Because of the substantial risk of thromboembolism early after valve replacement, perioperative initiation of anticoagulation is necessary, despite the increased risk for bleeding. Anticoagulation should be initiated within 24 h after the procedure with unfractionated heparin or low-molecular-weight heparin (LMWH).
Heparin is monitored by checking the activated partial thromboplastin time or anti-Xa activity.
Oral anticoagulants are monitored by INR.

Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a nonsurgical technique for treating obstructive coronary artery disease, including unstable angina, acute myocardial infarction (MI), and multivessel coronary artery disease (CAD).

Inferior STEMI is usually caused by occlusion of the right coronary artery, or less commonly the left circumflex artery, causing infarction of the inferior wall of the heart.

The ECG findings of an acute inferior myocardial infarction include the following:
ST segment elevation in the inferior leads (II, III and aVF)
Reciprocal ST segment depression in the lateral and/or high lateral leads (I, aVL, V5 and V6)

The clinical presentation of basilar artery occlusion (BAO) ranges from mild transient symptoms to devastating strokes with high fatality and morbidity. Often, non-specific prodromal symptoms such as vertigo or headaches are indicative of BAO, and are followed by the hallmarks of BAO, including decreased consciousness, quadriparesis, pupillary and oculomotor abnormalities, dysarthria, and dysphagia. When clinical findings suggest an acute brainstem disorder, BAO has to be confirmed or ruled out as a matter of urgency. If BAO is recognised early and confirmed with multimodal CT or MRI, intravenous thrombolysis or endovascular treatment can be undertaken. The goal of thrombolysis is to restore blood flow in the occluded artery and salvage brain tissue; however, the best treatment approach to improve clinical outcome still needs to be ascertained.

Answer: Yersinia enterocolitica

Yersinia enterocolitica (see the image below) is a bacterial species in the family Enterobacteriaceae that most often causes enterocolitis, acute diarrhoea, terminal ileitis, mesenteric lymphadenitis, and pseudo appendicitis but, if it spreads systemically, can also result in fatal sepsis. Symptoms of Y enterocolitica infection typically include the following:

Diarrhoea – The most common clinical manifestation of this infection; diarrhoea may be bloody in severe cases

Low-grade fever

Abdominal pain – May localize to the right lower quadrant

Vomiting – Present in approximately 15-40% of cases

Mesenteric adenitis, mesenteric ileitis, and acute pseudo appendicitis
These manifestations are characterized by the following symptoms (although nausea, vomiting, diarrhoea, and aphthous ulcers of the mouth can also occur):

Fever

Abdominal pain

Tenderness of the right lower quadrant

Leucocytosis

Pseudo appendicitis syndrome is more common in older children and young adults. Patients with Y enterocolitica infection often undergo appendectomy; several Scandinavian studies suggested a prevalence rate of 3.8-5.6% for infection with Y enterocolitica in patients with suspected appendicitis.

Analysis of several common-source outbreaks in the United States found that 10% of 444 patients with symptomatic, undiagnosed Y enterocolitica infection underwent laparotomy for suspected appendicitis.

Human clinical Y enterocolitica infections ensue after ingestion of the microorganisms in contaminated food or water or by direct inoculation through blood transfusion.

Y enterocolitica is potentially transmitted by contaminated unpasteurized milk and milk products, raw pork, tofu, meats, oysters, and fish. Outbreaks have been associated with raw vegetables; the surface of vegetables can become contaminated with pathogenic microorganisms through contact with soil, irrigation water, fertilizers, equipment, humans, and animals.

Pasteurized milk and dairy products can also cause outbreaks because Yersinia can proliferate at refrigerated temperatures.

Animal reservoirs of Y enterocolitica include swine (principle reservoir), dogs, cats, cows, sheep, goats, rodents, foxes, porcupines, and birds.

Reports of person-to-person spread are conflicting and are generally not observed in large outbreaks. Transmission via blood products has occurred, however, and infection can be transmitted from mother to new-born infant. Faecal-oral transmission among humans has not been proven.

