​What is Pathology - What are granulomas, exactly? 
Granulomas are clumps of epithelioid macrophages and lymphocytes, with the occasional multinucleated giant cell, that are the characteristics of granulomatous inflammation. The cytoplasm of epithelioid macrophages is loaded with vacuoles and lysosomes, which distinguishes them from other macrophages. Their cell boundaries are close together, giving the structure a "epithelioid" appearance (i.e., it resembles the epithelial layer of the skin).

What is Surgery – Thyroglossal cyst 

DEFINITION Remnants of the thyroglossal tract were discovered along the thyroid gland's course of descent. 

AETIOLOGY
The thyroglossal duct is an embryonic mesoderm tube that originates between the first and second branchial pouches, and is represented by the tongue's foramen caecum. During development, it descends to a pre tracheal location to produce the thyroid gland. The duct usually disappears  by the sixth week, but if some tissue remains along its path, it may grow into a cyst. lingual or ectopic thyroid tissue is seen in one to two percent of cases. 

EPIDEMIOLOGY 
It mostly affects children or adolescents, and the average age of onset is 5 years (but it can range from 4 months to 70 years). Branchial cysts are three times as prevalent than ovarian cysts. 

HISTORY
 In the midline of the anterior neck, a swelling or lump is seen, which is usually asymptomatic, but in 5% of instances, there may be discomfort or rapid expansion due to infection. 

EXAMINATION 
Smooth, spherical swelling in the midline (90 percent; 10% can be lateral, with 95 percent on the left side), usually between the thyroid notch and the hyoid bone, but also occasionally in the submental region. 

Moves upwards with tongue protrusion and swallowing, and is frequently transilluminated.

 Lymph node, epidermal inclusion (dermoid) cysts, salivary duct abnormalities, or ectopic thyroid tissue are all possible differential diagnoses. 

PATHOLOGY/PATHOGENESIS
 Thyroglossal cysts can appear anywhere along the thyroglossal duct route, with 75 percent occurring before the hyoid. Non-keratinising stratified squamous, columnar, or cuboidal epithelium lines the cyst, which is filled with mucoid debris. Ectopic thyroid tissue may be present. 

INVESTIGATIONS 
To distinguish cysts from other structures (cysts have a high signal on T2 weighting) considered Ultrasound or MRI scan. Thyroid function tests in the blood. Pre-operative fine-needle aspiration cytology (typically benign epithelia, respiratory or squamous). 

MANAGEMENT 
Antibiotics are used to treat any type of acute infection. Surgical: The Sistrunk procedure (removal of the cyst and any duct remnants, as well as the central section of the hyoid bone) is used for excision. The tract may occasionally extend to the mouth, necessitating the removal of a tiny part of the tongue. 

COMPLICATIONS
 The most prevalent consequence is infection. After infection and spontaneous rupture, attempted drainage, or incomplete excision, a thyroglossal sinus or fistula may occur. Carcinoma in the thyroglossal duct cyst is a rare occurrence. 

PROGNOSIS 
Good, however even with good technique, recurrence rates are 7–8%, with infection being the most prevalent cause.

​What Is Surgery – Salivary Gland Cancer Symptoms 

DEFINITION 
Tumors that arise in the major (parotid, submandibular, sublingual) or minor salivary glands, with a variety of histological subtypes. The parotid gland (20 percent malignant), the submandibular gland (30–50 percent malignant), and the minor salivary glands (15 percent malignant).Tumors of the sublingual gland are uncommon (0.3 percent , but nearly all malignant). 

AETIOLOGY 
The reason behind this is unknown

RISK FACTORS/ASSOCIATIONS 
Smoking (Warthin's), radiation (Warthin's and mucoepi-dermoid carcinoma), and the Epstein-Barr virus which is linked to lymphoepithelial tumours. 

