​Surgery -Laparoscopic Abdominal Surgery
Indications 
minimal access surgery of the abdomen or pelvis, in which a laparoscopic camera (either at a 0°, 30°, or 45° angle) is inserted through a port into the peritoneal cavity for inspection and to direct the manipulation of additional instruments inserted through other ports after a CO2 pneumoperitoneum has been created.

Diagnostic: Used for directed biopsy or emergency assessment of abdominal trauma, as well as for the study of abdominal or pelvic pain, focused liver illness, abdominal masses, and the staging of malignant disease.

Therapeutic: A lot of procedures involving the abdomen can now be completed with minimally invasive techniques. Laparoscopic cholecystectomy, appendixectomy, fundoplication, colectomies, hernia repairs, nephrectomy, prostatectomy, and bariatric operations are among the frequently performed procedures. Other operations, such as laparoscopic-assisted hysterectomy, can benefit from laparoscopy assistance.

Relative contraindications include respiratory insufficiency, the existence of dilated colon, and untreated coagulopathy. Conversion to open surgery may be more likely if prior open surgery was performed ("likelihood of adhesions").

Anatomy 
In otherwise healthy patients, the physiological effects of a pneumoperitoneum are typically well tolerated; however, patients with heart disease may find them more difficult to bear.
Cardiovascular: decreased cardiac output; elevated pulmonary and systemic vascular resistance; elevated cardiac preload; decreased renal, hepatic, and splanchnic flow.
Renin and aldosterone, sympathomimetic reaction, and renal vasoconstriction are examples of metabolic and autonomic processes.

Investigational studies
Blood: coagulation and FBC.
as suitable for the planned process.

Actions 
carried out while under general anesthesia.
Preparation: Depending on the planned procedure, a nasogastric tube or urinary catheterization can be used to decompress the bladder and stomach, respectively. The abdominal cavity is prepared and draped.
Pneumoperitoneum: There are three ways to gain access to the peritoneal cavity:
Open (Hassan): The fascia is visible after the initial incision. This is separated, and the Hassan trocar can be fastened using fascial sutures. Using two tissue forceps, the peritoneum is gripped, then the peritoneal cavity is forcefully opened, the Hassan trocar is put into it under direct vision, and insufflation is initiated.

Closed Veress needle: The peritoneal cavity is punctured using a Veress needle. There are two areas of resistance in the midline—the fascia and the peritoneum—and three points of resistance farther laterally—the anterior and posterior sheaths and the peritoneum. The free passage of salt aids in verifying accurate positioning. Low CO2 insufflation pressure is ideal; if it's high, move the needle. After the establishment of the pneumoperitoneum, the trocar is placed and the needle is removed. Because this is a blind treatment, there is a greater risk of injury to blood vessels or the bowel.

Optical trocar: Using a transparent, bladeless trocar and a 0 degree laparoscope, the layers of the abdominal wall can be seen while the trocar is being advanced through the wall by applying direct pressure and twisting. beneficial for those who are fat.

Laparoscope insertion: The laparoscope is used to view the peritoneal cavity and safely direct the insertion of additional ports. It is inserted after the white balance has been adjusted to account for the yellow light of the halogen bulb.

Closure: To ensure there is no bleeding, the instruments and ports are removed under direct eyesight, in accordance with the intended process. Pneumoperitoneum deflation and proper wound closure are carried out. Fascial closure is often not necessary for 5mm ports, but depending on their location, bigger ports (10–12 mm) frequently require it to prevent herniation.

Complications 
Immediate : Extraperitoneal insufflation, damage to the viscera or vessels (vascular injuries reported to occur 0.04–0.5%, visceral injuries 0.06–0.12%), and open Hassan technique against Veress needle or optical trocar had fewer incidences. diaphragmatic splinting brought on by a high inhalation pressure. Pneumothorax and gas embolism are uncommon.
Early signs and symptoms include shoulder tip pain, wound infection, and the aftereffects of an undiagnosed visceral injury (such as peritonitis after a bowel injury or bile duct damage).
Late : Incisional hernia

Surgery -  Cataracts
Introduction 
Opacification of the ocular lens.