The patient’s history and examination point towards a significant visceral injury. FAST scan is associated with a false-negative result in pregnancy which makes the normal result, in this scenario, less reassuring. CT scan of the abdomen remains the gold standard for diagnosis.

Sonography and FAST scanning are established in pregnancy and provide the advantage of avoiding ionising radiations. However, the sensitivity of the FAST scan is reduced in pregnancy especially with advanced gestational age. CT scan remains the first-line investigation in major trauma where significant visceral injury is suspected. The maximum permitted safe dose of radiation in pregnancy is 5 mSv.

Answer: Rupture of the aorta distal to the left subclavian artery

Aortic rupture is typically the result of a blunt aortic injury in the context of rapid deceleration. After traumatic brain injury, blunt aortic rupture is the second leading cause of death following blunt trauma. Thus, this condition is commonly fatal as blood in the aorta is under great pressure and can quickly escape the vessel through a tear, resulting in rapid haemorrhagic shock, exsanguination, and death.
Traumatic aortic transection or rupture is associated with a sudden and rapid deceleration of the heart and the aorta within the thoracic cavity. Anatomically, the heart and great vessels (superior vena cava, inferior vena cava, pulmonary arteries, pulmonary veins, and aorta) are mobile within the thoracic cavity and not fixed to the chest wall, unlike the descending abdominal aorta. Injury to the aorta during a sudden deceleration commonly originates near the terminal section of the aortic arch, also known as the isthmus. This portion lies just distal to the take-off of the left subclavian artery at the intersection of the mobile and fixed portions of the aorta.

High-probability ECG features of MI are the following:
ST-segment elevation greater than 1 mm in two anatomically contiguous leads
The presence of new Q waves

Intermediate-probability ECG features of MI are the following:
ST-segment depression
T-wave inversion
Other nonspecific ST-T wave abnormalities
Low-probability ECG features of MI are normal ECG findings. However, normal or nonspecific findings on ECGs do not exclude the possibility of MI.

Special attention should be made if there is diffuse ST depression in the precordial and extremity leads associated with more than 1 mm ST elevation in lead aVR, as this may indicate stenosis of the left main coronary artery or the proximal section of the left anterior descending coronary artery.

Localization of the involved myocardium based on the distribution of ECG abnormalities in MI is as follows:
– Inferior wall – II, III, aVF
– Lateral wall – I, aVL, V4 through V6
– Anteroseptal – V1 through V3
– Anterolateral – V1 through V6
– Right ventricular – RV4, RV5
– Posterior wall – R/S ratio greater than 1 in V1 and V2, and – T-wave changes in V1, V8, and V9
– True posterior-wall MIs may cause precordial ST depressions, inverted and hyperacute T waves, or both. ST-segment elevation and upright hyperacute T waves may be evident with the use of right-sided chest leads.

Hyperacute (symmetrical and, often, but not necessarily pointed) T waves are frequently an early sign of MI at any locus.
The appearance of abnormalities in a large number of ECG leads often indicates extensive injury or concomitant pericarditis.
The characteristic ECG changes may be seen in conditions other than acute MI. For example, patients with previous MI and left ventricular aneurysm may have persistent ST elevations resulting from dyskinetic wall motion, rather than from acute myocardial injury. ST-segment changes may also be the result of misplaced precordial leads, early repolarization abnormalities, hypothermia (elevated J point or Osborne waves), or hypothyroidism.
False Q waves may be seen in septal leads in hypertrophic cardiomyopathy (HCM). They may also result from cardiac rotation.
Substantial T-wave inversion may be seen in left ventricular hypertrophy with secondary repolarization changes.
The QT segment may be prolonged because of ischemia or electrolyte disturbances.
Saddleback ST-segment elevation (Brugada epsilon waves) may be seen in leads V1-V3 in patients with a congenital predisposition to life-threatening arrhythmias. This elevation may be confused with that observed in acute anterior MI.
Diffuse brain injuries and haemorrhagic stroke may also trigger changes in T waves, which are usually widespread and global, involving all leads.
Convex ST-segment elevation with upright or inverted T waves is generally indicative of MI in the appropriate clinical setting. ST depression and T-wave changes may also indicate the evolution of NSTEMI.
Patients with a permanent pacemaker may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.
To summarize, non-ischemic causes of ST-segment elevation include left ventricular hypertrophy, pericarditis, ventricular-paced rhythms, hypothermia, hyperkalaemia and other electrolyte imbalances, and left ventricular aneurysm.

