Showing posts with label Surgery. Show all posts
Showing posts with label Surgery. Show all posts

Friday, March 8, 2013

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Thoracic cage injuries - simple and complicated


Thursday, June 21, 2012

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Arteriovenous fistula - AVF


Definition:
It is an abnormal communication between an artery and a vein (or veins). It may be
1) a congenital malformation,
2) acquired by the trauma of a penetrating wound,
3) iatrogenic in which AVFs are created surgically in the arms or legs of patients undergoing renal dialysis. All arteriovenous communications have a structural and a physiological effect.

Structural effect:
The veins become dilated, tortuous and thick walled (arterialised).

Physiological effect:
There is high-pressure from the arterial system and an enhanced venous return/venous pressure. This results in an increase in pulse rate and cardiac output. The pulse pressure is high if there is a large and persistent shunt. Left ventricular enlargement and later cardiac failure may occur.
A congenital fistula in the young may cause overgrowth of a limb.
In the leg, indolent ulcers may result from relative ischaemia below the short circuit.

Clinical features:
Clinically, a pulsatile swelling or dilated tortuous veins may be present if the lesion is relatively superficial.
On palpation, a thrill is detected and auscultation reveals a buzzing continuous bruit.

Nicoladoni’s (1875) or Branham’s (1890) sign
Pressure on the artery proximal to the fistula causes the swelling to diminish in size, the thrill and bruit to cease and the pulse rate to fall. The pulse pressure also returns to normal.

Arteriography:
Arteriography confirms the lesion, which is noteworthy for the speed with which venous filling occurs. It is often difficult to pinpoint the actual site of the fistula.

Treatment:
Embolisation by the radiologist or excision is advocated only for severe deformity or recurrent haemorrhage. A plastic surgeon can also help for a proper ablation and reconstruction. Ligation of a ‘feeding’ artery is of no lasting value and is likely to be detrimental as it may preclude treatment by embolisation.

Clinical implications:
1) Autogenous AV fistulas have a lower risk of failure and require less revision compared to prosthetic grafts. The only problem with this is that a large number of patients lack suitable veins. This inability to make a proper vascular access is often termed as the Achilles tendon of hemodialysis. 

Saturday, April 28, 2012

Hypertrophic pyloric stenosis of infancy


Epidemiology: 
Incidence of 3/1000 births. 
4 times more in males. 
Aetiology is unknown. In some cases there seems to be a familial association. In such families the mother has suffered from the condition in 50 per cent of cases. Characteristically it is a first-born male child that is most commonly affected. The condition is most commonly seen at 4 weeks after birth ranging from the third week to, on rare occasions, the seventh. Inexplicably, it is the time following birth that seems important and not the child’s gestational age. A premature infant will also develop the condition at about 4 weeks after birth.

Pathology:
Grossly hypertrophied musculature of the pylorus and adjacent antrum, the hypertrophy being maximum in the pylorus itself. The mucosa is compressed such that only a probe can be inserted.

Clinical features:
Vomiting is the presenting symptom that after 2—3 days becomes forcible and projectile. The child vomits milk and no bile is present. Immediately after vomiting the baby is usually hungry. Weight loss is a striking feature and rapidly the infant becomes emaciated and dehydrated. Diagnosis can usually be made with a test feed. This may produce characteristic peristaltic waves that can be seen to pass across the upper abdomen. At the same time, using a warm hand, the abdomen is palpated to detect the lump.

Imaging:
Ultrasonography is the investigation of choice as it can, without difficulty, detect the classical features in the pyloric canal.
Contrast radiology was done in the past but is not necessary now.

Differential diagnosis:
The common D/D are gastro-oesophageal reflux, feeding problems, urinary tract infection and raised intracranial pressure.
 The condition cannot normally be confused with duodenal atresia or intestinal obstruction because of the absence of bile in the milk vomit.

Treatment:
Following diagnosis the first concern is to correct the metabolic abnormalities. Essentially this is the same situation that pertains in adults with the patient being dehydrated, with low sodium, chloride and potassium, and a metabolic alkalosis.
The child should be rehydrated with dextrose—saline and potassium (2.5 per cent dextrose plus 0.45 per cent sodium chloride plus 1 g of potassium chloride per 500 ml of fluid). This will restore the infant’s clinical condition and electrolytes to normal. Following stabilization of the patient, operation is required. 
Conservative treatment has little place in the management of this condition as with appropriate surgical treatment recovery is virtually 100 per cent.