Etiology 
The majority of occurrences are age-related idiopathic cataracts, or "senile cataracts."
Among the many secondary reasons are the following:
Local: Intraocular tumors, uveitis, and prior eye trauma.
Systemic conditions include diabetes, myotonic dystrophy, X-ray and UV radiation, medications (steroids), skin conditions (atopic dermatitis, scleroderma), metabolic abnormalities (galactosaemia, hypocalcaemia, Wilson's disease), and genetic syndromes (Down's).
Congenital: Rubella syndrome in children.

Epidemiology 
primary global cause of curable blindness. Age-related increases in cataracts, which impair vision, affect 30% of those over 65 in one or both eyes.

History 

gradual, painless blindness that occurs.
glare from bright lights: In strong light, eyesight might get worse (particularly if the center lens is opacified).
Some people may see haloes surrounding lights and suffer from monocular diplopia.
Some people may discover that they have "lens convergent power" (nuclear sclerotic cataract) and can read without glasses.
Nystagmus or amblyopia may occur in babies.

Examination 

blurry lens look and loss of red reflex. less sharpness in the eyes.


Investigation
In order to choose the best intraocular lens (IOL) implant, biometry is necessary.
Others are superfluous unless they happen early in life or are connected to a systemic illness.

Management 
To prevent amblyopia, congenital cataracts need to be treated as away.
The impact of the cataracts on the patient's life and vision will determine whether or not surgery is necessary.
Operative: It is therapeutic to do phacoemulsification (with an ultrasonic probe), aspirate the lens material, and then install the intraocular lens implant. Particular side effects include endophthalmitis, vitreous humour loss, and posterior capsule opacification. usually performed as day surgery under local anesthesia. Steroid drops (for inflammation), antibiotic drops (for infection prophylaxis), avoiding intense exercise, and ocular trauma should all be part of the post-operative treatment.

Complications 
None other from a lower standard of living due to diminished visual acuity.

Prognosis 
good in treating cataracts brought on by aging.

Surgery - Neck of Femur Fracture 
Introduction 
disruption in the femur's cortical bone continuity at or above the lesser trochanter.
There are two categories into which fractures fall:
Intracapsular: Including subcapital, transcervical, and basicervical; occurs close to the point where the hip joint capsule joins the femur.
 Extracapsular: Subtrochanteric or trochanteric

Etiology 
osteoporosis and a higher frequency of falls among the elderly; additional risk factors include smoking at the moment, having a BMI below 18.5, having had a mild trauma fracture after age 50, having a mother who has had a hip fracture, hyperparathyroidism, and Paget's disease.
anatomy Since the retinacular arteries that travel back along the capsule are the primary source of blood supply to the femoral head, intracapsular fractures have the potential to disrupt this supply and cause avascular necrosis.

Epidemiology 
Frequent in the elderly; lifetime risk for women is 18%, for men it is 6%. 12/100 (over 85 years old), 3/100 (65–74 years old).

History 
Hip pain and movement restriction may arise from a slight fall in the past.

Examination 
There is hip pain and the affected leg is shortened, adducted, and externally rotated.


Investigations
Blood: coagulation, G&S, U&Es, and FBC.
Imaging: Lateral images of the hip and plain AP radiographs. If the diagnosis is unclear, an MRI, a bone scan, or further plain radiographs should be taken 24 to 48 hours later. CXR in case elderly patients need surgery.


Management 
Prevention: Risk evaluation and fall-risk reduction measures.
Medical: For primary or secondary prophylaxis, calcium, vitamin D, HRT, selective oestrogen receptor modulators, bisphosphonates, calciumitonin, fluoride, and thiazides have been utilized.
Prompt: Analgesia, resuscitation, electrolyte and fluid imbalance correction, pressure area care. It is recommended that patients undergo surgery within a day to minimize the possibility of thrombotic problems and pressure damage.
Undisplaced intracapsular fractures: Hemiarthroplasty may be taken into consideration in the extremely old; internal fixation permits early mobilization and lowers the chance of fractures becoming displaced.
Displaced intracapsular fractures: Hemiarthroplasty or total hip replacement (may be acceptable in patients with pre-existing joint illness, good activity levels, and a fair life expectancy), open reduction and internal fixation (for younger, more active patients).
Unless there is a medical reason not to, extracapsular fractures should be surgically treated with reduction and internal fixation using either intramedullary (such as gamma nail implants) or extramedullary (such as sliding screws and plates).
Antibiotic prophylaxis during induction and DVT prevention have to be administered to all patients.