Twisting or rotational injuries to the knee in sports, followed by delayed onset of knee swelling and locking are strongly suggestive of a meniscal tear. Arthroscopic meniscectomy is the usual treatment.

Meniscal tear is one of the most common knee injuries, characterized by:
1. A popping sensation
2. Delayed swelling or stiffness of the affected knee
3. Pain, especially when twisting or rotating the knee
4. Difficulty straightening the knee fully
5. Locking of knee in place (patient may be able to unlock the knee)

In older adults, degenerative changes of the knee can also contribute to a torn meniscus with little or no trauma.

A torn meniscus may lead to knee instability, inability to move the knee normally, or persistent/recurrent knee pain. There is a strong likelihood of developing osteoarthritis in the injured knee.

Complications of Transurethral Resection: TURP
T URP syndrome
U rethral stricture/UTI
R etrograde ejaculation
P erforation of the prostate

TURP syndrome can cause a wide variety of symptoms that include asymptomatic hyponatremia, ECG changes, fatigue, vomiting, confusion, visual loss, coma and death. In a conscious and alert patient, changes in the mental state of may be the first sign of TURP syndrome and bladder perforation.

Active, serious haemorrhage due to Warfarin should be treated with four-factor prothrombin complex concentrate (PCC), if available.
While costly, an essential advantage FFP confers to emergency care is that, in contrast to FFP, it results in a more rapid reversal of coagulopathy and does not require thawing or blood group typing. Additionally, it has a reduced risk of volume overload, transfusion-related acute lung injury, transfusion reactions, and infectious disease transmission. Despite these advantages, no mortality benefit has been proven for PCC compared with FFP.
Alternatively, recombinant factor VIIa (rFVIIa) has been reported to be effective in rapidly lowering INR due to warfarin toxicity and may be considered if PCC is not available. FFP is effective at lowering the INR and was historically first-line therapy for warfarin toxicity with serious or life-threatening bleeding, although it has now been superseded by PCC, which lowers the INR more rapidly. If PCC or rFVIIa is not available, 4 units of FFP may be administered instead.
Administer vitamin K1, 10 mg, by slow IV infusion,

Mitral valve stenosis is the most common cause of cardiac abnormality occurring in pregnant women. It is becoming less common in the UK population; however, it should be considered in women from countries where there is a higher incidence of rheumatic heart disease. Physiological changes in pregnancy may cause an otherwise asymptomatic patient to suddenly deteriorate.

Mitral stenosis causes a mid-diastolic murmur which may be difficult to auscultate unless the patient is placed in the left lateral position. These patients are at risk of atrial fibrillation (up to 40%) which can also contribute to rapid decompensation such as pulmonary oedema (hence, whiteout of lungs seen on CXR). Balloon valvuloplasty is the treatment of choice in patients with mitral valve stenosis.

Answer: 6

Eye Opening Response
Spontaneous–open with blinking at baseline – 4 points
Opens to verbal command, speech, or shout – 3 points
Opens to pain, not applied to face – 2 point
None – 1 point

Verbal Response
Oriented – 5 points
Confused conversation, but able to answer questions – 4 points
Inappropriate responses, words discernible – 3 points
Incomprehensible speech – 2 points
None – 1 point

Motor Response
Obeys commands for movement – 6 points
Purposeful movement to painful stimulus – 5 points
Withdraws from pain – 4 points
Abnormal (spastic) flexion, decorticate posture – 3 points
Extensor (rigid) response, decerebrate posture – 2 points
None – 1 point

He opens his eyes to pain and groans or grunts. He extends his hands at the elbow on application of painful stimulus. This gives him a Glasgow score of 6: eye opening response of 2, verbal response 2 and motor response 2.

