In performing noncardiac surgery on patients on anticoagulation, the major concern is when it is safe to perform surgery without increasing the risk of haemorrhage or increasing the risk of thromboembolism (e.g., venous, arterial) after discontinuing treatment.
Any patient who is on long-term anticoagulation and is to undergo a major surgery needs proactive management.
Heparin is discontinued 6-12 hours before surgery and restarted at 200-400 U/h at 4-6 hours after surgery. Coumadin is restarted as soon as tolerated by the patient. Stop oral anticoagulants at least 5 days preoperatively, and do not perform the procedure until the PT is in the reference range.

Scalp wounds often bleed and the addition of adrenaline is, therefore, desirable. Lignocaine is fast acting and the preferred agent for local anaesthesia.

Lignocaine, also called lidocaine, is a local anaesthetic and a less commonly used antiarrhythmic. Its increased doses may be used when combined with adrenaline to limit systemic absorption. Adrenaline may be added to local anaesthetic drugs. It prolongs the duration of action at the site of injection and permits usage of higher doses. It is, however, contraindicated in patients taking monoamine oxidase inhibitors or tricyclic antidepressants.

Other listed options are ruled out in this case because:
1. Bupivacaine: has a much longer duration of action than lignocaine and, thus, may be used for topical wound infiltration at the conclusion of surgical procedures.
2. Prilocaine: the agent of choice for intravenous regional anaesthesia.

The ophthalmic nerve is the smallest of the three trigeminal divisions. The cutaneous branches of the ophthalmic nerve supply the conjunctiva, the skin over the forehead, the upper eyelid, and much of the external surface of the nose.

Pilar or Trichilemmal cysts are common dermal cysts. They occur in less than 10% of the population. Of all skin cysts, Pilar cysts are the most common cysts. Pilar cysts usually occur in areas with dense hair follicle so that they are most commonly seen on the head especially the scalp, but they can also be found on the face, head, and neck.
Trichilemmal cysts never give rise to malignant lesions. They are usually sporadic. The cysts contain keratin and are outlined by stratified squamous epithelium similar to what we see in the outer(external) root sheath of the hair follicle. Proliferating trichilemmal cysts are the tumour form of pilar cysts, and it would appear in less than 3% of all cases of pilar cysts, and it might ulcerate and may be locally aggressive.

Pilar cysts are lined by thick capsules containing small layers of cuboidal, dark-staining basal epithelial cells in a palisade arrangement without an obvious intercellular gap. Those cells coalesce with multiple layers of keratinocytes forming squamous epithelium; these cells showed more maturation with dense eosinophilic-staining keratin in the absence of a granular cell layer. Sometimes we might see some areas of calcifications. Keratin in the pilar cysts stains with antikeratin antibodies similar to that seen in keratin derived from human hair. Trichilemmal cysts might rupture and of their components will leak into the dermis leading to the formation of foreign-body reaction.
Trichilemmal cysts are usually asymptomatic unless they calcify or rupture their contents leading to inflammatory process and pain in the affected site. Sometimes, the presence of pilar cyst overpressure or bony prominence might lead to pain. Trichilemmal cysts usually present as flesh-coloured, smooth, mobile, firm, and well-circumscribed nodules. Family history is very important since this condition can have an autosomal dominant pattern of inheritance. Usually, they are slow-growing nodules but sometimes they increase in size rapidly and it would indicate infection or malignant transformation. Young females are affected more than males.

The gastroduodenal artery is a branch of the hepatic artery and descends near the pylorus between the first part of the duodenum and the neck of the pancreas to divide at the lower border of the duodenum into the right gastroepiploic and pancreaticoduodenal arteries. Before it divides, it gives off a few branches to the pyloric end of the stomach and to the pancreas. The artery that is most likely involved in this situation is the gastroduodenal artery since it is posterior to the first part of the duodenum.

Among all body organs, the brain is most susceptible to ischaemia. Comprising of only 2.5% of total body weight, the brain receives 15% of the cardiac output. Oxygen extraction is also higher with venous oxygen levels approximating 13 vol%, and arteriovenous oxygen difference of 7 vol%.