Complications 
Early symptoms include pain, immobility, infections, pressure sores (20%), pulmonary problems (ARDS, fat embolism, pneumonia), DVT (asymptomatic up to 45%, symptomatic up to 11%), and PE (3–13%).
Implant failure, non-union, and avascular necrosis of the femur head are late symptoms.

Prognosis 
After a hip fracture, the elderly have a high death rate (30% at one year), with 25% needing more extensive long-term care.

Surgery -  Septic Arthritis
intra-articular joint infection.

Introduction 
Bacteria can penetrate the joint directly, such as through a puncture wound, or they might spread hemorrhagically from nearby osteomyelitis or from a contaminated prosthesis. An inflammatory response in the joint is triggered by bacteria. A joint effusion is caused by permeability and fluid secretion. Activation of neutrophils and macrophages results in the production of proteolytic enzymes, which, in conjunction with bacterial toxins, cause destruction to the articular cartilage. Fibrosis and bony ankylosis may occur as a result of the raw articular surfaces recovering during the healing process.
Staphylococcus aureus, Neisseria gonorrhoeae in adults, and Haemophilus influenzae or coliforms are the most often occurring causal organisms in children under three years old.

R isk Factors 
Septic arthritis is more common in those with diabetes, IV drug misuse, immunocompromised individuals, and those with chronic joint diseases (such as rheumatoid arthritis).


Epidemiology 
 50% of cases in children under three years old, incidence 6/100,000.

History 

fever, malaise, and joint or limb pain.
usually only affects one big joint, such as the hip in young children, who may exhibit a limp and a refusal to bear weight. While it can affect any joint, older children and adults are more likely to have knee pain.

Examination 

a red, swollen joint; if it's the hip, hold the leg flexed and move it slightly outside to loosen up the ligaments and lessen joint strain.
widespread joint soreness accompanied by a sharp decrease in range of motion.
Skin pustules in the vicinity of the joint may be present if gonococcal arthritis is present.


Investigations

Blood: CRP, ESR, FBC, and blood cultures.
Together with microscopy, culture, and sensitivity, aspiration Aspirate typically murky material including several neutrophils; culture to determine the causing pathogen.
Joint space, soft tissue edema, and in severe cases, subchondral bone loss are all seen on a joint radiograph.
Joint region shows increased absorption on a bone scan.
USS: May direct aspiration in order to detect a joint effusion.

Management 
Surgical: To remove pus and infectious material, surgical washout of the joint is usually necessary. may be carried out through an open operation (arthrotomy) or by arthroscopy.
When a prosthetic joint develops sepsis, the prosthesis must be removed in order to completely eradicate the infection.
Health: IV antibiotics for two weeks at first, then oral antibiotics for a further four to six weeks.
For pain relief, analgesics and a splint should be applied to the joint.
To keep joints mobile and avoid fibrosis, physiotherapy is offered.

Complications 
Joint damage or dislocation, growth disturbance, ankylosis, avascular necrosis of the epiphysis, or subsequent osteoarthritis.

Prognosis 
Outcomes are depending on the virulence of the organism, duration of infection previous to diagnosis, the pre-morbid status of the patient and the joint affected; e.g. knees have better outcomes than ankles. The prognosis is often favorable with prompt, proper therapy.

​Surgery - Skin cancer (basal cell carcinoma) 
Introduction 
Most prevalent type of skin cancer; also referred to as a "rodent ulcer"

Etiology 
prolonged exposure to UV light or the sun. correlated with anomalies of the hedgehog/patched intracellular signaling cascade, as observed in naevoid basal cell carcinoma syndrome, or Gorlin's syndrome. Pitch that becomes photosensitized, tar, and arsenic are additional danger concerns.

Epidemiology 
Frequent in the elderly, uncommon before the age of 40, common in people with fair skin and locations with considerable sun exposure. For Caucasians, the lifetime risk is 1:3.

