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

Divarication

The rectus abdominis muscles should meet in the midline at the linea alba. Superior to the umbilicus, some people have a congenital defect that results in a widened linea alba. As a result, when a patient flexes the abdominal muscles the rectus muscles spread apart (divaricate).

Divarication and abdominal hernias appear very similiar. To differentiate between a divarication and a hernia clinically:

• get the patient to do a sit-up - rectus muscles spread apart in both a hernia and a divarication
• get the patient to cough - rectus muscles will only split apart if its a hernia. When coughing all abdominal muscles are used (not just the rectus), so a divarication will show a diffuse bulging, rather than locally down the midline.
  

Divarication is common in obese men. It can be surgically corrected, although such an operation would be almost entirely for cosmetic purposes and not of any functional value (unlike a hernia).

Blood flow patterns

Peripheral muscular arteries always show a triphasic pattern (forward-reverse-forward flow):

• forward - steep rise during ventricular systole
  
• reverse - brusque return to baseline with a small negative wave in early diastole caused by the high resistance of small peripheral arteries and capillaries
• forward - slow late diastolic rise due to the compliance of the peripheral arterial walls.
  

A monophasic waveform without the reverse component occurs when the volume in the artery is insufficient and extra flow is required during diastole. This is usually because stenosis or occlusion reduces the blood available to fill the reservoir during systole, but may also occur when there is a large flow to the limb caused by exercise or gross infection.

Neostigmine methylsulfate

Actions

• An anticholinesterase agent which reversibly inhibits the hydrolysis of acetylcholine by competing with acetylcholine for attachment to acetylcholinesterase. As a result, acetylcholine accumulates at cholinergic synapses and its effects are prolonged and exaggerated.
  
• Produces a generalised cholinergic response, including miosis, increased tonus of intestinal and skeletal musculature, constriction of bronchi and ureters, bradycardia and stimulation of salivary and sweat glands.
  
• Used mainly for its direct cholinomimetic effect on skeletal muscle and to a lesser extent to increase the activity of smooth muscle.
• Because of its quaternary ammonium structure, neostigmine in moderate doses, does not cross the BBB to produce CNS effects. Extremely high doses, however, produce CNS stimulation followed by CNS depression.

Indications

• Reversal of the effects of neuromuscular blocking agents (e.g. tubocurarine, pancuronium).
  
• Prophylaxis and treatment of postoperative intestinal atony and urinary retention.
  
• Treatment of myasthenia gravis during acute exacerbations, when the condition is severe, or in neonates.

Pharmacokinetics

• For IV administration the elimination half-life is 47-60 minutes.
• For IM administration the elimination half-life is 50-91 minutes.
  
• Approximately 80% of a single IM dose of neostigmine is excreted in the urine in 24 hours, about 50% as unchanged drug and the remainder as metabolites.
  
• The major site of uptake is in the liver. It is metabolised partly by the hydrolysis of the ester linkage and partly by microsomal enzymes in the liver.

Difference between purpura and ecchymoses

Moved to http://didiaskfor.freehostia.com/index.php?n=CR.AbnormalBleeding

Common postoperative problems

Postoperative complications are common, despite good pre-op assessment, surgical technique and perioperative management.

Complications can be minimised by regular and close postoperative patient observation. Managing complications effectively requires quick diagnosis and treatment before the complication gets out of hand.

Postoperative pain

• Pain from surgical wounds should subside over the first few days, and should be controlled by planned analgesia. Some types of wounds (e.g. vertical abdominal incisions) are more painful than others.
• Postoperative pain can be reduced by:
  
  • Preoperative counselling - letting the patient know in advance what to expect after the operation in terms of wounds, IV lines, catheters, extent of pain, plans for pain relief and degree of mobility.
    
  • Peroperative measures - preemptive analgesia to ensure pain does not become established after operation e.g. long acting analgesics, local anaesthetic infiltration into the sound edges, regional nerve blocks, morphine epidurals etc.
    
  • Postoperative analgesia - better to prevent pain than to react to established pain!
    
