Breast cancer histology

Grade - modified Bloom-Richardson (grades I-III)

Grade I = good prognosis; grade III = bad prognosis.

• Tubule formation = happy sign.
• Mitotic count per high-power field.
• Nuclear size and pleomorphism (enlargement and variation are bad).

DCIS

90% of DCIS are identified on mammography as suspicious calcifications, linear, clustered, segmental, focal, or mixed distribution. DCIS is divided into comedo (i.e. cribriform, micropapillary, solid) and noncomedo subtypes, which prognosticates on the likelihood of progression or local recurrence:

DCIS Characteristic	Comedo	Noncomedo
Nuclear grade	High	Low
ER	-	+
HER2 overexpression	Present	Absent
Distribution	Continuous	Multifocal
Necrosis	Present	Absent
Local recurrence	High	Low
Prognosis	Worse	Better

LCIS

Arises from the terminal duct apparatus and shows a diffuse distribution throughout the breast, which explains its presentation as a nonpalpable mass in most cases.

Infiltrating ductal carcinoma

The most commonly diagnosed breast tumour (75%). Has a tendency to metastasise via lymphatics. Has no specific histologic characteristics other than invasion through the basement membrane. DCIS is a frequently associated finding on pathologic examination. Typically metastasises to axillary LNs first.

Infiltrating lobular carcinoma

Much lower incidence (15%). Characterised histologically by the 'Indian file' arrangement of small tumour cells. Like ductal carcinoma, infiltrating lobular carcinoma typically metastasises to axillary LNs first. However, it also has a tendency to be more multifocal. Despite this, the prognosis is comparable to that of ductal carcinoma.

Medullary carcinoma

Relatively uncommon (5%). Generally occurs in younger women. Most present with a bulky palpable mass with axillary lymphadenopathy. Diagnosis depends on a histological triad:

1. Sheets of anaplastic tumour cells with scant stroma.
2. Moderate or marked stromal lymphoid infiltrate.
3. Histological circumscription or a pushing border.

DCIS may be observed in the surrounding normal tissues. Typically ER-, PR- and HER2-. TP53 is commonly mutated.

Mucinous carcinoma

Rather rare (fewer than 5%). Usually presents in the 60s as a palpable mass or appears mammographically.

Excellent prognosis (80% 10-year survival).

Mucin production is the histological hallmark with 2 main forms, type A and B, with AB lesions possessing features of both. Type A represents the classic variety with larger quantities of extracellular mucin, whereas type B shows endocrine differentiation.

DCIS is not a frequent occurrence, although it may be found. Most are ER+ and PR+. HER2 overexpression in rare. These carcinomas predominantly express glycoproteins MUC2 and MUC6.

Tubular carcinoma

1-2%. Single layer of epithelial cells with low-grade nuclei and apical cytoplasmic snoutings arranged in well-formed tubules and glands. L

ow incidence of LN involvement and very high overall survival rate. Because of its good prognosis, patients are often treated only with breast-conserving surgery and local radiation therapy.

Papillary carcinoma

1-2%. Women older than 60y. Centrally located in the breast and can present as a bloody nipple discharge. Strongly ER+ and PR+.

2 common types: Cystic (non-invasive) and micropapillary ductal carcinoma (invasive). The cystic type has a low mitotic activity, which results in a more indolent course and good prognosis. Micropapillary ductal carcinoma has a more aggressive phenotype, even though 70% are ER+. LN metastasis is seen frequently.

Metaplastic breast cancer (MBC)

1%. Older women. Higher incidence in blacks. Combination of adenocarcinoma + mesenchymal and epithelial components.

A wide variety of histologic patterns including:

• Spindle cell carcinoma
• Carcinosarcoma
• Squamous cell carcinoma of ductal origin
• Adenosquamous carcinoma, etc.

The diverse group of malignancies is identified as a single entity based on a similarity in clinical behavious. When compared with infiltrating ductal carcinomam MBC tumours are larger, more rapidly growing, commonly LN-negative, and typically ER-, PR-, HER-.

Mammary Paget disease

Relatively rare (1-4%). Peak incidence in the 50s.

This adenocarcinoma is localised within the epidermis of the nipple-areola complex and composed of the histologic hallmark Paget cells within the basement membrane. Paget cells are large, pale epithelial cells with hyperchromatic, atypical nuclei, dispersed between the keratinocytes singly or as a cluster of cells.