History 
a persistent, gradually developing skin lesion that mainly affects the face but can also affect the scalp, ears, or trunk.

Examination
Most frequently, nodulo-ulcerative: tiny, shimmering, translucent skin covering a colored papule that initially grows slowly or a core ulcer known as a "rodent ulcer" that has elevated, pearly margins. The surface of the tumor is commonly covered in fine telangiectatic arteries. Lesions that are bigger and more protuberant may exhibit cystic transformation.
Morphoeic: Waxy, yellow-white, expanding plaque with a fuzzy border that tends to be more aggressive.
Superficial: Usually on the trunk, several brown or pink scaly plaques with a thin "whipcord" border that steadily expand to a diameter of more than 10 cm.
Pigmented: Any kind of basal cell carcinoma may have small amounts of brown or black pigment.

Pathogenesis 
The dermis is invaded by small, dark blue-staining basal cells that form in distinct clusters and have palisade-like arrangements on their outer layer. There are several mitotic and apoptotic entities visible. Typically, growth is subtle, consistent, and sluggish. Although it doesn't spread, it has the ability to infiltrate and kill nearby tissues.

Investigations
Rarely is a biopsy required (clinical suspicion is the primary basis for diagnosis).

Management 
For minor superficial lesions, photodynamic treatment, curettage, cauterization, and cryotherapy are employed.
Operative: For discrete nodular or cystic nodules, excision is recommended with a 0.5 cm margin of surrounding normal skin; for large tumors (1 cm in diameter) and lesions close to the eyes, nose, and ears, Mohs' micrographic surgery is the preferred method of treatment. This procedure involves a meticulous examination of tissue removed under frozen section. There may be a need for excision and skin flap covering.
Radiation therapy: beneficial for basal cell carcinomas affecting tissues (such as eyelids and tearducts) that are challenging to repair surgically. There is a chance of adverse effects include radiation dermatitis, ulceration, and depilation, and repeated treatments might be required.


Complications 
The tumor progresses slowly but unabatedly. can cause facial disfigurement. has the ability to infiltrate and cause blindness in the orbit.

Prognosis 
good when given the proper care. If ignored, it could spread, infiltrate, and become ulcerated. To identify further lesions or a local recurrence, routine follow-up is required.

​Surgery - Burns 
Introduction 
Damage to tissue brought on by electrical, thermal, or chemical shock.

Etiology 
contact with chemicals, electricity, liquids, fire, hot objects, UV light, or radiation.

Epidemiology 
Annually, more than 12,000 admissions occur in Wales and England.

History 
Burn circumstances; record duration of contact with agent, temperature, and time. Take into account the possibility of breathing in smoke and poisonous gas poisoning (carbon monoxide). Examine non-accidental injuries in children and adults who are at risk.

Examination 
Watch out for symptoms such as stridor, shortness of breath, hoarse voice, soot in the nostrils, singed nose hairs, and carbonaceous sputum that indicate an inhalational injury or airway compromise. Analyze the burn's location, depth, and dispersion. Examine every surface area of the body. Seek for burns that are circumferential.
Partially thick: separated into the deep and superficial layers. Painful symptoms include blistering and mottling in severe dermal burns and red, oedematous skin in superficial burns.
Full thickness: Both the dermis and the epidermis are destroyed. a stiff, painless, leathery eschar that has lost all sensation due to burning.
Burn size (percentage of body surface area): The Wallace "Rule of Nines" should be applied (arm or head: 9%, anterior or posterior trunk: 18%, leg: 18%, palm area: 1%, and perineum: 1%), or the Lund–Browder chart (for kids).

Pathogenesis 
Burns that are superficially partial thickness cause damage to the epidermis; dead skin peels off after 7 days of recovery. Deep partial burns penetrate the dermis, but sweat and sebum glands are unaffected. Over the course of three weeks, epithelial regrowth heals the wounds, usually leaving no scars unless an infection arises. Completely destroying all skin layers in a full thickness burn necessitates skin grafting; else, scarring and contractures will result in healing.