EPIDEMIOLOGY 
The majority of cases are in adults, and they are rather uncommon. Pleomorphic adenoma: 42 years on average, Warthin's tumour: 60 years on average (male>female); acinic cell carcinoma: women in their 50s; squamous carcinomas: men in their 70s. 

HISTORY A swelling that is normally painless and grows slowly. When a tumour is malignant, it is more likely to cause pain. 

EXAMINATION 
The edoema should be thoroughly inspected for signs of fixation. induration or ulceration of the surrounding skin or mucosa in locally advanced instances. A bimanual palpation of the submandibular gland is recommended. Deep lobe parotid tumours may expand into the parapharyngeal space, necessitating an examination of the oral cavity. Evidence of regional lymphadenopathy and facial nerve function in parotid lesions (weakness should trigger concern of malignancy). 

INVESTIGATIONS 
Ultrasound, CT, or MRI scanning are utilised to delineate the mass and its connection to adjacent structures, as well as to stage the procedure. FNA can be utilised for tissue biopsy, but it cannot be depended on completely for histological diagnosis. Because of the potential of tumour leakage, incisional or excisional biopsy of tumours in large glands should be avoided. 

Histology: Tumors that are benign: Pleomorphic adenoma accounts for 80-85% of all parotid gland tumours. Without a genuine capsule, epithelial or myoepithelial cells are more likely to return following excision. Warthin's tumour (papillary cystadenoma lymphomatosum, formerly known as adeno-lymphoma) accounts for 15% of parotid neoplasms, 10% of which are bilateral or multi-centric and contain glandular and cystic features, as well as eosinophilic epithelium. Acinic cell carcinoma is the most prevalent type of malignant cancer in the parotid gland. Lymphocytic infiltrates can be found throughout a wide histological spectrum. Mucoepidermoid carcinoma: The most frequent malignant tumour of the parotid gland, ranging in severity from low to high. Adenoid cystic carcinoma (6 percent of all submandibular malignancies) is aggressive, with perineural progression into the brain and the possibility for late metastases. 

Squamous, adenocarcinoma, and undifferentiated carcinomas are all aggressive cancers. 

Non-epithelial tumours (such as haemangiomas and lymphomas) are extremely rare. 

MANAGEMENT 
Medical: Lymphoma or infective masses are treated with the medication. Excision is a surgical procedure that is used to remove both benign and malignant tumours. 

Parotid: Superficial or whole parotidectomy with careful preservation of the facial nerve and its branches that run between the deep and superficial lobes (for benign or low-grade cancers). If the nerve is affected, it can be sacrificed and immediately rebuilt with a nerve graft. 

Submandibular: Tumours are accessed with a submandibular triangular incision. The lingual or hypoglossal nerves may be involved in malignant tumours, necessitating excision. The patient should be informed about the partial loss of sensation and movement of the tongue as a result of this. There's also a chance that the mandibular branch of the facial nerve will be injured, resulting in asymmetry in the mouth and lower lip. If lymph nodes are implicated, a neck dissection is performed. 

Carcinomas of the palate: Excision of a large portion of the palate, which may necessitate difficult repair. If the cancer is malignant, adjuvant post-operative radiotherapy should be provided. Chemotherapy is mainly reserved for palliation because it is not particularly effective. 


CONSEQUENCES OF PAROTIDECTOMY: Facial nerve injury, haemorrhage, skin flap necrosis, salivary fistula, and Frey's syndrome (10–50 percent, abnormal regeneration of postganglionic parasympathetic nerve fibres that normally innervate the parotid to sympathetic nerves of sweat glands, resulting in gustatory sweating.Because of the existence of pseudopod-like extensions from the tumour, pleomorphic adenomas have a high rate of recurrence if only simple enucleation is performed. 

PROGNOSIS 
Pleomorphic adenomas gradually increase if not removed, and there is a risk of malignant transformation (5 percent ). The 5-year survival rate for mucoepidermoid carcinoma is 70%. (but worse for higher-grade forms). Because perineural invasion is difficult to eliminate and has a tendency for late recurrence, adenoid cystic carcinoma has a poor prognosis. Low-grade tumours have a 10-year survival rate of 80–95 percent, but high-grade tumours have a survival rate of only 25–50 percent.