Ramstedt’s operation
1) In preparing the child for operation it is important that the stomach is emptied and washed out with saline, and that hypothermia is avoided. To achieve this, the patient is encased in cotton wool allowing exposure of the upper abdomen. 
2) Operation is performed under general anaesthesia, although it is possible to perform the procedure under a local anesthetic. 
3) The skin is opened through a transverse incision placed in the upper abdomen over the right rectus sheath, which is opened in the same line. The rectus muscle is then split along the line of its fibres and the posterior rectus sheath opened in the line of the skin incision. 
4) The hypertrophied pylorus is delivered and rotated so that its superior surface comes into view. Thus, the least vascular portion can be selected for incision. To ascertain the distal limit of the hypertrophy the surgeon invaginates the duodenum with the index finger. 

5) The incision is made through the serosa only and from this point along the whole length of the pylorus and, importantly, the distal antrum. The hypertrophied pylorus has the consistency of an unripe pear, hence splitting the muscle coats can be accomplished by blunt dissection. On separating the edges with artery forceps the pyloric mucosa bulges into the cleft which has been made in the muscle as shown in the diagram above. 
6) Great care is taken not to penetrate the mucosa. When this injury occurs it is almost always in dividing the most distal part of the constricting fibres which are in the vicinity of the duodenal fornix. To be sure that there is no perforation some air is squeezed from the stomach into the duodenum. If a perforation has occurred it is closed and a piece of omentum placed over the closure. 
7) Haemostasis should be meticulous.


After operation the nasogastric tube can be removed and feeding commenced on the morning after operation. If the infant manages to feed without difficulty it can be discharged early from hospital. If the mucosa is inadvertently opened it is wise to delay feeding for 48 hours and to retain the child in hospital longer.

Saturday, March 17, 2012

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Hypertrophic scars


Pathology:
In some cases, the scarring process remains in the remodelling phase for longer than usual. These hypertrophic scars are more cellular and more vascular than mature scars.  There is increased collagen production and collagen breakdown but the balance is such that excess collagen is produced. 

Clinical features:
The hypertrophic scars are red, raised, itchy and tender. They will eventually mature to become pale and flat, and it is this spontaneous resolution which distinguishes hypertrophic scars from keloid scars. 

Cause:
Hypertrophic scars typically occur in wounds where healing was delayed, e.g. in cases where infection or dehiscence has occurred. 

Incidence:
They are more common in children and where skin tension is high such as the tip of the shoulder or any scar that runs across relaxed skin tension lines.

Prevention and treatment:
The risk of developing a hypertrophic scar can be minimised by ensuring quiet primary healing. Where hypertrophy does occur patience is usually rewarded by improvement with time. Massage of the scar with moisturising cream or the application of pressure to the remodelling scar can accelerate the natural process of maturation. Patients with hypertrophic bum scars are supplied with custom made Lycra pressure garments that promote acceleration of scar maturation. Revision of hypertrophic scars is appropriate where they cross skin tension lines or where a specific wound healing complication occurred. In the absence of these factors scar revision should be avoided as it will usually be met with recurrence.

Monday, March 12, 2012

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Barrett's esophagus

Definition:
Barrett’s esophagus is characterized by an intestinal metaplastic change in the lining mucosa of the esophagus in response to chronic gastro­esophageal reflux. 
The condition is named after Norman Barrett, an Australian surgeon who drew attention to the columnar-lined esophagus in 1950.
It is still not well understood why some people develop esophagitis and others develop Barrett’s esophagus often without significant esophagitis. 

Pathology:
In Barrett’s esophagus the junction between squamous esophageal mucosa and gastric mucosa moves proximally. The columnar epithelium is more acid resistant than the squamous epithelium. So this metaplasia appears to be a protective adaptation. The patient of chronic reflux esophagitis will find his symptoms decrease when he has developed Barrett's esophagus.