Investigations 
Bloods: In the event of an inhalational injury, carboxyhemoglobin, arterial blood gases, and O2 saturations. Crossmatch, FBC, U&Es, and G&S in cases of severe burns.
ECG, urine myoglobin indicating muscle injury, and creatine kinase are tested for electrical burns.

Management 
Emergency protocol: Airway security, oxygen administration, and prompt endotracheal intubation in case of inhalational harm are the ABCs. Determine the extent of the burn. If it covers more than 15% of the body's surface (10% in children), IV fluids are needed to avoid hypovolaemic shock. The following methods can be used to estimate fluid requirements:
& the Parkland formula [4 ml weight (kg) %burn, with half the volume given over first 8 hours, the other half over next 16 hours]; or the Muir and Barclay formula [(% burn weight, kg)/2]½fluid (ml) per time period (each 4 hours from time of burn for 12 hours, then each 6 hours for 12 hours, and then over 12 hours).
A sterile dressing should be applied to the burn, along with analgesic medication and tetanus prevention.
There is no preventative use of antibiotics due to the possibility of resistance growing. nutritional assistance for severe burns because of the highly catabolic state. Early physical therapy helps stop contractures from forming. Think about moving to a specialized unit.
Surgery: An escarotomy is a longitudinal incision made over circumferential burns to relieve constrictions that could impair perfusion in the limbs or chest movement.
Skin grafting: After stability, for deep partial thickness or complete thickness

Complications 
Early symptoms include dyspnea, hypothermia, cardiac depression, rhabdomyolysis, compartment syndrome, peptic ulcers (such as Curling's ulcer), or erosive gastritis.
Late: Contractures and hypertrophic scarring.

Prognosis 
Depending on the age of the patient, the depth and severity of the burn, and the emergence of complications (mortality risk is roughly equal to the product of age and burn percentage).

​Surgery -  Necrotizing Fasciitis and Gangrene
Introduction 
Gangrene is a type of tissue necrosis that can be dry (due to desiccation), wet (due to infection), or gas-filled.
A potentially fatal illness that spreads quickly along fascial planes is necrotizing fasciitis.
Perineum necrotizing fasciitis is a symptom of Fournier's gangrene.

Etiology 
Infection, accidental arterial injection (e.g., thiopentone), physical trauma, heat injury, and tissue ischaemia and infarction are all causes of gangrene. Clostridium perfringens is the cause of gas gangrene.
Group A streptococcus infection or a polymicrobial infection involving streptococci, staphylococci, bacteroides, coliforms, or clostridial forms can cause necrotizing fasciitis. 

Risk Factors 
Risk factors for peripheral vascular disease, leg ulcers, cancer, immunosuppression, and steroid use include diabetes. Necrotizing fasciitis can sometimes develop in the absence of a clear risk factor or in connection with surgical, ulcerative, or puncture wounds.

Epidemiology 
While necrotizing fasciitis and gas gangrene are rare, gangrene is somewhat frequent.

History 

Gangrene: Pain and discoloration in the affected location, which is usually one of the extremities or a pressure point.

Necrotizing fasciitis: Pain that is frequently excruciating and excessive for the visible physical symptoms.
History of risk factors or events that predispose (such as surgery, ulcers, and trauma).

Examination 
Gangrene: The erythematous area surrounding the gangrenous tissue is typically the painful area; the latter is usually black due to products of hemoglobin breakdown, lifeless, and insensate. The line of demarcation is the point where the living and dead tissues converge. Wet gangrene is characterized by a strong stench produced by anaerobes, swollen tissue, and possibly pus. Overlying oedema, discoloration, and crepitus are brought on by gas production in gas gangrene, which is caused by the infection spreading and the muscle and tissue being destroyed.

Necrotizing fasciitis: Palpably, there may be crepitus in areas of erythema and oedema as well as areas of hemorrhagic blisters. Pyrexia, tachycardia, tachypnea, and hypotension are related symptoms of sepsis and systemic inflammatory response.

Pathogenesis 
Gangrene: Damage to the tissues and ischemia make bacteria more likely to colonize and multiply. An anaerobic environment fosters organismal synergy, which feeds the cycle of bacterial development and tissue destruction. C. perfringens, C. novyi, and C. septicum are rod-shaped, spore-forming saprophytes that are gram-positive. In the anaerobic environment of injured tissue, they proliferate and generate exotoxins, such as a-lethicinase, which disrupt the local microcirculation and result in sepsis, hemolysis, and necrosis.