​What is Surgery – Parathyroid Gland Disease
 
DEFINITION
Primary hyperparathyroidism with hypercalcemia and osteomalacia is caused by benign tumours of the parathyroid gland (parathyroid adenomas) or parathyroid hyperplasia with excessive parathyroid hormone (PTH) release.
Malignancy is a rare occurrence (parathyroid adenocarcinomas).
 
AETIOLOGY
The specific reason for the formation of these benign tumours is unknown. Previous radiation to the head, neck, and chest has been linked to a higher risk of parathyroid adenomas. Endocrine tumour syndromes (such as MENI and MENIIa) can cause parathyroid adenomas.
 
EPIDEMIOLOGY
Uncommon. Approximately 1 in 1000; most common in people between the ages of 50 and 70.
 
HISTORY
Hypercalcaemia is frequently asymptomatic and detected with basic blood tests. Hypercalcaemia can cause the following symptoms: Fatigue, myalgia, ,arthralgia bone ache,nephrolithiasis depression, anxiety, and a loss of consciousness as well as pancreatitis
 
EXAMINATION
Other than the consequences of hypercalcaemia, there is usually nothing to uncover on inspection.
 
INVESTIGATIONS
 U&E (to determine fluid balance and electrolytes), bone profile (Ca2+, phosphate), and plasma PTH Urine: Urinary calcium levels have increased. Simple radiographs: Osteopenia is also known as osteoporosis. Lesions in the bones that are cystic.
 
CXR: To rule out sarcoidosis. The location of the adenoma may be determined by technetium-99 scintigraphy.
 
DEXA bone scan: Required to determine the degree of osteopenia or osteoporosis. US neck: Parathyroid adenomas can have a characteristic look.
 
MANAGEMENT
 IV rehydration is used to treat hypercalcemia (normal saline). To increase renal calcium excretion, continue to maintain fluids using loop diuretics (e.g. furosemide) after rehydrated. Other electrolytes should be kept an eye on.
 
Consider intravenous pamidronate (which increases bone resorption), calcitonin, or steroids (which are only useful in other types of hypercalcemia). Neck exploration and total parathyroidectomy (removal of all aberrant glands) are the procedures used. Directed parathyroidectomy may be an option if the adenoma site is clearly recognised (needs more than one modality); alternatively, parathyroidectomy guided by intraoperative monitoring of PTH levels can be conducted because PTH levels diminish within minutes after the adenoma is removed.
 
COMPLICATIONS
 Surgical risks include: Hypoparathyroidism caused by 'hungry bone syndrome' after surgery may necessitate short-term calcium and vitamin D supplements. The likelihood of recurrent laryngeal nerve damage is high, especially if the neck is extensively explored. Vocal cord paralysis can be detected using a laryngoscopy, and an early intervention to repair a severed nerve can help to reverse some of the damage. A neck haematoma can obstruct the airway by compressing the trachea; large haematomas may necessitate surgery to remove the haematoma. Hypercalcaemia complications include nephrolithiasis, osteoporosis, and cognitive impairment.
 
PROGNOSIS It's ideal if the adenoma is completely eradicated. Many patients don't require any extra supplements.

​What is Surgery – Branchial Cyst, Sinus, Fistula  
DEFINITION 
Neck swelling or discharge caused by incomplete pharyngeal clefts and pouches obliteration during embryonic development. 

AETIOLOGY
Although the specific embryological origin is contested, 95% of them derive from congenital remains of the second pharyngeal pouch or branchial cleft (possibly incomplete involution or ectopic tissue). 

EPIDEMIOLOGY 
Uncommon. Branchial cysts are the most prevalent, appearing most frequently in the third decade and presenting with variations. Children are more likely to have fistulae and sinuses. 