Lesions are predominantly unilateral, developing insidiously as a scaly, fissured, oozing, or erythematous nipple-areola complex. Retraction or ulceration of the nipple is often noted, along with symptoms of itching, tingling, burning or pain.

Ovarian cancer

3 cell types make up the normal ovary: Surface epithelial cells (multipotential); sex cord/stromal cells (multipotential); germ cells (totipotential).

Risk factors: Nulliparity and Fx. OCP reduces the risk :)

Genetics: 5-10% of all ovarian cancers are familial. Most are caused by mutations in BRCA1 and BRCA2. The average lifetime risk for ovarian cancer approximates 30% for BRCA1 carriers; somewhat lower in BRCA2 carriers.

Sporadic cancers:

• BRCA1 and BRCA2 mutations are seen in only 10% of sporadic ovarian cancers.
• HER2/NEU is overexpressed in 35%, and is associated with a poor prognosis.
• K-RAS protein is overexpressed in up to 30%, mostly mucinous cystadenocarcinomas.
• p53 is mutated in about 50% as with other cancers.

Surface epithelial cells

• Serous
• Mucinous
• Endometrioid
• Clear cell
• Brenner
• Cystadenofibroma

Germ cell

• Teratoma
• Dysgerminoma
• Endodermal sinus tumour
• Choriocarinoma

Sex cord-stroma

• Fibroma
• Cranulosa-theca cell tumour
• Sertoli-Leydig cell tumour
  

Surgery is also out.

All OK :)

Medicine is out.

My first result is out. I was reading in bed when my mobile groaned on my bedside table. I groaned too. Who was it now? ‘Medicine is out’, said the message. Oh, I see.

I allowed myself to fall back into bed and became very aware of my beating heart and of a whirlpool of doom forming in my gut. Slowly I got out of bed and walked calmly to the computer. I almost whistled to convince myself that I was completely calm and in control of the freaky situation. I took the book with me, so that I could pretend to read while my computer switched itself on, the browser coughed into motion and esims loaded.

But I couldn’t read, so I prayed instead. A D, please please please! Give me a D! A D! A D! While I went on with my sad mantra I entered esims. And there it was, my result.

I prayed for a D because the last time I did well in my exams (four whole years ago), I prayed for a C when I wanted a B. And I actually got an A and a B in the subjects that mattered. So I repeat, like a superstitious monkey, the small things that led me to success four years ago. I beg for the minimum I need to scrape by to perhaps get something better.

I almost forgot: My result was OK. OKish.

ARDS - acute respiratory distress syndrome

Info from Burkitt pg 179

Characterised by rapid, shallow breathing, severe hypoxaemia, stiff lungs, diffuse pulmonary opacity on CXR.

Pathophysiology

1. Insult to the lung.
2. Increased permeability of pulmonary capillaries + damaged type I pneumocytes.
3. Leakage of protein-rich fluid into alveolar interstitium (interstitial oedema).
4. Lung compliance is reduced - stiff lungs.
5. Reduced alveolar ventilation.
6. Leakage of fluid into alveolar spaces until they are filled.
7. Disruption of V/Q ration, causing R to L shunting of blood.
8. The intra-alveolar fluid later condenses to form a hyaline membrane which lines the alveoli. This is histologically similar to the natal form of the disease.
9. If the patient recovers, the interstitial damage may result in diffuse interstitial fibrosis.

Note that cardiac failure plays no party in the development of ARDS, although cardiac failure may later complicate ARDS.

Clinical features

• Rapid shallow respiration.
• Only scattered crepitations on auscultation.
• Usually no cough, no chest pain, no haemoptysis.
• ABG reveals low PaO2 but usually normal PaCO2 unless very severe.
• CXR may be normal initially, with interstitial markings progressively increasing to complete or partial 'white out'.
• May be difficult to distinguish from cardiac failure. Cardiac diameter is usually normal in ARDS, and heart failure usually responds to diuretic therapy.

Treatment

The overall objective is to maintain respiratory function and cardiovascular stability while the underlying causes e.g. sepsis is treated. This should be carried out in ITU.

Most patients need mechanical ventilation with PEEP (positive end-expiratory pressure).

Fluid balance is complex; they need a CVP. Cardiac output can be measured with TOE (trans-oesophageal echo).

One of the treatment aims is to produce a negative fluid balance and thus help minimise accumulation of fluid in the lung and interstitial tissue. Loop diuretic infusions or continuous veno-venous haemofiltration can be used to achieve this.