Incidence:
It is mainly seen in white man and the prevalence increases with age. 
Several types of gastric-type mucosa may be found in the lower esophagus. When intestinal metaplasia occurs there is an increased risk of adenocarcinoma of the esophagus of the order of 25 times that of the general population. A recent (Dec 2011) large scale study in Denmark however shows that the incidence of adenocarcinoma in Barrett’s esopahgus is actually much lower i.e. around 7 times that of general population.

Clinical features:
The patient will have all the complaints of reflux esophagitis. Heartburn, described as a substernal burning sensation that moves from the region of the xiphoid up toward the neck. Regurgitation, water-brash and  odynophagia may be the other symptoms.

Diagnosis:
Barrett’s esophagus is diagnosed by endoscopic examination and  2  criteria  must  be  fulfilled.
1) The endoscopist must ascertain that columnar epithelium lines the distal esophagus.
2) Biopsy specimens of that columnar epithelium must show evidence of metaplasia.

To ascertain that columnar epithelium lines the distal esophagus, the endoscopist first must locate the esophagogastric junction (EGJ, which is recognized as the most proximal extent of the gastric folds) and then determine that columnar epithelium extends above the EGJ into the esophagus. Endoscopically, columnar epithelium has a reddish color and velvet-like texture that can be distinguished readily from normal esophageal squamous epithelium, which is pale and glossy.
There is disagreement among experts regarding the histologic type of epithelium required to confirm that there is evidence of metaplasia in the esophagus.
Virtually all would agree that the finding of an intestinal type epithelium with goblet cells (which has been called intestinal metaplasia, specialized intestinal metaplasia or specialized columnar epithelium) is clear evidence of metaplasia.

Treatment:
Patients who are found to have Barrett’s esophagus may be submitted to regular screening endoscopy with multiple biopsies every year or two in the hope of finding dysplasia or in situ cancer rather than allowing invasive cancer to develop and cause symptoms. There is as yet no general agreement about the benefits of screening endoscopy, nor about the ideal frequency of endoscopy. 
When Barrett’s esophagus is discovered the treatment is that of the underlying GERD. Several methods of ablation of Barrett’s mucosa are under active study, including laser, photodynamic therapy and argon beam plasma coagulation. In conjunction with high-dose PPI treatment or an antireflux operation these endoscopic methods can restore the squamous lining of the esophagus. It is not yet known whether this reduces the risk of malignant transformation since there are often remnants of glandular mucosa underneath the new squamous lining.

Friday, January 6, 2012

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Cullen's sign


It refers to the superficial peri-umbilical bruising of the subcutaneous fat.
It can be seen in the following cases:
1) acute pancreatitis (classically),
2) bleeding from blunt abdominal trauma, rupture of abdominal aorta and ruptured ectopic pregnancy.

The sign was actually first described by Thomas Cullen in 1916 in a case of ruptured ectopic pregnancy.

Saturday, December 24, 2011

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Subcutaneous injection - Insulin / Heparin

Definition:
It is defined as the introduction of a fluid drug under pressure using a syringe equipped with a hollow needle into the loose connective tissue below the dermis i.e. into the hypodermis.
It has a low absorption there because of the low vascularisation but since it contains pain receptors, injection can be painful depending on the volume administered.
For structure of skin, consider this page : Skin structure

Sites:
1) outer sides of arm,
2) front of upper outer thigh,
3) above and below the spine of scapula,
4) abdomen extending from the costal margin to the iliac crest except 5 cm all around the umbilicus.


Angle of insertion of needle:
1) 90 degrees with a short needle,
2) 45 degrees with a longer needle.

Techniques:
1) Pinch skin slightly to make 3 cm fold,
2) Insert needle quickly and firmly,
3) Release skin,
4) Aspirate and make sure that needle is not in a vessel,
5) Remove needle by gentle pressure with antiseptic swab,
6) Massage lightly to diffuse drug.

Caution must be taken when injecting anticoagulant. The preferred site is the abdomen. The drug usually comes in ready to use syringe fitted with a needle. We should not remove any air trapped inside. The air is to make sure that all the medication has been delivered. Also do not release the skin after inserting the needle. Finally do not massage the medication!!



Monday, December 19, 2011

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CSF rhinorrhea - Double-ring sign / ring sign / halo sign


The double-ring test is clearly shown in this photo. It is also known as the ring sign or halo sign. The patient was brought following an injury to the head and was bleeding moderately from the nose but the blood was more watery than normal. CSF rhinorrhea was suspected.