Sodium nitroprusside is a potent peripheral vasodilator that affects both arterioles and venules. It is often administered intravenously to patients who are experiencing a hypertensive emergency. It reduces both total peripheral resistance as well as venous return, so decreasing both preload and afterload. For this reason it can be used in severe cardiogenic heart failure where this combination of effects can act to increase cardiac output. It is administered by intravenous infusion. Onset is typically immediate and effects last for up to ten minutes. The duration of treatment should not exceed 72 hours.

The classic symptom of subarachnoid haemorrhage is thunderclap headache (a headache described as like being kicked in the head, or the worst ever, developing over seconds to minutes). This headache often pulsates towards the occiput (the back of the head). About one-third of people have no symptoms apart from the characteristic headache, and about one in ten people who seek medical care with this symptom are later diagnosed with a subarachnoid haemorrhage. Vomiting may be present, and 1 in 14 have seizures. Confusion, decreased level of consciousness or coma may be present, as may neck stiffness and other signs of meningism.
In 85 percent of spontaneous cases the cause is a cerebral aneurysm—a weakness in the wall of one of the arteries in the brain that becomes enlarged. They tend to be located in the circle of Willis and its branches. While most cases are due to bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture. Aspirin also appears to increase the risk.
In 15–20 percent of cases of spontaneous SAH, no aneurysm is detected on the first angiogram. About half of these are attributed to non-aneurysmal perimesencephalic haemorrhage, in which the blood is limited to the subarachnoid spaces around the midbrain (i.e. mesencephalon). In these, the origin of the blood is uncertain. The remainder are due to other disorders affecting the blood vessels (such as cerebral arteriovenous malformations), disorders of the blood vessels in the spinal cord, and bleeding into various tumours.
Genetics may play a role in a person’s disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid haemorrhage. But lifestyle factors are more important in determining overall risk. These risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption.
The absence of trauma and skull fracture rules out the other types of haemorrhages and haematomas.

Answer: Meckel’s diverticulum

Meckel’s diverticulum is the most common congenital malformation of the gastrointestinal tract (present in 2%-4% of population) due to persistence of the congenital vitello-intestinal duct. Bleeding from Meckel’s diverticulum due to ectopic gastric mucosa is the most common clinical presentation, especially in younger patients, but it is rare in the adult population. This is due to the persistence of the proximal part of the congenital vitello-intestinal duct. It is a true diverticulum, typically located on anti-mesenteric border, and contains all three coats of intestinal wall with its separate blood supply from the vitelline artery. Meckel’s diverticulum is lined mainly by the typical ileal mucosa as in the adjacent small bowel. However, ectopic gastric, duodenal, colonic, pancreatic, Brunner’s glands, hepatobiliary tissue and endometrial mucosa may be found, usually near the tip. The main mechanism of bleeding is the acid secretion from ectopic mucosa, leading to ulceration of adjacent ileal mucosa. It is possible that the recurrent intussusception may cause trauma, inflammation, mucosal erosion and bleeding. The pathogenic role of Helicobacter pylori in the development of gastritis and bleeding in the ectopic gastric mucosa is still debatable. NSAIDs’ effect on the ectopic gastric mucosa is yet to be proved. Bleeding from Meckel’s diverticulum can cause the iron deficiency anaemia, but it may also cause megaloblastic anaemia due to the bacterial overgrowth and vitamin B12 deficiency as a result of the dilatation and stasis in adjacent obstructed ileal loop. The presence of bleeding with hypoalbuminemia and low ferritin due to ongoing slow unrecognized bleeding may lead to the diagnosis of inflammatory bowel disease.

Constant cerebral blood flow is maintained by autoregulation in the brain, which causes an increase in local vascular resistance to offset an increase in blood pressure. There will be an increase in cerebral blood flow (and decrease in resistance to cerebral blood flow) with a decrease in arterial oxygen or an increase in arterial CO2. Similarly, a decrease in viscosity will also increase the blood flow. Due to increased brain metabolism and activity during a seizure, there will also be an increase in the cerebral blood flow.