Unstable angina is a common cardiovascular condition associated with major adverse clinical events. Over the last 15 years, therapeutic advances have dramatically reduced the complication and mortality rates of this serious condition. The standard of therapy in patients with unstable angina now incorporates the combined use of a potent antithrombotic (aspirin, clopidogrel, heparin and glycoprotein IIb/IIIa receptor antagonists) and anti-anginal (β-blockade and intravenous nitrates) regimens complemented by the selective and judicious application of coronary revascularisation strategies.
Increasingly, these invasive and non-invasive therapeutic interventions are being guided not only by the clinical risk profile but also by the determination of serum cardiac and inflammatory markers.
Moreover, rapid and intensive management of associated risk factors, such as hypercholesterolaemia, would appear to have potentially substantial benefits even within the acute in-hospital phase of unstable angina. Aspirin 300mg should be given as soon as possible. If the patient has a moderate to high risk of myocardial infarction, then Clopidogrel should be given with a low molecular weight heparin. Thrombolysis or urgent percutaneous intervention should be given if there are significant ECG changes.

Absence of comorbidities and a small procedure with no likelihood of systemic compromise will equate to an ASA score of 1.

The ASA physical status classification system is a system for assessing the fitness of patients before surgery. It has six grades, as described below:

ASA 1: No physiological, biochemical, or psychiatric disturbance. The surgical pathology is localised and has not invoked systemic disturbance.

ASA 2: Mild or moderate systemic disruption caused either by the surgical disease process or through an underlying pre-existing disease.

ASA 3: Severe systemic disruption, not life-threatening, caused either by the surgical pathology or a pre-existing disease.

ASA 4: Patient has severe systemic disease that is a constant threat to life.

ASA 5: Patient is moribund and will not survive without surgery.

ASA 6: A brain-dead patient whose organs are being removed with the intention of transplanting them into another patient.

Abdominal CT with IV contrast would be carried out in this case and this presentation has most likely resulted due to an anastomotic leak with abscess formation which is a common complication following surgery. This can occur in any of the branches and anticipating the likely complication and appropriate avoidance will minimize their occurrence. Detailed imaging is required to allow accurate diagnosis and further planning.

Torsade de pointes is an uncommon and distinctive form of polymorphic ventricular tachycardia (VT) characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line. Torsade de pointes, often referred to as torsade, is associated with a prolonged QT interval, which may be congenital or acquired. Torsade usually terminates spontaneously but frequently recurs and may degenerate into ventricular fibrillation. This woman is likely to have hypokalaemia and hypomagnesaemia as a result of vomiting. In addition to this, the erythromycin will predispose her to torsades de pointes. The patient should be given Magnesium 2g over 10 minutes. Knowledge of the management of this peri arrest diagnosis is hence important in surgical practice.

Bile leak may be classified into a minor leak with low output drainage (<300 ml of bile/24 hours) or leaks due to major bile duct injury with high output drainage (>300 ml/24 hours).

The majority of minor bile leak results from Strasberg type A injuries with intact biliary-enteric continuity and includes leaks from cystic duct (CD) stump (55%-71%) or small (less than 3 mm) subsegmental duct in gall bladder (GB) bed (16%) and minor ducts like cholecystohepatic duct or supravesicular duct of Luschka (6%). An injury to the supravesicular duct occurs if the surgeon dissects into the liver bed while separating the gall bladder. This duct does not drain the liver parenchyma.
A leak from the cystic duct stump may occur from clip failure due to necrosis of the stump secondary to thermal injury/pressure necrosis or when clips are used in situations where ties are appropriate (acute cholecystitis) and in a significant majority from distal bile duct obstruction caused by a retained stone and resultant blow out of the cystic stump.
Strasberg type C and type D injuries usually present with a minor leak as well. The former results when an aberrant right hepatic duct (RHD) or right posterior sectoral duct (RPSD) is misidentified as the CD and divided because of the anomalous insertion of CD into either of these ducts.
Type D injuries are lateral injuries to the extrahepatic ducts (EHD) caused by cautery, scissors or clips.