Necrotizing fasciitis: Usually a polymicrobial infection that works in concert and spreads along fascial planes. frequently brought on by gram negative and anaerobic synergistic infections, such as enterococci and bacteroides, or Group A b-haemolytic Streptococcus pyogenes.


Investigations 

Blood: blood culture, glucose, CRP, U&Es, and FBC.
Swab from wound, pus/fluid aspirate: Gram stain, culture, sensitivity, and microscopy.
X-ray or CT scanning: may reveal gas in the tissues that an organism has generated.

Management 

In cases of gangrene, rapid surgical debridement of all pus and necrotic tissues is combined with fluid resuscitation and broad-spectrum IV antibiotics.
Necrotizing fasciitis: In addition to broad-spectrum antibiotics (such as penicillin, aminoglycoside, and metronidazole), aggressive debridement of all diseased tissues is required to prevent spread and systemic sepsis. Regular examination of the wound is required because recurrent debridement is frequently required.
Amputation: Suggested when there is no chance of saving the limb or when the gangrene spreads quickly.

Complications 

tissue damage, amputation, sepsis, septic shock, multiple organ failure syndrome, and death are examples of systemic inflammatory response syndrome symptoms.

Prognosis 
Changeable. Recovery is good if a gangrenous limb is amputated early. Poor peripheral vascular health and diabetes are not good predictors of prognosis. Necrotizing fasciitis and gas gangrene are linked to significant morbidity and fatality rates.

​Surgery - Lymphoedema 
introduction 
excessive buildup of lymphatic fluid in the extracellular space as a result of the lymphatic system's compromised performance.

Etiology 
Primary (hereditary): The genetic alterations in the majority of families remain unknown.
Those named are:
Milroy's illness: A mutation in the vascular endothelial growth factor receptor VEGFR-3 gene results in autosomal dominant inheritance.
An inactivating mutation in the transcription factor FOXC2 gene causes lymphoedema distichiasis syndrome. correlated with additional eyelash rows.
Mutations in the transcription factor SOX18 gene cause the hypotrichosis-lymphoedema-telangiectasia syndrome.
Secondary (acquired): Occurs after blockage or damage of lymphatic channels, such as a TB infection, silica, or Wuchereria bancrofti infection (filariasis).
& regional lymphatics can be surgically excised or treated with post-radiotherapy for cancer, most often breast cancer.
malignant lymph node invasion in the area.

Epidemiology 
Principal: Rare; yearly incidence 1/6000–10,000; 2-3 times more prevalent in females.
Secondary: Far more typical. The most frequent cause globally is filariasis.

History 
can appear at any age (lymphoedema distichiasis), during puberty (Milroy's), or at birth. Lower limb swelling occurs most frequently gradually, getting worse towards the end of the day. Other times, the swelling is in the genitalia or arms. Chylothorax, chylous ascites, or leaky skin vesicles are possible presentations in megalymphatics.

Examination 
Skin oedema in its early stages is pitting. Subsequently, the skin turns brawny, fibrotic, and non-pitting; vesicles may start to cry. Toes get squared off, and ankles lose their shape. Areas of skin that become thicker (condylomas) may form.

Pathogenesis 
Primary/congenital lymphoedema is caused by lymphatic valve hypoplasia, hyperplasia, or inadequate function. The buildup of protein-rich fluid and oedema that follows, frequently accompanied by inflammation, causes fibrosis and an overabundance of connective and adipose tissue, which causes swelling in the extremities.

Investigations 

Isotope lymphography: a gamma counter is used to quantify movement after a subcutaneous injection of a colloid labeled with 99 mTc into the foot's first web space.
Contrast lymphangiography is no longer often used.
A CT or MRI scan can reveal lymphoedema-related abnormalities, such as oedema in the fascial planes or thickening of the skin. If an obstructive lesion is present, it can reveal the cause.
Other: tissue/lymph node biopsies or bioelectric impedance analysis.