In these patients, diuretics alone do not control pulmonary oedema but instead aggravate the hypovolaemia and shock associated with the underlying cause.

Renal failure is a common complication, sometimes prevented by early use of drugs such as dopamine.

Mortality rate for complicated ARDS approaches 90%.

Causes

Direct insults to the lung = ARDS Causes.

Systemic insults to the lung = STAN BEC DEAD.

Respiratory complications of surgery

Up to 15% of patients suffer from respiratory complications associated with general anaesthesia and major operations. The most common of these are atelectasis and pneumonia.

Pre-existing lung disease greatly increases the risk of complications. Severely ill patients, including those with acute pancreatitis, and burns or trauma victims, are susceptible to the development or ARDS.

Effects of anaesthesia and surgery on respiratory function
Anaesthesia and surgery predispose to postoperative complications by altering lung function and compromising normal defence mechanisms as follows:

• Lung tidal volume may be reduced by as much as 50%, depending on the incision site. Thoracic, upper abdominal and lower abdominal incisions (in decreasing order of effect) reduce lung volume.
  
  
• Lung expansion is reduced by the supine posture during and after operation, pain, abdominal distension, abdominal constriction by bandages and the effects of sedative drugs.
  
  
• Ventilation rate usually increases and there is loss of normal periodic hyperinflation.
  
  
• Diminished ventilation and pulmonary perfusion result in reduced gaseous exchange.
  
  
• Airway defences are compromised by loss of the cough reflex and diminished ciliary activity, which both lead to accumulation of secretions.
  
  
• Problems associated with laparoscopic abdominal surgery - the pneumoperitoneum and head-down position lead to diaphragmatic splinting, a reduction in functional residual capacity and changes in intrathoracic blood volume. These lead to atelectasis, pulmonary shunting and hypoxaemia.

Atelectasis

Atelectasis or alveolar collapse occurs when airways become obstructed and air is absorbed from the air spaces distal to the obstruction.

Bronchial secretions are the main cause of this obstruction. Predisposing factors include shallow ventilation, loss of periodic hyperinflation, inhibition of coughing and pooling of mucus. All of these are particular problems after thoracic or abdominal surgery.

The resulting V/Q mismatch produces a degree of R to L shunting of the blood and tends to cause a fall in PaO2.

If the obstructed airways are small, there is only minor segmental collapse, in which case localising signs are minimal and x-ray appearance is unremarkable. Despite this, the overall extent of collapse may be large and cause significant hypoxia.

Obstruction of a major airway causes collapse and consolidation of a whole lobe, resulting in the typical clinical signs of dullness to percussion and reduced breath sounds or bronchial breathing.

CXR will show the lobe to be contracted and opacified with mediastinal shift and compensatory expansion of other lobes.

Most cases of atelectasis are relatively mild and pass undiagnosed, although the patient may be slow to recover from operation.

The patient may be cyanosed, resulting from mild hypoxaemia, and have a mild tachypnoea, tachycardia and low-grade pyrexia, which all resolve spontaneously within a few days. Sputum culture (if any is produced) is usually negative but infection may complicate severe cases.

Prevention and Rx:

1. Preop and postop physiotherapy. This includes deep breathing exercises, regular adjustments of posture and vigorous coughing. During physiotherapt, wounds should be supported by the patient's hand.
2. Analgesia, e.g. infiltration of the wound with local anaesthetic or epidural analgesia, facilitates physiotherapy and mobility.
3. Nebulised bronchodilators e.g. salbutamol may assist the patient to cough up secretions.
4. Severe cases of diffuse atelectasis may require endotracheal intubation and positive-pressure ventilation.
5. Lobar or whole lung collapse requires intensive physiotherapy and sometimes flexible bronchoscopy to aspirate occluding mucus plugs.

Pneumonia

Bronchopneumonia is the usual form of chest infection seen in surgical patients. It occurs secondarily to chronic lung disease, chronic smoking or following atelectasis or aspiration of gastric contents.

Haemophilus and Strep. pyogenes are the common infecting organisms but coliforms may be responsible in elderly, debilitated or seriously ill patients.

Pseudomonas bronchopneumonia occurs in patients on ventilators or with bronchiectasis.

Infection is manifest by pyrexia, tachypnoea, tachycardia, increased leucocyte count.

Mucopurulent sputum is thick, copious and green.