High output biliary fistulas are the result of major transactional injury of EHD (Strasberg type E). Here the common bile duct (CBD) is misidentified as the CD and is clipped, divided and excised. This not only results in a segmental loss of the EHD but often associated with injury or ligation of right hepatic artery as well. Such devastating injuries are peculiar to LC and have been described by Davidoff as “classic laparoscopic biliary injury”.

Early recognition is the most important part of the management of bile leak due to iatrogenic injuries.
Unfortunately, most of the bile duct injuries are not recognized preoperatively. Optimal management of BDI detected postoperatively requires good coordination between the radiologist, endoscopists and an experienced hepatobiliary surgeon.

There is a scope of re-laparoscopy, within 24 hours of surgery, in situations where a low output fistula (<300 ml/day) is confirmed (by reviewing the operative video), to be because of a slipped CD clip. Through lavage, clipping or tying the CD stump with an endoloop may be a simple solution. Such an approach is not useful after 24 hours as inflammatory adhesions and oedema will make the job difficult. If low output controlled biliary fistula is detected after 24 hours, a wait and watch policy should be followed as many of the minor leaks will close within 5 to 7 days. If the leak fails to resolve or if the drainage amount is >300 ml/day (high output), an ERCP should be performed both to delineate the biliary tree and some therapeutic interventions if indicated.

A surgical drain is a tube used to remove pus, blood or other fluids from a wound. They are commonly placed by surgeons or interventional radiologists. Suction is applied through the drain to generate a vacuum and draw fluids into a bottle. Following breast surgery, it is standard practice to use a Redivac type system that is made of polypropylene.

Answer: Aspirin

Aspirin increases bleeding time when taken orally. Aspirin causes several different effects in the body, mainly the reduction of inflammation, analgesia (relief of pain), the prevention of clotting, and the reduction of fever. Much of this is believed to be due to decreased production of prostaglandins and TXA2. Aspirin’s ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (COX) enzyme. Cyclooxygenase is required for prostaglandin and thromboxane synthesis. Prostaglandins are local chemical messengers that exert multiple effects including but not limited to the transmission of pain information to the brain, modulation of the hypothalamic thermostat, and inflammation. They are produced in response to the stimulation of phospholipids within the plasma membrane of cells resulting in the release of arachidonic acid (prostaglandin precursor). Thromboxanes are responsible for the aggregation of platelets that form blood clots.
Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation.

Antihypertensive and antidiabetic medications do not need to be stopped when a patient is undergoing local anaesthesia. Steroid (Prednisolone) use cannot be stopped abruptly; tapering the drug gives the adrenal glands time to return to their normal patterns of secretion. Withdrawal symptoms and signs (weakness, fatigue, decreased appetite, weight loss, nausea, vomiting, diarrhoea, abdominal pain) can mimic many other medical problems. Some may be life-threatening.

Hepatitis A is a viral liver disease that can cause mild to severe illness. The hepatitis A virus (HAV) is transmitted through ingestion of contaminated food and water or through direct contact with an infectious person.
The risk of hepatitis A infection is associated with a lack of safe water, and poor sanitation and hygiene (such as dirty hands). Unlike hepatitis B and C, hepatitis A does not cause chronic liver disease and is rarely fatal, but it can cause debilitating symptoms and fulminant hepatitis (acute liver failure), which is often fatal.
Prodrome
In the prodrome, patients may have mild flulike symptoms of anorexia, nausea and vomiting, fatigue, malaise, low-grade fever (usually < 39.5°C), myalgia, and mild headache. Smokers often lose their taste for tobacco, like persons presenting with appendicitis. Icteric phase
In the icteric phase, dark urine appears first (bilirubinuria). Pale stool soon follows, although this is not universal. Jaundice occurs in most (70%-85%) adults with acute HAV infection; it is less likely in children and is uncommon in infants. The degree of icterus also increases with age. Abdominal pain occurs in approximately 40% of patients. Itching (pruritus), although less common than jaundice, is generally accompanied by jaundice.