Management 
Conservative measures include massage using pneumatic devices or manual lymphatic drainage, limb elevation, exercise, graduated compression stockings, and skin or foot care. Venesection or blood pressure monitoring shouldn't be done on limbs that are impacted.
Medical: Infection treatment (e.g., cellulitis antibiotics, tinea pedis antifungals).
Diuretics don't have any advantages.
Surgery: Not often utilized. Surgical techniques employed comprise liposuction combined with forceful postoperative compression; the Homan's procedure entails generating skin flaps, removing subcutaneous tissue, and then resuturing the skin. After skin and subcutaneous tissue are removed, skin grafting is the next step in the Charles reduction process.

Complications 
Boost Skin that is deficient in fluid and protein is more vulnerable to cellulitis, poor cosmesis, pain from enlarged tissue, decreased mobility, and ulceration.

Prognosis 
Good, usually responds to conservative therapy for primary lymphoedema.
Depending on the cause, secondary lymphoedema may occur.

Surgery - Malignant Melanoma
Introduction 
malignancy brought on by the neoplastic alteration of skin pigment-forming melanocytes. the primary reason why skin diseases cause death. can also develop in the leptomeninges, GI tract, eye, or ear.

Etiology 
Multiple factors contribute to the neoplastic transformation, with a build-up of genetic alterations. Inheritable mutations in the tumour suppressor genes CDKN2A and CDK4 have been found in 10% of cases of uncommon familial melanoma syndrome (autosomal dominant). Birth defects, such as xeroderma pigmentosum.
Four categories of histopathology:
(1) Superficial spreading (70%): Usually develops from an already-existing naevus, a flat or elevated brown lesion, potentially with variegate coloring, and it spreads radially prior to the vertical growth phase.
Nodular (15%): De novo, aggressive, ulcerative or bleed readily, lacks radial development phase.

Lentigo maligna (10%): This condition is more prevalent in elderly people who have sun exposure, has large, flat lesions, and grows more slowly. Typically on the arms, neck, or face.
(4) Acral lentiginous (5%): These lesions appear on the soles, palms, and subungual regions. most prevalent kind in non-White populations, with an often postponed diagnosis.
linked to UV radiation exposure (sun exposure, particularly if there is a history of blistering burns, tanning lamp use, and PUVA). Increased number of dysplastic moles and fair skin.

Epidemiology 

steadily rising incidence: in the UK, 6,000 cases are diagnosed annually, whereas in the USA, the lifetime risk is 1/60. Non-white races are at a 20 percent risk from white races. causes 3/4 of skin cancer fatalities but just 4% of skin cancer cases.
H HISTORY
A pigmented skin lesion's size, form, or color changing, as well as any redness, bleeding, crusting, or ulceration. But more than 60% don't start from pre-existing moles.


Examination 
ABCDE criteria for examining moles:
A Asymmetry
B Border irregularity/bleeding
C Colour variation
D Diameter >6mm
E Elevation/evolving changes over time
Amelanotic melanoma is non-pigmented, often associated with nodular subtype or
metastases of undifferentiated melanoma to the skin.

Investigations 
Excisional biopsy: To determine Breslow thickness or Clark's levels and provide a histological diagnosis.
Sentinel lymph node biopsy: Histological examination is used to determine the presence of metastases after lymphoscintigraphy and blue dye are used to identify the nodes.
Staging: CT, MRI, CXR, and PET scans for imaging.
Bloods: LFTs and LDH (metastases frequently occur in the liver).


Management 

Primarily, prevent sunburn, limit excessive sun exposure, and raise public awareness.
Operation: Broad local excision with a margin that varies according to the depth of invasion (<1 mm: 1 cm, 1-4 mm: 2 cm border). Skin grafting can be necessary. If the melanoma is more than 1 mm, a sentinel lymph node biopsy is done; if the results are positive, a complete lymph node dissection is done. Careful follow-up is necessary after treatment.
Diseases with metastases: Chemotherapy: not very effective. Response to dacarbazine in combination with paclitaxel and cisplatin during clinical studies. ought to be included in a trial. High-dose interferon a-2b immunotherapy has been demonstrated in trials to enhance relapse-free survival, but not overall survival (for high-risk tumors >4mm with regional lymph node metastases). Research on vaccinations against melanoma is ongoing.