HISTORY The patient has a lateral neck swelling that can change in size over time; it is normally painless until inflammation and infection occur, at which point it becomes painful and red. A sinus or fistula appears as a depression in the neck that discharges mucus or mucopurulent fluid. 



EXAMINATION 
A lump (cyst) is located just deep to the sternocleidomastoid at the intersection of its upper and lower two-thirds.  The swelling is normally ovoid, smooth, and firm on palpation, but it can be soft in the early stages, fluctuate, and transilluminate. 2% are bilateral.

 The intersection of the middle and lower one-third of the anterior edge of the sternocleidomastoid is where the external opening of a branchial sinus or fistula is located. 

PATHOLOGY/PATHOGENESIS
In the fifth week of development, branchial clefts, or grooves in the neck, with branchial arches in between, are form. The external auditory meatus remains in the first cleft, while the others usually fade away. 

A cyst, sinus, or fistula may form if parts of the second cleft remain. Squamous or respiratory epithelium lines the cysts, which contain turbid fluid containing epithelial debris and cholesterol crystals, as well as lymphoid tissue in rare cases.

 A branchial fistula connects the internal and external carotid arteries in the oropharynx, terminating superior to the hypoglossal nerve and inferior to the glossopharyngeal nerve in the posterior section of the tonsillar fossa. 

INVESTIGATIONS 
The cyst can be visualised with ultrasound, CT, or MRI scanning. FNA: Used to distinguish thyroid cancer and mucoepidermoid carcinomas of the salivary glands that may have a significant cystic component from cervical lymph node metastases in older people (e.g. thyroid cancer and mucoepidermoid carcinomas of the salivary glands that may have a significant cystic component). 

MANAGEMENT
 Surgery: The cyst and any related sinus or tract are surgically removed. A transverse neck incision is commonly used for this procedure. To gain access to the cyst, the platysma is split and the sternomastoid is retracted posteriorly. It is then carefully dissected with identification and nerve injury avoided before being removed (especially the vagus, hypoglossal and spinal accessory nerves). Before removing a branchial cyst, the abscess should be drained and medicines provided to prevent infection. 

COMPLICATIONS 
Infection, branchial cyst abscess, nerve injury during surgery, and inadequate sinus or fistula tract excision are all possible complications. 

PROGNOSIS 
Good, with full excision resulting in cure. If there has been a previous infection, the chances of recurrence are higher.

​What is Surgery – Ruptured Spleen Symptoms 

Splenic rupture is a condition in which the spleen ruptures. 

DEFINITION
A significant intra-abdominal haemorrhage can arise from a splenic rupture. a severity rating system (American Association for the Surgery of Trauma) 

Minor subcapsular rupture (1 cm) or haemorrhage, (grade 1) (10 percent of surface area) 

Non-expanding subcapsular haematoma (Grade 2) Intraparenchymal haematoma, 10–50% of surface area, 5 cm diameter 

ruptured subcapsular or intraparenchymal haematoma involving more than 50% of the surface area, intraparenchymal haematoma involving more than 5 cm, laceration involving more than 3 cm or involving trabecular arteries (Grade3 )

Laceration of segmental or hilar arteries, resulting in severe devascularization (Grade 4) 

Spleen devascularization, broken spleen, and hilar vascular injury (Grade 5) 

AETIOLOGY
The most common causes are non-penetrating trauma or rapid deceleration injury. This syndrome has also been associated to traumatic internal organ injuries, such as the liver, kidney, pancreas, and diaphragm, as well as rib fractures. Splenomegaly and its causes, such as infectious mononucleosis, malaria, and leukaemia, are linked to an increased risk of rupture even from minor trauma. 

EPIDEMIOLOGY
It's fairly common, with up to 25% of major trauma patients experiencing some kind of it. 

HISTORY 
A history of blunt trauma exists. Kehr's sign is abdominal pain that can be generalised or specific to the left flank, with referred pain to the left shoulder point. 