Arthralgias and skin rash, although also associated with acute HAV infection, are less frequent than the above symptoms. Rash more often occurs on the lower limbs and may have a vasculitic appearance.

Relapsing hepatitis A
Relapsing hepatitis A is an uncommon sequela of acute infection, is more common in elderly persons, and is characterized by a protracted course of symptoms of the disease and a relapse of symptoms and signs following apparent resolution.

Open haemorrhoidectomy is traditionally viewed as a painful procedure. Most operations are performed under general or regional anaesthesia. Following excisional haemorrhoidectomy, severe pain is not unusual, a well placed caudal anaesthetic will counter this. A pudendal nerve block is an alternative but is less effective than a caudal.

Perioperative administration of antibiotics is very important for reducing the risks of postoperative wound infection. Clips make infections easier to manage but do not reduce the risks. Drains have no effect on the skin wounds in these cases.

Surgical site infections (SSI) comprise up to 20% of all healthcare-associated infections and at least 5% of patients undergoing surgery will develop an SSI as a result. SSIs may occur following a breach in tissue surfaces and allow normal commensals and other pathogens to initiate infection. The organisms are mostly derived from the patient’s own body.

SSIs are a major cause of morbidity and mortality.
Some preoperative measures that may increase the risk of SSI include:
1. Shaving the wound using a razor (disposable clipper preferred)
2. Tissue hypoxia
3. Delayed administration of prophylactic antibiotics in tourniquet surgery

SSIs can be prevented by taking certain precautionary steps pre-, intra-, and postoperatively.

1. Preoperatively:
a. Do not remove body hair routinely
b. If hair needs removal, use electrical clippers (razors increase the risk of infection)
c. Antibiotic prophylaxis if:
– placement of prosthesis or valve
– clean-contaminated surgery
– contaminated surgery

2. Intraoperatively:
a. Prepare the skin with alcoholic chlorhexidine (Lowest incidence of SSI)
b. Cover surgical site with dressing

3. Postoperatively:
a. Prevention of incisional infection by appropriate cleansing, skin care, and moisture management
b.Tissue viability advice for management of surgical wound healing by secondary intention

In adults 50% of the cases of brain death follow severe head injury, 30% are due to subarachnoid haemorrhage and 20% are due to a severe hypoxic-ischaemic event. Thus supra-tentorial catastrophes lead to pressure effect which cause the irretrievable death of the brain-stem.

The Criteria for Diagnosis of Brain-Stem Death

All the pre-conditions must be satisfied and
there should be demonstrably no pharmacological or
metabolic reason for the coma before formally testing the
integrity of the brain-stem reflexes.

Pre Conditions
1. The patient is comatose and mechanically ventilated
for apnoea.
2. The diagnosis of structural brain damage has been
established or the immediate cause of coma is known.
3. A period of observation is essential.

Exclusions
1. Drugs are not the cause of coma e.g. barbiturates.
Neuromuscular blockade has been demonstrably reversed.
2. Hypothermia does not exist.
3. There is no endocrine or metabolic disturbance.

Testing for Brain-Stem Death
Reflexes involving brain-stem function.
1. No pupillary response to light.
2. No corneal reflex.
3. No vestibulo ocular reflex (Caloric test).
4. Doll’s eye reflex
5. No motor response to pain – in the Vth nerve distribution.
6. No gag reflex in response to suction through endotracheal tube or tracheostomy.
7. Apnoea persists despite a rise in PaCO2 to greater than 50 mmHg (6.6kPa) against a background of a normal PaO2.