Complications 
Localized: ulcers and bleeding.
Metastases: mass effect and bleeding.
Post-surgical: Block dissection of lymph nodes may cause wound issues or lymphoedema.

Prognosis 
Five-year survival is 90–95% for lesions that are less than 1 mm deep, 13–69% for node-positive disease, and a 9-month median survival for metastatic disease. Every stage of cancer survival is decreased by ulceration.
Lesions in the trunk as opposed to the limb, ulceration, and an elevated mitotic rate are poorer prognostic indications.
The prognosis is worse for men than for women.

​Surgery - Pressure Sores 
Introduction 
an area usually over bony prominences where pressure, shear, and/or friction have damaged the skin and underlying tissue.

Etiology 
Tissue perfusion is hampered when external pressure rises over the capillary filling pressure (32 mmHg), which leads to ischaemia, acidosis, and waste product buildup. Early tissue damage symptoms include non-blanching erythema in the dermis, which is a sign of perivascular hemorrhage from capillaries. Cell death and tissue necrosis occur in the dermis, subcutaneous tissue, and finally the epidermis over time.

RIsk Factors 
extrinsic: moisture, friction, shear, and pressure.
 Intrinsic factors include age, incapacity, sensory impairment, incontinence, protein-calorie deficiency (a threefold increase in risk is associated with every 10 g/L drop in albumin), comorbidity, and prior pressure injury.

Epidemiology 
Typically, 3–10% of hospitalized patients and residents of nursing homes are over 70 years old, and the UK's annual costs—which primarily consist of nursing time—are expected to be over £2.1 billion.


History 
Caretaker may observe an area of erythema or ulcer; less often, patient complaints of pain in the affected area occur. contributing elements. The majority of injuries develop within the first two weeks of hospitalization, and the causing injury may have happened early in the stay, such as while the patient was on the operating table.

Examination 
The sacrum, coccyx, ischial tuberosities, greater trochanter, malleoli, heels, occiput, and scapulae are among the vulnerable regions.
Stage I: Irritable skin that does not blanch and has unbroken skin. 
Stage II: Dermal ulcer involving the shallow layer (may form a blister).
Stage III: The entire dermis thickness, spreading into the subcutaneous layer.
Stage IV: Invading a tendon, bone, muscle, or joint in addition to deep fascia.
As an example, Stage IV ulcers do not always begin and proceed through Stages I, II, and III. Therefore, this system cannot be used to monitor progression or healing.
It is normal and inevitable for bacteria to colonize wounds; nevertheless, an infection should only be recognized in the event that purulent exudates, erythema, an odor, or systemic symptoms (such as fever) are present.

Investigations 
blood cultures and wound swabs in case of suspected infection.
If underlying osteomyelitis is suspected, standard radiographs, MRIs, bone or 67Gallium scans, or needle bone biopsies may be used.


Management 

The secret is to prevent: Risk evaluation (e.g., Waterlow scores), nutritional status evaluation, and avoiding prolonged bed rest.
Reducing pressure by rotating the patient every two hours. By distributing the pressure between the patient and the bed, pressure-reducing devices—static or dynamic—such as foam or air mattresses, can help prevent pressure on sensitive areas, such as the sacrum, trochanters, and heels.
Management of wounds: decrease in pressure. evaluating the wound's severity, removing necrotic tissue, and adjusting the surrounding conditions to encourage granulation and reepithelialization.
Use of suitable dressings (e.g., hydrocolloid, hydrogel, or alginates) that offer moisture balance, bacterial balance, and debridement. Infection prevention and treatment, nutritional considerations (supplementing zinc and vitamin C deficient individuals).
Surgery: Only available for Stage III or IV ulcers. Debridement of necrotic material and myocutaneous flap rebuilding of the damaged area are crucial because they have a high complication rate and require careful pre- and post-operative management.

Complications 
infection (such as osteomyelitis or cellulitis), persistent sores, and recurrent tendencies.

Prognosis 
Since just one-third of Stage IV pressure ulcers have healed after six months and Stage III may require several weeks of care, prevention is essential.