Antibiotics, usually amoxicillin or co-trimoxazole, are given on a best-guess basis until sputum culture and sensitivities are available.

Physiotherapy and encouragement to cough are equally important for recovery.

Incomplete - Missing aspiration pneumonitis, aspiration pneumonia, ARDS. INfo from Burkitt pg 177.

Thyroid adenoma

from http://www.fpnotebook.com/Endo/Hemeonc/ThyrdAdnm.htm.

1. Simple or colloid Macrofollicular Adenoma

• Most common type
• Follicles of normal size

2. Embryonal (Trabecular) adenoma

• Mostly stroma and minimal follicles

3. Fetal Microfollicular Adenoma

• Small follicles with minimal colloid
• Follicular cancer found in 5% of cases

4. Hurthle Cell Adenoma (uncommon)

Papillary carcinoma of the thyroid

Papillary carcinoma constitutes about two thirds of thyroid malignancies in adults and nearly all thyroid malignancies in children. Females are affected at least three times as often as males and the peak incidence is between 30y and 45y.

Histologically, the tumour forms a complex branching papillary structure with a fibrovascular stroma, often containing calcified 'psammoma bodies'.

Tumours vary over a wide range of epithelial dysplasia between apparently benign and obviously malignant.

Whatever the degree of dysplasia, the tumours grow slowly.

Papillary carcinomas are microscopically multicentric in about 80% of cases and about one third affect both lobes; this is important in planning treatment.

The tumour occasionally invades locally into trachea or oesophagus. Metastasis is to central cervical and later lateral cervical LNs and only rarely to distant sites such as lung or bone.

By presentation, LN are involved in about 40% of patients (90% in children).

LN enlargement is often the sole presenting feature and the histology of involved LNs is so close to normal thyroid tissue that at one time this condition was known as 'lateral aberrant thyroid'.

The prognosis of papillary carcinoma is the best of all thyroid carcinomas with only about 10% of patients dying of the tumour after 10y; it is remarkable that survival is hardly prejudiced by the presence of LN mets.

Symptoms and signs

Papillary ca presents as a slow-growing thyroid nodule.......... incomplete

Management

Total thyroidectomy because of the high risk of other foci within the gland.

Palpable cervical nodes are removed at the same operation. The operation is no more difficult than subtotal thyroidectomy but carries a higher risk of post-op hypoparathyroidism.

Total thyroidectomy has the added advantage that recurrent local disease, LN or distant mets can then effectively be treated with radioiodine (131I). This requires a very high TSH level which only occurs if no normal thyroid tissue remains.

A further advantage is that plasma thyroglobulin can then be used as a tumour marker to detect recurrent disease.

After treatment, hormone replacement is necessary to keep TSH close to zero to minimise the risk of stimulating any residual malignant cells.

Since papillary ca progress so slowly and only 15% develop contralateral lobe recurrence, some surgeons prefer to retain one thyroid lobe if the primary tumour is small and there are no palpable or isotope-detectable nodules. Their reasoning is that any further tumours can be removed later without reducing life expectancy.

Follicular carcinoma of the thyroid

Info from Burkitt pg 720

Follicular carcinoma is another well-differentiated thyroid malignancy.

Histologically, the neoplastic cells form a well-developed follicular pattern which is impossible to distinguish from benign adenomatous hyperplasia on FNA cytology; even on histology of the surgical specimen, it may also be difficult to diagnose malignancy unless there is evident capsular or vascular invasion.

Unlike papillary carcinoma, multicentricity is common.

The peak incidence of follicular carcinoma is between 40y and 50y, older than for papillary ca, but it is still three times more common in women. Generally, follicular carcinoma grows slowly and metastasises at a late stage.

In contrast to papillary carcinoma, metastasis tends to occur via the bloodstream to the lungs, bone and other remote sites rather than to local lymph nodes.

Since follicular carcinoma is rarely multicentric, management depends on the extent of local invasion. A tumour with only microinvasion of the capsule has a very good prognosis and only requires removal of the thyroid lobe containing the tumour. If, however, there is gross capsular invasion or vascular invasion (or known remote mets), total thyroidectomy is performed.

The purpose of total thyroidectomy is not to treat the local tumour but to enhance radioiodine uptake by metastatic lesions should this be required later for diagnosis, or any consequent Rx with high-dose radioiodine (as with papillary carcinoma).