Diagnosis is to be made by two doctors who have been registered for more than five years and are competent in the procedure. At least one should be a consultant. Testing should be undertaken by the doctors together and must always be performed completely and successfully on two occasions in total.

Complications related to stapled anastomoses include bleeding, device failure, and anastomotic failure, which include stricture or leak.
Stricture: Patient discomfort, need for additional procedures
Bleeding: Hemodynamic implications, difficult intraoperative visualization
Anastomotic leak: Increase in local recurrence, decreased overall survival, sepsis, need for diverting ostomy, increased hospital cost, increased use of hospital resources, decreased quality of life.
Anastomotic bleeding is a common complication of stapled anastomoses, and it can lead to hemodynamic instability and anaemia, sometimes requiring transfusion or additional procedures. To this end, there are efforts aimed at reducing staple line haemorrhage by using buttressing techniques.

It has been well established that any delay in the resumption of normal oral diet after major surgery is associated with increased rates of infectious complications and delayed recovery. Early oral diet is safe 4 h after surgery in patients with a new non-diverted colorectal anastomosis. Some report that low residue diet, rather than a clear liquid diet, after colorectal surgery is associated with less nausea, faster return of bowel function, and a shorter hospital stay without increasing postoperative morbidity when administered in association with prevention of postoperative ileus. Spontaneous food intake rarely exceeds 1200–1500 kcal/day. To reach energy and protein requirements, additional oral nutritional supplements are useful.

The flattened appearance of the face is a classical description of the dish-face deformity associated with Le Fort III fracture of the midface.

The term Le Fort fractures is applied to transverse fractures of the midface involving the maxillary bone and surrounding structures in either a horizontal, pyramidal, or transverse direction. There are three grades of Le Fort fractures:

1. Le Fort I
It is the horizontal fracture of the maxilla. Violent force over a more extensive area above the level of the
teeth will result in this type of fracture. Horizontal fracture line is seen above the apices of the maxillary teeth, detaching the tooth-bearing portion of the maxilla from the rest of the facial skeleton. Floating maxilla and Guerin’s sign is seen in such patients.

2. Le Fort II
It is a pyramidal or subzygomatic fracture. Violent force in the central region extending from glabella to the alveolus results in this type of fracture, resulting in ballooning or moon-face facial deformity.

3. Le Fort III
It is a high-level transverse or suprazygomatic fracture associated with craniofacial disjunction. The entire facial skeleton moves as a single block as a result of the trauma. The patient develops a characteristic panda facies and dish-face deformity.

High-voltage electrical burns are associated with rhabdomyolysis. Acute tubular necrosis may also occur.

Electrical burns occur following exposure to electrical current. Full-thickness burns are third-degree burns. With these types of burns, the epidermal and dermal layers of skin are destroyed, and the damage may even penetrate the layer of fat beneath the skin.

Following the burn, there is a local response with progressive tissue loss and release of inflammatory cytokines. Systemically, there are cardiovascular effects resulting from fluid loss and sequestration of fluid into the third space. There is a marked catabolic response as well. Immunosuppression is common with large burns, and bacterial translocation from the gut lumen is a recognised event. Sepsis is a common cause of death following major burns.

After the initial management and depth assessment of the burn, the patient is transferred to burn centre if:
1. Needs burn shock resuscitation
2. Face/hands/genitals affected
3. Deep partial-thickness or full-thickness burns
4. Significant electrical/chemical burns

Management options include:
1. The initial aim is to stop the burning process and resuscitate the patient. Adults with burns greater than 15% of total body surface area require burn fluid resuscitation. Fluids administration is calculated using the Parkland formula. Half of the fluid is administered in the first eight hours. A urinary catheter should be inserted and analgesics should be started.

2. Conservative management is appropriate for superficial burns and mixed superficial burns that will heal in two weeks. More complex burns may require excision and skin grafting. Excision and primary closure is not generally practised as there is a high risk of infection.

