =2.5mL)
• Pantoprazole 80mg in N/Saline 100mL at 10mL/hr (each mL is 0.8mg , 10mL/hr = 8mg/hr,1mg=1.25mL)

References

• Pantoprazole infusion guidelines, http://www.philippelefevre.com/JHH-ICU-guidelines/adult-drug-infussions/pantoprazole-infusion.pdf
  
• Pantoprazole Infusion as Adjuvant Therapy to Endoscopic Treatment in Patients With Peptic Ulcer Bleeding: Prospective Randomized Controlled Trial, medscape.com
  

Peutz–Jeghers syndrome

• Peutz–Jeghers syndrome is also known as hereditary intestinal polyposis syndrome.
• An autosomal dominant genetic disease characterized by the development of benign hamartomatous polyps in the GIT and hyperpigmented macules on the lips and oral mucosa.
• Prevalence of approximately 1 in 100,000 to 200,000 births.
  

Diagnosis

Need 2 of 3 of:

• Family history
• Mucocutaneous lesions causing patches of hyperpigmentation in the mouth and on the hands and feet.
  
  • Oral pigmentations are the first to appear and play an important part in early diagnosis. Intraorally, they are most frequently seen on the gingiva, hard palate and inside of the cheek. The mucosa of the lower lip is almost invariably involved as well.
• Hamartomatous polyps in the gastrointestinal tract. These are benign polyps with an extraordinarily low potential for malignancy.
• Mutation in the tumour supressor gene STK11 on chromosome 19.

Natural history

• Most patients will develop melanotic macules during the first year of life.
• Intussusception usually first occurs between the ages of six and 18 years old.
  
• Most people will have developed some form of neoplastic disease by age 60.
• Cumulative lifetime cancer risk begins to rise in middle age.
• Cumulative risks by age 70 for all cancers, gastrointestinal (GI) cancers, and pancreatic cancer are 85%, 57%, and 11%, respectively.

References

• http://en.wikipedia.org/wiki/Peutz-Jeghers_syndrome
• http://www.answers.com/topic/peutz-jeghers-syndrome
  

IV Fluids

Standard fluid regime for NBM patients:

• N/2 * 2 bags
• 4 % dextrose + N/5 + 30mmol KCl

In terms of fluid requirements,

• 65% of body is water (TBW)
• 2/3 of this is intracellular, 1/3 extracellular

Ways you can lose electrolytes:

• Vomiting → loss of K
• Diarrhoea→ loss of K
• Sweat→ loss of NaCl
• Burns → loss of protein and Na
• Third space losses → loss of NaCl + H20

Ways to assess dehydration:

• Urine dipstick - concentration
• ↑ Ur and ↑ Na

Correction of hypernatremia begins with a calculation of the fluid deficit. Predicted insensible and other ongoing losses are added to this number and the total is administered over 48 hours. Recheck serum electrolyte levels frequently during therapy. To avoid cerebral edema and associated complications, the serum sodium level should be raised by no more than 1 mEq/L every hour. In patients with chronic hypernatremia, an even more gradual rate is preferred.

Free Water Deficit (L) = Body Weight (kg) X Percentage of Total Body Water (TBW) X ([Serum Na / 140] - 1)

Percentage of TBW should be as follows:

• Young men - 0.6%
• Young women and elderly men - 0.5%
• Elderly women - 0.4%

Example:

• A serum sodium level of 155 in a 60-kg young man represents a fluid deficit of 60 X 0.6 X ([155 / 140] - 1) or 3.9 L
  

• With another 900 mL of insensible losses, the patient requires 4.8 L of fluid in the next 48 hours, resulting in an infusion rate of 100 mL/h.

SIADH

• Pure water depletion and ↑ Na → use 4% D + N/5 to treat it.
• Stimulating the bowel e.g. abdo surgery → release of ADH → SIADH

References

• http://www.merck.com/mmpe/print/sec12/ch156/ch156e.html
• http://emedicine.medscape.com/article/766683-treatment
  

Ileus

Ileus is a partial or complete non-mechanical blockage of the small and/or large intestine. It causes colic, vomiting, and constipation.

Ileus occurs because peristalsis stops. Causes of ileus include:

• peritonitis
• disruption or reduction of the blood supply to the abdomen e.g. post-operatively
• kidney diseases, especially when potassium levels are decreased
• gallstone ileus - obstruction of the large intestine by a gallstone that has blocked the intestinal opening.

References:

• http://www.answers.com/topic/ileus
• http://www.answers.com/gallstone%20ileus
  

Pneumoperitoneum

Pneumoperitoneum is air or gas in the abdominal (peritoneal) cavity.

A pneumoperitoneum is deliberately created by the surgical team in order to perform laparoscopic surgery. This is achieved by insufflating the abdomen with carbon dioxide.

Aetiology

The most common cause is a perforated abdominal viscus, generally a perforated ulcer, although any part of the bowel may perforate from a benign ulcer, tumor or trauma.

A perforated appendix seldom causes a pneumoperitoneum.

Diagnosis

It is often seen on x-ray, but small amounts are often missed and CT is nowadays regarded as the gold standard in the assessment because CT can visualize as small as 5 cm cubic air.

Complications

Increased intrathoracic pressure -> decreased venous return. This means that DVT prophylaxis is required!!

References:

• http://en.wikipedia.org/wiki/Pneumoperitoneum

Indomethacin

Drug class

NSAID

Action

Potent inhibitor of prostaglandin synthesis. Affords relief of symptoms but does not alter the progressive course of the underlying disease.

Uses

Arthritis and related inflammatory disorders; low back pain; postop bone pain; primary dysmenorrhoea, IBD.

Contraindications

NSAID sensitive asthma; active peptic ulcer, recurrent GI ulceration; pregnancy, lactation

Sold as

Athrexin

Pyloric stenosis

Congenital hypertrophic pyloric stenosis

• Seen in infants as a disorder that affects males three to four times more often than females, occurring in 1 in 300-900 live births.
  
• Familial occurrence implicates a multifactorial pattern of inheritance; monozygotic twins have a high rate of concordance of the condition.
• May occur in association with Turner syndrome, trisomy 18, and esophageal atresia.
  
• The stenosis from hypertrophy, and possibly hyperplasia, of the muscularis propria of the pylorus. Edema and inflammatory changes in the mucosa and submucosa may aggravate the narrowing.

• Regurgitation and persistent, projectile, nonbilious vomiting usually appear in the second or third week of life.
  
• Physical examination reveals visible peristalsis and a firm, ovoid palpable mass in the region of the pylorus or distal stomach.
• Investigations include barium swallow to look for narrowing, blood tests to check for electrolyte imbalances.
  
• A pyloromyotomy - surgical muscle splitting - is curative.

• After surgery, most babies are able to return to normal feedings quickly. The baby starts feeding again 3 to 4 hours after the surgery, and the baby can return to breast-feeding or the formula that he was on prior to the surgery. Because of swelling at the surgery site, the baby may still vomit small amounts for a day or so after surgery. As long as there are no complications, most babies who have undergone pyloromyotomy can return to a normal feeding schedule and be sent home within 48 hours of the surgery.

Acquired pyloric stenosis

• Seen in adults.
• One of the long-term risks of antral gastritis or peptic ulcers close to the pylorus.
  
• Carcinomas of the pyloric region, lymphomas, or adjacent carcinomas of the pancreas are more ominous causes. In these cases, inflammatory fibrosis or malignant infiltration narrow the pyloric channel, producing pyloric outlet obstruction.
  
• In rare instances, hypertrophic pyloric stenosis is the result of prolonged pyloric spasm.