  
  
• Patients vary in their tolerance for pain and need for analgesics. Anxiety, exhaustion and sleep deprivation all reduce pain tolerance.
  
• If the pain is not controlled by what seems to be a normal dose and frequency of analgesia, complications should be suspected.
  
  • Review dose in relation to expected severity of pain and the weight of the patient.
    
  • Consider local postoperative complications such as haematoma -> wound pain, bleeding into fascial compartment -> compartment syndrome, wound infection -> pain increasing after 48 hours.
    
  
  

Pyrexia

• Infection is not the only cause of postoperative pyrexia, however it should always be considered and investigated as a cause.
• Common postoperative infections include superficial and deep wound infections, chest infections (pneumonia), UTIs and IV cannula site infections.
• Infection is not likely to be a cause in fever developing within 2 hours of surgery - it normally takes longer to develop.
  
• Common non-infective causes of pyrexia include transfusion reactions, drug reactions, wound haematomas, DVT and pulmonary emboli.

Tachycardia

Tachycardia can be benign or malignant.
Benign causes of postoperative tachycardia:

• pain
• anxiety

Malignant causes of postoperative tachycardia:

• infection
• circulatory disturbances
• thyrotoxicosis
• Mild tachycardia can be a sign of incipient hypovolaemic shock resulting from haemorrgahe or dehgydration.
• Cardiac failure.
• AF or flutter.
• Anastomotic leakage - after bowel surgery.
  

Week 2 eve

Well I've officially been in the OC for just over a week. It feels like a lot longer. My emotions tonight are very different to how I felt sitting here at my desk this time last week.

I'm not really nervous about tomorrow (except about getting grilled about pyloric stenosis). I'm actually looking forward to it, although I'm not looking forward to the 6:30am start. The main thing I'm worried about is mucking up my timetable and inadvertently missing a teaching session in the afternoon. I think the only session I have on is a procedural skills one, but I wouldn't bet my life on it.

I'm hoping that this week I can start working out how to come home at the end of the day and do something productive in the afternoon. The main problem so far is in working out what to do. Let's see how tomorrow goes, one day at a time!

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.

New kids on the block

I’ve got absolutely no idea where to start in describing day 1 in hospital. The morning, and indeed most of the day up until 4pm was the usual orientation stuff – getting id issued, hospital tour etc

I’m doing General Surgery for my first rotation, along with another student, who I’ll call Kate here (all names changed to protect the guilty, remember).

At around 4pm myself and Kate paged our registrar to say hello and find out what time we should turn up tomorrow. He asked if we were close by, and when I said we were in the student’s quarters across the road he asked could we meet him in the ED in 5 mins. We were free for the rest of the afternoon, so why not?

The next few hours we were thrown in the deep end taking histories and doing abdominal physical exams of patients in the ED. Although we had just done this stuff last year, I felt so ill-prepared.

Our reg is a lovely, lovely guy, more than a little crazy and I have no doubt that in the next 4 weeks we are going to learn a hell of a lot, and have fun in the process. He is not of the old-school humiliate-your-students-into-learning way of teaching, but will teach us what we are seeing on the day, and expect us to go and learn about it that night, instead of drilling the crap out of us when it’s the first time we are seeing a given case.

Things were off to an eeirily rosy start, right up until we met our consultant. This week is not a good week to get sick because the teams across the state are basically rebuilt from the ground up: brand new interns first week out of uni, new registrars etc. Chaos.

Our reg hadn’t even met his consultant right up until the consultant walked into the room where I was interviewing a patient who presented earlier that day with a palpable mass and right groin pain. Not long after the consultant walked in, our reg walked in. Not long after he walked in, Kate walked in. Our consultant had obviously had enough of people walking in the room, because he then yelled at us all to get out. The reg was mortified and apologized that we had to witness that. He’d never seen anyone act like that before.

Since then he has talked to the consultant who has calmed down and is apparently apologizing to us tomorrow morning. Talk about drama. Let’s see how this unfolds tomorrow!