Prognosis can be predicted by the degree of capsular and vascular invasion by the primary lesion and on histology. If there is no invasion, 10y survival is close to 100% but this falls to 30% if there is extensive local invasion.

ERCP

Procedure

A catheter is advanced from a side-viewing duodenoscope into the CBD. Contrast medium is injected and x-rays taken to show lesions in the biliary tree and pancreatic ducts.

Diagnostic indications

1. Cholangitis.
2. Jaundice with dilated intrahepatic ducts.
3. Jaundice with normal calibre ducts and a non-diagnostic liver biopsy.
4. Recurrent pancreatitis.
5. Post-cholecystectomy pain.

Therapeutic indications

1. Sphincterotomy for CBD stones.
2. Stenting of malignant strictures.

Pre-procedure

1. LFT, clotting, platelet count.
2. Antibiotic prophylaxis e.g. ciprofloxacin 750mg PO 2h before.
3. Analgesia e.g. pethidine.
4. Sedation e.g. midazolam 2.5-10mg IV.

Complications

1. Pancreatitis.
2. Bleeding.
3. Cholangitis.
4. Perforation.
5. Mortality less 0.2% overall; 0.4% if performing stone removal.

Complications of bowel stoma

Early complications

• Mucosal sloughing or necrosis of the terminal bowel due to ischaemia.
  Rx = Reoperation and refashioning.
  
  
• Obstruction of stoma due to oedema/faecal impaction/adhesions.
  Rx = Exploration with a gloved finger and sometimes glycerol suppositories or softening enemas.
  
  
• Persistent leak between skin and appliance causing skin erosion and patient distress, often due to inappropriate location of stoma (e.g. over skin crease).
  Rx = May respond to stoma nursing care or require a resiting operation.
  
  
• Haemorrhage at stoma site.
  
  
• Stoma ischaemia - colour progresses from dusky grey to black.
  
  
• High output - can lead to hypokalaemia. Consider loperamide +/- codeine to thicken the output.
  

Late complications

• Obstruction (failure at operation to close the lateral space around stoma).
  
  
• Parastomal hernia due to abdominal wall weakness. Risk increases with time.
  Rx = Resiting.
  
  
• Prolapse of bowel.
  Rx = refashioning.
  
  
• Parastomal fistula.
  Rx = refashioning.
  
  
• Retraction of spout ileostomy
  Rx = refashioning.
  
  
• Stenosis of stomal orifice.
  Rx = refashioning.
  
  
• Perforation after colonic irrigation.
  Rx = emergency operation.
  
  
• Dermatitis around stoma site (worse with ileostomy).
  
  
• Psychological and psychosexual dysfunction.
  Rx = Counselling or measures to reverse stoma.
  

Causes of haematuria

Renal causes TTP PING

• Tubulointerstitial nephritis
• Trauma
• PCKD
• Papillary necrosis
• Neoplasia
• Infection (pyelonephritis)
• GN

Extrarenal CINT

• Calculi
• Infection (cystitis, prostatitis, urethritis)
• Neoplasia (bladder, prostate, urethra)
• Trauma (E.g. from catheter)

Causes of false +ve dipstick haematuria

• Haemoglobinuria
• Myoglobin e.g. in rhabdomyolysis
• Beetroot
• Porphyria
• Alkaptonuria
• Rifampicin
• Phenindione
• Phenolphthalein

Tests
Urine MC&S
CBC
ESR & CRP
U&E
Clotting
...
AXR/KUB
Urine cytology
Estimation of proteinuria
Renal US +/- renal biopsy

What is liver fibrosis?

1. Activated stellate cells ('myofibroblast').
   
   
2. Dense ECM in the space of Disse (types I and III collagen are deposited... normal liver has type IV collagen in the space of Disse).
   
   
3. Loss of fenestrations between sinusoidal endothelial cells.
   
   
4. Hepatocytes lose their microvilli (which normally project into the space of Disse).
   
   
5. Kupffer cells are activated and produce plenty a cytokine.

Information from Robbins diagram on pg 636.

What is cirrhosis?

1) Diffuse loss of normal hepatic architecture.
2) Fibrosis.
3) Nodular regeneration.

Complications of thyroidectomy

From Burkitt's Essential Surgery.

Complications during operation

1. Uncontrollable haemorrhage - uncommon, usually results from a slipped ligature on the upper pole vessels which then retract.
   