EXAMINATION 
In the abdomen, there is tenderness, guarding, and rigidity (generalised or left flank only). Symptoms of shock (e.g. hypotension, tachycardia). There may be a delay in rupture for several days following the trauma due to the formation of a subcapsular haematoma that grows in size before rupturing. 

INVESTIGATIONS 
Blood tests include FBC, U&Es, LFTs, clotting, and crossmatch. A targeted sonographic examination for trauma in order to detect fluid in the peritoneal cavity, which could indicate an intra-abdominal haemorrhage. To detect splenic damage as well as other organ trauma, a CT scan is used. CXR may reveal rib fractures, diaphragmatic rupture, or a left pulmonary contusion. 

Diagnostic peritoneal lavage: Detects free intraperitoneal blood; now that FAST and CT scanning are available, this test is rarely done. 

MANAGEMENT
 It is determined by the patient's hemodynamic status as well as the degree of the lesion. Resuscitation includes wide-bore IV access, fluids, transfusion if necessary, and avoiding overinfusion (permissive hypotension may be tolerated). 

Grade 1 and Grade 2: Proceed with caution, keeping a close check on everything and conducting regular reviews. Consider interventional radiological methods to embolize a bleeding location.

 Grade 3: A laparotomy as well as splenorrhaphy/splenectomy may be necessary. 

Grades 4 and 5 require splenectomy. Following surgery, vaccination against pneumococcal, meningococcal (Men C), and haemophilus organisms is suggested. 

Children as young as 15 years old can receive antibiotic prophylaxis, with patients given a home supply of medicines to take at the first sign of infection. 

COMPLICATIONS 
As a result of the damage, there was haemorrhage and mortality. Splenectomy carries a number of risks, including haemorrhage, post-splenectomy sepsis, the risk of encapsulated organism infections, thrombotic vascular event (splenic/splanchnic venous thrombosis), pancreatic damage, pancreatitis, subphrenic abscess, gastric distension, and localised gastric necrosis. After splenorrhaphy, the leftover spleen bleeds or thromboses. 

PROGNOSIS There is a 75% likelihood of mortality if the condition is not treated. After treatment, the typical death rate ranges between 3% and 23%.

​What is Surgery – Sepsis Diagnosis 
Sepsis and the systemic inflammatory response syndrome (SIRS) 

DEFINITION 
When two or more of the following are present, SIRS is considered: Heart rate >90 beats per minute. Temperature should be 36°C or higher (>38°C). PaC024.3 kPa or tachypnoea >20/minute (32 mmHg). >12,000 cells/mm3 or >10 percent immature neutrophils (WCC 4000). 

SIRS Plus infection = sepsis. Sepsis with organ failure, hypotension, or hypoperfusion is known as severe sepsis. Sepsis-induced hypotension despite adequate fluid resuscitation is referred to as septic shock. SIRS is a frequent inflammatory response to a wide range of physiological stressors, including infection, ischaemia, inflammation, e.g. pancreatitis, trauma, and burns. Multiple organ dysfunction syndrome (MODS) occurs when an acutely unwell patient's organ function is disrupted to the point where haemostasis cannot be maintained without intervention. 

EPIDEMIOLOGY 
All ages, extremes of age, and comorbidities have a detrimental impact on the result. 

HISTORY Whether infectious, traumatic, ischemic, or inflammatory, it depends on the aetiology. 

EXAMINATION 
For diagnosis, a thorough examination is performed, paying close attention to vital signs, urine output, and mental status. The respiratory rate is a sensitive indicator of sickness severity. 

PATHOLOGY/PATHOGENESIS 
Local cytokines induce an inflammatory response in response to an insult in order to fight infection and promote recovery. To improve the local response, cytokines are released into circulation. The release of endogenous antagonists and a decrease in pro-inflammatory mediators normally govern the acute-phase response. If homeostasis is not restored, inflammation and coagulation take over, resulting in microcirculatory thrombosis, hypoperfusion, ischaemia, loss of circulatory integrity, and tissue damage. 