The dextrose stick test was positive to the sample and when placed on a filter paper, we got an inner ring of blood and a halo, followed by an outer ring of CSF. Though this has been a classical medical test, it is not 100% reliable.

Battle sign / Battle's sign




Battle sign refers to the post auricular ecchymosis that occurs following trauma to the middle cranial fossa of the skull. It may indicate underlying brain trauma.

The picture above shows one patient who came to the emergencies few hours after the head injury while in the one below it, patient was brought in a confused state few days after trauma to his head.

The sign was named after William Henry Battle, who was a English professor of surgery and pathology.

Thursday, November 24, 2011

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I.V catheters - precautions

1. For adults requiring a peripheral catheter, upper extremity site is preferred. If it is for a child, then we can use both upper or lower extremities as well as scalp sites.
2. The catheter site should be evaluated everyday and if there is any sign of phlebitis, the catheter should be removed immediately.
3. For central catheters in adults, it is better to use the jugular or subclavian route rather than the femoral one.
4. Systemic antimicrobial prophylaxis is not essential when using I.V catheters.

Friday, October 21, 2011

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Acute limb ischaemia / Peripheral Vascular Diseases (PVD) - 6 P's

The 6 P's are:
1) Pain,
2) Pallor,
3) Pulselessness,
4) Paralysis,
5) Paraesthesia,
6) Perishingly cold.

Friday, September 2, 2011

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Differences between hemoptysis and hematemesis

1) There is usually a tingling sensation in the throat in hemoptysis while in hematemesis the patient will usually complain from nausea and upset stomach.

2) The blood is usually frothy and bright red in hemoptysis while it is dark red in hematemesis, non-frothy and food particles may also be present at the same time.

3) Blood in hematemesis will give an acidic pH when tested with litmus paper whereas that in hemoptysis will be neutral to alkaline.

4) Stools will be almost always positive for occult blood in hematemesis while it is usually negative in case of hemoptysis. But it can also be positive at times if the patient has swallowed his sputum.

Last reviewed on: 1 September 2015

Tuesday, July 12, 2011

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Chronic gastritis/peptic ulcer - pathogenesis


Peptic ulcers are created by an imbalance between the gastroduodenal mucosal defenses and the damaging forces that overcome such defenses. It is very well depicted above.

H.pylori does not invade the tissues but it causes intense local inflammation. It has flagella that allows it to move in the viscous mucous. Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in the gastric mucous, thus weakening the first line of mucosal defense. It also produces urease that breaks down endogenous urea to form ammonia. This causes the pH to increase locally. The H.pylori also has adhesins that make it bind to the cells and finally they elaborate toxins that cause further damage like metaplasia.

NSAIDs and aspirin are inhibitors of cyclooxygenase (COX). Thus they prevent the synthesis of prostaglandins. The latter is responsible for the promotion of mucin synthesis and vasodilation. In the absence of prostaglandins, the mucinous layer is depleted and the decreased vascular perfusion does not help in the regeneration of the damaged layer.

Ischaemia, shock and cigarette smoking also act by decreasing the blood flow.

Sunday, July 3, 2011

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Hypokalemia - Potassium replacement calculation


 DEFINITION 
Hypokalemia is defined as a serum potassium level of less than 3.5 mmol/L.

Normal level= 3.5-5.5 mmol/L.
It is encountered in >20% of patients.

Patients are usually asymptomatic but severe arrhythmias and rhabdomyolysis can occur. Non-specific complaints include easy fatiguability and skeletal muscle weakness.

The preferred method of replacement is via the oral route but at times this is not possible. The article below will give you an idea about how to calculate the amount of KCl to be given I.V.






1) Potassium deficit in mmol is calculated as given below:


Kdeficit (mmol) = (Knormal lower limit - Kmeasured) x kg body weight x 0.4


2) Daily potassium requirement is around 1 mmol/Kg body weight.
3) 13.4 mmol of potassium found in 1 g KCl. (molecular weight KCl = 39.1 + 35.5 = 74.6)




Suppose we get an asymptomatic patient of  70 Kg with a serum potassium level of 3.0 mmol/L and he is on nil by mouth but having an adequate diuresis, we proceed this way. 