   
2. Unilateral or bilateral recurrent laryngeal nerve damage - bilateral nerve damage presents as laryngeal obstruction after tracheal extubation and necessitates immediate tracheostomy. Unilateral damage causes hoarseness and a weak voice and impairs coughing.
   
   
3. Inadvertent damage to other structures - tracheal or oesophageal perforation or damage to laryngeal muscles or nerves.

Early post-op (within 12h)

1. Major haemorrhage - presents as rapid swelling of the neck or a large volume of blood loss via the wound drain. Instantly remove sutures for clot evacuation + emergency surgical exploration of the wound to release the clot (to prevent laryngeal oedema) and achieve haemostasis.
   
   
2. Mediastinal haemorrhage - Presents with hypovolaemic shock.
   
   
3. Laryngeal oedema - Presents as stridor, rapidly progressing to respiratory obstruction. This requires endotracheal intubation.
   
   
4. Thyrotoxic crisis - Abrupt onset of extreme agitation and confusion, hyperpyrexia, profuse sweating and rapid tachycardia or other arrhythmia. This requires emergency beta-adrenergic blockade, IV hydrocortisone and KI therapy.
   
   The mortality of thyrotoxic crisis is 10% from coma, pulmonary oedema or circulatory collapse. The condition is very rare if the patient is rendered euthyroid before surgery.
   

Later post-op complications

1. Hypoparathyroidism - Due to inadvertent parathyroid gland damage. Presents with muscle cramps, paraesthesiae and tetany within 36h of operation. Treat with calcium and vitamin D analogues.
   
   
2. Unilateral recurrent laryngeal nerve damage - Hoarseness and defective cough.
   
   
3. External laryngeal nerve damage - Changes the quality of the voice.

Long-term complications

1. Hypothyroidism - often overlooked because it develops insidious;y. Features are loss of energy, weight gain, depression and intellectual deterioration and intolerance of cold weather.
   
   
2. Recurrent thyrotoxicosis - Insufficient gland removed.
   

Pneumonia

What's in the alveoli?

• Consolidation = Many bacteria + scattered polymorphs + oedema fluid.
  
  
• Red hepatisation = Packed with polymorphs + red cells + fibrin + fibrinous pleurisy.
  
  
• Grey hepatisation = Red cells lyse + fibrinous exudate persists.
  
  
• Resolution = Exudate resorbed/digested/expectorated + intact structure + pleura resolves or organises with adhesions.

This happens in both lobar and broncho pneumonia, but is more 'dramatic' in bronchopneumonia.

Pleural involvement is more common in lobar pneumonia, and complications are more common in lobar pneumonia.

Uncommon complications of pneumonia

1. Lung abscess (a localised suppurative area, characterised by necrosis).
2. Empyema.
3. Alveolar fibrosis in organisation.
4. Bacteraemia with metastatic abscesses --> endocarditis, meningitis, arthritis.
5. Pleural adhesions.
6. Bronchiectasis (caused by necrotising pneumonias, commonly due to anaerobes +/- aerobes and uncommonly due to S. aureus, Klebsiella, or S. pyogenes type 3 pneumococcus).
   

How is VSD a complication of MI?

The question is: Isn't VSD a congenital defect? So how come it is a complication of MI?

The pathogenesis is: MI --> rupture of intraventricular septum as a complication of the MI --> new VSD (ventricular septal defect).

Robbins lists three types of myocardial rupture:

1. Rupture of the ventricular free wall --> haemopericardium --> cardiac tamponade (usually fatal)
2. Rupture of intraventricular septum --> new VSD and L to R shunt
3. Papillary muscle rupture --> mitral regurgitation.

Causes of clubbing

Idiopathic

Lung

• Suppurative lung disease (bronchiectasis, empyema, abscess)
• Malignancy
• Fibrosis

Cardiac

• Infective endocarditis
• Cyanotic congenital heart disease

GIT

• IBD
• Cirrhosis

Thyroid

• Thyroid acropachy (due to autoimmune thyroid disease)
  

Postoperative wound management

Once a wound has been closed, the doctor has three main responsibilities: Choosing the dressing, monitoring the progress of healing and deciding when to remove the sutures.

Dressings

The purposes of dressings for surgical wounds are:

• To maintain the wound in a warm and moist state most conducive to healing.
• To absorb or contain any superficial bleeding or inflammatory exudate.
• To protect the delicate healing tissue from trauma, bacterial contamination and interference.
• To prevent suture catching on clothing or other objects.
• To conceal the wound from view.
• To apply pressure to the wound if haematoma formation is likely.