INVESTIGATIONS
 FBC, U&E, LFT, amylase, and cardiac enzymes are all tested in the blood. CRP and ESR are two inflammatory markers, as are IL6, IL8, pro-calcitonin, and LPS-binding protein. 
ABG: Indicates the severity of acidosis and lactate levels. Blood, sputum, urine, lines, CSF, joint fluid, ascites, pleural effusion and other possibly contaminated locations are all cultures. 

Imaging studies are used to identify and sample the source of infection. 

MANAGEMENT 
Stabilization of the patient as soon as possible.ABC resuscitation. In sepsis, start empirical antibiotics right away and support organ function. 

With a systematic approach developed into the Surviving Sepsis Campaign, targeted and protocol-driven early 'goal-directed therapy' of fluid and inotropic support has been shown to enhance the prognosis from sepsis. 

The following are also some of the goal-directed therapy : venous pressure in the heart 8–12 mmHg, a mean arterial pressure of less than 65 mmHg ,0.5 ml/kg/hour urine output. Oxygen saturation in the central venous system is greater than 70%.

Supportive measures include critical care, glycemic control, nutrition, DVT prevention, and stress ulcer prevention. 

Acute renal failure is a common complication of severe sepsis, and it may necessitate renal replacement treatment. 

Even if a septic patient's renal function is normal, early high-volume continuous veno-venous haemofiltration may be recommended. Some of the pro-inflammatory or pro-coagulant cytokines that drive the septic cascade are hypothesised to be removed during this process. 

Activated protein C (drotrecogin alpha): The PROWESS research found that recombinant-activated protein C (drotrecogin alpha) lowers mortality in patients with severe sepsis (higher risk of bleeding). 

Surgical: Acute surgical difficulties, such as abscess drainage and infected tissue removal/debridement, should be deal  correctly. 

COMPLICATIONS 
Renal failure, coagulopathy, liver failure, ARDS, and mortality are all symptoms of multi-organ dysfunction. 

PROGNOSIS 
SIRS has a 7% mortality rate, severe sepsis has a 30% mortality rate, and septic shock has a 50% mortality rate. Each new organ failure increases mortality rates by 15–20 percent.

What is Surgery – Sebaceous Cyst Removal 

DEFINITION 
A blocked hair follicle causes an epithelium-lined, keratinous, debris-filled cyst. Epidermal cyst is the correct term. 

AETIOLOGY 
The pilosebaceous gland is occluded. Common in Gardner's syndrome.

EPIDEMIOLOGY
Is quite common in people of all ages. 

HISTORY 
Skin swelling that is non-tender and grows slowly, frequently in multiples. If there is a superimposed inflammation or infection, the skin may become red, hot, and painful. 

EXAMINATION
Overlying punctum on a smooth tethered mass in the skin. Hair-bearing parts of the body, such as the scalp, trunk, and scrotum, are common. It's possible to get granular creamy stuff with an unpleasant odour. 

PATHOLOGY/PATHOGENESIS 
These cysts are not made up of sebaceous glands, despite their name. The cystic growth of epidermal cells within the dermis causes sebaceous cysts. The infundibulum of the hair follicle is frequently the source of this epidermis. 

INVESTIGATIONS 
In most cases, none is required. FNA or excision biopsy are only used in rare cases. 

MANAGEMENT 
Conservative: If it isn't causing the patient any discomfort, it can be left alone. Surgical: Cyst excision can be performed under local anaesthetic. If the cyst is not completely removed, it is likely to return. If an abscess forms, it should be drained. Antibiotics may be provided if there is an infection; nevertheless, once the acute inflammation has subsided, the definitive therapy is excision. 