3. Circumferential full-thickness burns affecting a limb or severe torso burns impeding respiration may require escharotomy to divide the burnt tissue.

4. There is no evidence to support the use of antimicrobial prophylaxis or topical antibiotics in burn patients.

The latissimus dorsi myocutaneous flap (LDMF) is one of the most reliable and versatile flaps used in reconstructive surgery. It is known for its use in chest wall and postmastectomy reconstruction and has also been used effectively for coverage of large soft tissue defects in the head and neck, either as a pedicled flap or as a microvascular free flap.

The latissimus dorsi may be transferred as a myofascial flap, a myocutaneous flap, or as a composite osteomyocutaneous flap when harvested with underlying serratus anterior muscle and rib. For even greater reconstructive flexibility, the latissimus can be harvested for free tissue transfer in combination with any or all of the other flaps based on the subscapular vessels (the so-called subscapular compound flap or “mega-flap”), including serratus anterior, scapular, and parascapular flaps

Carcinoid syndrome occurs in ∼20% of cases of well-differentiated endocrine tumours of the jejunum or ileum (midgut neuroendocrine tumours (NET) and consists of (usually) dry flushing (without sweating; 70% of cases) with or without palpitations, diarrhoea (50% of cases) and intermittent abdominal pain (40% of cases); in some patients, there is also lacrimation and rhinorrhoea.
Carcinoid syndrome occurs less often with NETs of other origins and is very rare in association with rectal NETs. It is usually due to metastasis to the liver, with the release of vasoactive compounds, including biogenic amines (e.g., serotonin and tachykinins), into the systemic circulation. However, it may also occur in the absence of liver metastases if there is direct retroperitoneal involvement, with venous drainage bypassing the liver. Pain due to hepatic enlargement may also be a presenting feature, as may upper right abdominal pain (similar to that of pulmonary infarction) secondary to either haemorrhage into, or necrosis of, a hepatic secondary tumour. Wheezing and pellagra are less common presenting features. CHD is present in ∼20% of patients at presentation and usually indicates that the syndrome has been present for several years.

The aim of treatment should be curative where possible but it is palliative in the majority of cases.
Surgery is the only curative treatment.
Administration of specific medications to treat symptoms should, therefore, start as soon as clinical and biochemical signs indicate the presence of hypersecretory NETs, even before the precise localisation of primary and metastatic lesions is confirmed.

The only proven hormonal management of NETs is by the administration of somatostatin analogues.
Somatostatin analogues bind principally to SSTR subtypes 2 (with high affinity) and 5 (with lower affinity), thus inhibiting the release of various peptide hormones in the gut, pancreas and pituitary; they also antagonise growth factor effects on tumour cells, and, at very high dosage, may induce apoptosis. The effects of somatostatin analogues are demonstrable as biochemical response rates (inhibition of hormone production) in 30–70% of patients and as symptomatic control in the majority of patients.
There are two commercially available somatostatin analogues: octreotide and lanreotide.

Answer: Flail chest injury

Flail chest is a life-threatening medical condition that occurs when a segment of the rib cage breaks due to trauma and becomes detached from the rest of the chest wall. Two of the symptoms of flail chest are chest pain and shortness of breath.

It occurs when multiple adjacent ribs are broken in multiple places, separating a segment, so a part of the chest wall moves independently. The number of ribs that must be broken varies by differing definitions: some sources say at least two adjacent ribs are broken in at least two places, some require three or more ribs in two or more places. The flail segment moves in the opposite direction to the rest of the chest wall: because of the ambient pressure in comparison to the pressure inside the lungs, it goes in while the rest of the chest is moving out, and vice versa. This so-called paradoxical breathing is painful and increases the work involved in breathing.

Flail chest is usually accompanied by a pulmonary contusion, a bruise of the lung tissue that can interfere with blood oxygenation. Often, it is the contusion, not the flail segment, that is the main cause of respiratory problems in people with both injuries.

Surgery to fix the fractures appears to result in better outcomes.