Types of wound dressing:

• For small surgical wounds, particularly on the face, a dressing is often unnecessary as the linear crust of inflammatory exudate performs this task admirably.

• For other simple wounds, plastic spray dressing is suitable e.g. Opsite.

• In most other cases, prepacked adhesive dressings are used, incorporating an absorbent pad with non-stick film in contact with the wound surface.
  
  While convenient, these dressings may conceal accumulations of blood, inflammatory exudate or infected discharge. Wound inspection then requires painful removal of the dressing which can be an opportunity for infection to enter.
  
  
• Transparent semi-permeable plastic film dressings neatly overcome this problem but are unsuitable for discharging wounds.
  
  
• Paraffin gauze (tulle gras) is used mainly for covering raw areas e.g. skin-graft donor sites. However, its non-stick paraffin content rapidly diminishes and blood clot and tissue proliferation soon incorporate the dressing via its open weave. As removal tends to damage the delicate new epithelium, a better alternative dressing is:
  
  
• A flexible polyamide net coated with soft silicone (e.g. Mepitel). This has very low wound adherence and is usually easy to remove when necessary.
  
  
• Other dressings include saline-soaked gauze, calcium alginate (seaweed orgin), hydrocolloids and hydrogels.
  
  
• Gamgee is a thick cotton wool dressing material enveloped in a thin layer of gauze; this is variously used for padding sites vulnerable to trauma (e.g. amputation stumps), as pads beneath pressure bandages or as absorbent dressings for leaking wounds.

Dry dressings need regular replacement and may be prevented from sticking by first placing a piece of non-adherent dressing material, e.g. Melonin, against the wound.

If dry dressings are used for infected wounds, exudate must not be allowed to permeate to the surface as bacteria rapidly spread from here to the environment ('strike-through').

Removal of dressings

Provided the dressing remains clean and dry and the patient afebrile and generally well, there is no need to inspect clean surgical wounds until the time of suture removal.

If wound complications are suspected, the dressing should be removed and the wound checked and redressed as appropriate.

If infection is apparent, a wound swab should be taken for C&S. Localised abscess formation requires removal and probing to effect drainage, whilst spreading cellulitis requires antibiotic therapy in addition.

Removal of sutures

Skin sutures should be removed as soon as the wound is strong enough (i.e. the edges are sticky enough) to remain intact without support.

On the back and around joints, this can rake 14 days; on the abdomen it takes about 7 days (longer in the case of steroid therapy or infection). Factors that may delay healing are age, chrinic illnesse e.g. DM and IHD, steroids, infection, tension.

On the face and neck healing is rapid and less influenced by functional stresses. Here, sutures can be removed after 3-5 days, giving a better cosmetic result - where cosmesis matters remove sutures as early as possible.

Management of infected surgical wounds

Grossly infected surgical wounds must be opened up to ensure free drainage, and cleaned.

All necrotic tissue is excised (necrosectomy) leaving only healthy tissue, and the wound packed daily afterwards with saline-soaked gauze.

The wound is usually allowed to heal by secondary intention, although a large wound can be sutured later when infection is no longer a problem (delayed primary closure).

In the case of deep, slowly healing wounds, a silicone foam dressing can be employed.

Drains in the post-operative period

Abdominal drains provide a potential route for infection top enter the abdomen even though the intra-abdominal pressure nearly always exceeds the external pressure.

The risk can be minimised by ensuring the drain opens into a sterile environment such as a drainage bag (closed drainage) and by removing the drain as soon as its task is completed.

Decisions about removal of drains should rest with the operating surgeon who will undoubtedly have personal preferences.

The general principles of drain management are as follows:

• Suction drains help to collapse down spaces lift in the tissues at operation, e.g. in mastectomy, thyroidectomy, excision of the rectum, as well as to drain blood and inflammatory exudate.
  
  A suction drain is usually retained only for 24 hours after operation unless susbtantial drainage (e.g. more than 30mL/24h) persists.
  
  
• Non-suction drains, e.g. large-bore silicone or rubber tubes or corrugated drains, are mainly used for bowel and biliary anastomoses and in abscess drainage.
  
  They are left in place for about 5 days. Some surgeons prefer to withdraw the drain in stages so that the deep part of the drainage tract can collapse progressively, reducing the risk of leaving a deep pool of fluid.
  