COMPLICATIONS 
Infection leads to the creation of an abscess. If the excision is not complete, the cyst will return. It's possible that it'll ulcerate and seem like a skin cancer (Cock's unusual tumour). If the discharged fluids dry out and create a horn-shaped protrusion, a sebaceous horn may arise. PROGNOSIS: Good; most don't need therapy, and excision is usually curative.

​What is Surgery – Pilonidal Sinus Surgery
 
DEFINITION
A pilonidal sinus (Latin for "hair nest") is a hair-filled aberrant epithelium-lined duct that opens to the skin surface, most commonly in the natal cleft.
 
AETIOLOGY
Shed or sheared hairs are thought to penetrate the skin, causing an inflammatory reaction and sinus formation, with occasional negative pressure drawing in additional hair and perpetuating the cycle.
 
EPIDEMIOLOGY
Male > female, annual incidence of 26 per 100,000, mean age of presentation 19 (women) and 21 years (men).Associated with hirsute individual.
 
Certain occupation may predispose to for example, hairdressers may develop interdigital pilonidal sinus. Due to soldiers suffering the illness during World War II, it is known as 'jeep bottom.'
 
HISTORY
A painful natal cleft, especially if inflamed or infected, with concomitant discharge or swelling, which the patient may complain of. This is a recurring issue.
 
EXAMINATION Between the buttocks, midline holes or pits can be visible, from which hairs may protrude. A sensitive swelling occurs if there is an accompanying infection or abscess, which may be fluctuant or exude pus or bloodstained fluid when compressed. Secondary opening, often known as pits, are very prevalent.
 
Squamous epithelium lines the sinus tract, which reaches a varied distance into subcutaneous tissue and frequently has branching side channels. In the accompanying granulation tissue, hair shafts and foreign body giant cells can be detected. Inflammation and the creation of a polymicrobial abscess packed with granulation tissue, pus, and hair result from the tracking of bacteria.
 
INVESTIGATIONS For diagnosis, none is required. Check glucose (for diabetes) if there is  infection WCC might be elevated.
 
MANAGEMENT
Acute pilonidal abscess: Removal of pus and hair usually involves incision and drainage (which can be done under local anaesthetic if the abscess is minor). The cavity is irrigated and packed, with dressings changed on a regular basis until secondary closure is achieved. Antibiotics are usually not required after surgery. Excision of the sinus tract, skin healing, and avoidance of recurrence are the treatment principles for chronic pilonidal sinus. Excision under general anaesthesia with examination, laying open, and removal of tracts (methylene blue staining may be used to identify them). It is possible to split the fibrous tissue tracts linked to the sacrococcygeal bone. Wound closure by primary intention (midline or off midline) or secondary intention (wound left open and healing).
 
Wounds that have been closed heal faster on average, but there is a higher chance of recurrence. Wounds that are off the midline heal faster and are less likely to reoccur.
 
The Karydakis procedure flattens and lateralizes the midline cleft by performing an asymmetric excision with a lateral closure.
 
Bascom technique: Midline pits are excised and closed, then the chronic abscess cavity is removed via a lateral incision, leaving the lateral wound exposed. Preventing recurrence requires attention to hygiene in the affected area, as well as depilation or shaving.
 
COMPLICATIONS
 Pain, infection, abscess, and recurrence are all possible outcomes.
 
PROGNOSIS With the right management, it's great. Complicated disease is inconvenient and can lead to recurrent infection. By the age of 40, the condition is usually resolved.

​What is Surgery – Peritonitis Signs and Symptoms 

DEFINITION 
Peritonitis is an inflammation of the peritoneal lining of the abdominal cavity that can be localised or generalised, with the latter being either primary or secondary.