1) Deficit of potassium in mmol = (3.5 - 3.0) x 70 x 0.4 = 14 mmol
2) Daily potassium requirement = 1 x 70 = 70 mmol
3) Total requirement = 14+70 = 84 mmol = (84/13.4) = 6.3 g KCl 


Therefore we can give the patient 1.0 g KCl (around 13 mmol of K+) in 500 mL Normal Saline (N/S) solution to run 4 hourly and reassess the serum potassium level after 1 day. So, in around 24 hours, we have given the patient around (24/4 = 6 pints of N/S solution, total KCl administered = 6.0 g i.e. around 80 mmol K+). Now if on the next day, he is still nil by mouth and there is still some degree of hypokalemia, we can repeat the above calculations to find his new total requirement and adjust the dosage accordingly.

But, if we have a symptomatic patient or someone with changes on the EKG, then better give 20 mmol of K+ in 50 mL of N/S via syringe pump over an hour through a central line and then recheck the serum potassium 1-2 hours after completion of the infusion. In extreme cases we can even go for up to 40 mmol of K+ per hour.


1) Never give potassium I.M or rapid I.V push
2) Never give more than 1.5 g KCl or 20 mmol of K+ over 1 hour without any continuous ECG monitor.
3) Do not just add the KCl solution to the hanging I.V fluid bag. Fully invert it around 10 times to ensure proper mixing.
4) 1 tab of Slow K gives around 8 mmol potassium.
5) 10 mL of KCl syrup = 20 mmol of K+.
6) Peripheral veins are damaged by a potassium concentration greater than 30 mmol/L i.e. 1.1 g KCl/ 500 mL I.V infusion solution. For higher concentrations, central lines are preferred.
7) Hypokalemia is associated with hypomagnesemia and the severity of the hypokalemia correlates with a similar degree of hypomagnesemia. Magnesium replacement should usually accompany potassium repletion. Unless the patient receives at least 0.5 g/hr of magnesium sulfate along with potassium replacement, potassium will not move intracellularly and the patient will lose potassium through excretion.
8) Correction of large potassium deficits may require several days. Oral and intravenous replacement can occur simultaneously.
9) Monitoring the plasma potassium level as an index of total body potassium is like evaluating the size of an iceberg by its tip since only 2% of total body potassium is extracellular. Thus repeated measurements of the serum potassium should be done. In an averaged-size adult with a normal serum K+ of  4 mEq/L, a total body K+ deficit of 200–400 mEq is required to produce a decrease in plasma K+ of 1 mEq/L.
10) Please leave a comment stating how useful the calculation turned out to be in your clinical practice (if ever you used it).

Further readings:
Alcoholic liver disease - complete review
Hypokalemia- ecg changes

Last reviewed on : 1 September 2015

Thursday, April 28, 2011

Richter hernia

The Richter hernia occurs when only the antimesenteric border of the bowel herniates through the fascial defect. The Richter hernia involves only a portion of the circumference of the bowel. As such, the bowel may not be obstructed, even if the hernia is incarcerated or strangulated, and the patient may not present with vomiting.
The Richter hernia can occur with any of the various abdominal hernias and is particularly dangerous, as a portion of strangulated bowel may be reduced unknowingly into the abdominal cavity, leading to perforation and peritonitis.

Friday, February 4, 2011

Mammography : age, frequency?

Doing annual mammograms from age 40-84 can greatly save lives. If annual mammograms are done as from the age of 40, the risk of dying from breast cancer decreases by nearly 71%. 

Thursday, August 12, 2010

Antibiotic fever

Fever that occurs on starting a drug without any other probable cause of fever is known as antibiotic fever. It may be part of an allergic reaction to the drug or a preservative of the drug. It usually occurs with beta lactam antibiotics, procainamide, alpha methyl dopa and isoniazid.

Sunday, June 13, 2010

Abnormal gas under left dome of diaphragm

This is also a case of perforated duodenal ulcer in a 34 yr old lady. Note the rim of gas above the fundal gas.

Gas under diaphragm

Massive  gas under diaphragm was seen in this case of perforated duodenal ulcer. Patient was a 28 yr old male with past history of chronic gastritis. He presented to A&E with acute abdomen. O/E rigidity of abdomen was positive and bowel sound was absent.