Principles of haemostasis

Bleeding is an unavoidable part of surgery. Blood loss should be minimised because bleeding obscures the operative field and hampers operative technique and because the loss has to be made up later.

Excessive bleeding can be averted by judicious dissection with control of bleeding as the operation proceeds, and by minimising the area of raw tissue exposed at the operation site by accurately siting the incision and by avoiding opening unnecessary tissue planes.

Clipping, ligation and under-running

Ligation is obligatory when large vessels are divided and is desirable for vessels larger than 1mm calibre.

If the end of a bleeding vessel cannot be grasped by haemostat forceps, a suture can be used to encircle the vessel and its surrounding tissues, a technique often referred to as under-running. It is particularly useful for a bleeding artery in the fibrous base of a peptic ulcer.

Diathermy

Diathermy achieves haemostasis by local intravascular coagulation and contraction of the vessel wall caused by heat generated by electrical waveforms.

However, enough heat is also produced to burn the tissues and these may be needlessly damaged by careless use, particularly near the skin or nerves.

Diathermy is ineffective for large vessels, which should be ligated.

There are three main variants of diathermy; all three modes are available on diathermy machines:

1. Monopolar diathermy
   
   Is the most widely used, but there is wide dispersion of the coagulating and heating effects, making it unsuitable for use near nerves and other delicate structures.
   
   Since the current passes through the patient's body, there is a risk of coagulating vessels en passant (e.g. monopolar diathermy used in circumcision may cause penile thrombosis), as well as provoking arrhythmias in patients with cardiac pacemakers.
   
   Monopolar diathermy mat also result in skin burns at the indifferent electrode plate if skin contact is poor or if the plate becomes wet during operation.
   
   Current recommendations to improve contact include shaving hair from the skin where the plate is used and using disposable self-adhesive diathermy plates.
   
   
2. Bipolar diathermy
   
   Used mainly for finer surgery. The current passes only between the blades of the forceps and it requires fairly accurate grasping of the bleeding vessel.
   
   It uses low levels of electrical power, there is almost no electrical dispersion from the tip of the forceps and much less heat is generated.
   
   The main advantages are minimal tissue damage around the point of coagulation and safety in relation to nearby nerves, blood vessels and cardiac pacemakers.
   
   
3. Cutting diathermy
   
   Mainly used for dividing large masses of muscle (e.g. during thoracotomy or access to the hip joint) and cutting vascular tissues (e.g. breast).
   
   The intention is a form of sharp dissection, at the same time coagulating the numerous small blood vessels as the tissue is cut - this is not always effective. A blend of cutting and coagulation is sometimes used.

Tourniquet and exsanguination

This technique is used in surgery of the limbs and hands where a bloodless field is particularly desirable.

A pneumatic tourniquet is placed proximally around the limb. The limb is exsanguinated by elevation and spiral application of a rubber bandage (Esmarck) or ring exsanguinator from the periphery; the tourniquet is then inflated.

UL tourniquets must not be left inflated for more than 30 minutes and LL tourniquets for more than 1 hour to avoid the risk of necrosis.

Pressure

Pressure is a useful means of controlling bleeding until platelet aggregation, reactive vasoconstriction and blood coagulation take over.

It can be used for emergency control of severe arterial or venous bleeding but is equally useful for controlling diffuse small-vessel bleeding from a large raw area, e.g. liver bed after cholecystectomy.

Pressure is usually applied with gauze swabs which must be kept in position for at least 10 minutes.

Even if bleeding is not arrested completely, this process usually allows a clearer view and allows haemostasis by standard means.

For intractable bleeding which is not amenable to ligature, diathermy or suture, various resorbable packing materials, e.g. oxidised cellulose, can be left in position until haemostasis occurs, allowing the wound to be closed.

If bleeding simply cannot be controlled, e.g. after liver injury, the bleeding cavity can be packed with gauze swabs which are left in situ and removed 48-72 hours later at a further operation. Bleeding, once controlled by this method, rarely recurs.

When a raw cavity has been created beneath the skin, external pressure dressings are sometimes a useful method of controlling potential postoperative oozing and minimising haematoma formation, e.g. after breast lump excision.

Hypotensive anaesthesia

Sometimes employed when marked diffuse bleeding is anticipated, e.g. prostatectomy, or where a bloodless field is desirable for fine dissection but where a tourniquet is impossible, e.g. parotid surgery.

The anaesthetist achieves controlled hypotension by the judicious infusion of drugs such as nitroprusside.