 AETIOLOGY
 Appendicitis, cholecystitis, diverticulitis, and salpingitis are common causes. Bacterial infection of the peritoneal cavity with no evident focus is the primary cause. Streptococcus penumoniae can cause primary pneumococcal peritonitis in children. Adults with CAPD are frequently linked with cirrhosis and ascites (spontaneous bacterial peritonitis) or renal failure (continuous ambulatory peritoneal dialysis). Peritonitis spreads from a localised infective focus, either polymicrobial or nonbacterial, due to leakage of bile, blood, gastric contents, e.g. perforated peptic ulcer, pancreatic secretions (a chemical peritonitis that frequently becomes secondary infected). 

EPIDEMIOLOGY
Primary peritonitis is uncommon and usually affects adolescent females; however, localised and secondary generalised peritonitis are more prevalent. 

HISTORY 
An in-depth history of the origin, type, course, and spread of abdominal pain, as well as exacerbating, alleviating, and related factors, should be collected. Peritonitis causes persistent, sharp, localised pain that is aggravated by movement and coughing (parietal peritoneum is supplied by somatic A-fibers coming from T7–L2 spinal neurons). 

EXAMINATION 
Examine vital signs, evidence of dehydration, and signs of perfusion compromise (e.g., hypovolaemia, sepsis, or circulatory failure). Localised: Tenderness with involuntary guarding: reflex contraction of overlaying abdominal wall muscles; rebound tenderness: pain caused by movement of the inflamed peritoneum when a palpating hand is suddenly removed, comparable to percussion tenderness or pain provoked by coughing. 

Generalized: The patient is frequently quite sick, with systemic indications of toxaemia or sepsis (e.g., fever, tachycardia); movement aggravates pain. Due to paralytic ileus, the abdomen is rigid with generalised guarding and rebound, and bowel sounds are attenuated or nonexistent. 

INVESTIGATIONS
 As evidenced by the patient's medical history and clinical evaluation. FBC, U&Es, LFT, amylase, CRP, clotting, G&S or crossmatch, blood cultures, pregnancy test, and ABG (to check for metabolic acidosis, lactate levels, or respiratory failure). 

Pneumoperitoneum is treated by an erect CXR. AXR is used to treat bowel blockage. To determine the cause of the peritonitis, a CT scan of the abdomen or a laparoscopy may be used. When the peritoneum is inflamed, it loses its lustrous aspect and becomes erythematous, producing copious serous inflammatory exudate that is rich in white blood cells, protein, and inflammatory mediators. The larger omentum adheres to the inflamed organ, forming a barrier to infection spread.
 
If you have ascites, you should: Gram stain and culture, ascitic tap and cell count (diagnostic of SBP if >250 neutrophils/mm3) 

MANAGEMENT Localized: Treatment will be determined by the underlying cause (appendectomy in appendicitis), as well as IV antibiotics (cholecystitis, salpingitis, and most cases of acute diverticulitis). 

Generalized: The patient is in danger of dying as a result of sepsis and shock. IV fluid resuscitation, volume and electrolyte balance correction, and IV antibiotics are required. To monitor fluid balance and surgical intervention, a urinary catheter, NG tube, and CVP line are used. To identify and treat the source, remove infected or necrotic tissue, and perform profuse peritoneal lavage, an urgent laparotomy/laparoscopy is required. Acute non-necrotising pancreatitis is an exception. Primary peritonitis is treated with antibiotics, however the diagnosis is often missed until after operational intervention has been attempted. 

COMPLICATIONS 
Septic shock, respiratory or multi-organ failure, paralytic ileus, wound infection, tertiary peritonitis (persistence of intra-abdominal infection), abscesses, portal pyaemia/hepatic abscesses are all common early complications.
 Late complications: adhesions and incisional hernia. 

PROGNOSIS
 Localised peritonitis usually goes away with proper treatment of the underlying cause. Generalised peritonitis has a substantially greater fatality rate, which can be as high as 30–50%. The development of septic shock or multi-organ dysfunction at the same time can increase the mortality rate to more than 70%. With the right antibiotics, primary peritonitis has an excellent prognosis. If diagnosis and treatment are delayed, the total death rate of patients with SBP may surpass 30%.