The patient has a Weber type A fracture, based on the Danis-Weber classification system for lateral malleolar fractures. It is a stable ankle injury and can, therefore, be managed conservatively. Whilst this patient could also be treated in a below-knee plaster, most clinicians, nowadays, treat this injury in an ankle boot. Patients are also advised to mobilise with the ankle boot as pain allows and can wean themselves off as the symptoms improve.

The Danis-Weber classification system is based on the level of the fibula fracture in relation to the syndesmosis (the connection between the distal ends of the tibia and fibula). The more proximal, the greater the risk of syndesmotic injury and, therefore, fracture instability.

1. Weber type A: fracture below the level of the syndesmosis
2. Weber type B: fracture at the level of the syndesmosis/level of the tibial plafond
3. Weber type C: fracture above the level of the syndesmosis. This includes Maisonneuve fracture (proximal fibula fracture) which can be associated with ankle instability.

Ankle fractures are common. They affect men and women in equal numbers, but men have a higher rate as young adults (sports and contact injuries), and women have a higher rate post-menopausal (fragility-type fractures). Patients present, following a traumatic event, with a painful, swollen ankle, and reluctance/inability to bear weight.

Radiographs of clearly deformed or dislocated joints are not necessary, and removing the pressure on the surrounding soft tissues from the underlying bony deformity is the priority. If the fracture pattern is not clinically obvious, then plain radiographs are appropriate. Antero-posterior, lateral, and mortise views are essential to evaluate fracture displacement and syndesmotic injury. Decreased tibiofibular overlap, medial joint clear space, and lateral talar shift all indicate a syndesmotic injury.

When deciding upon treatment for an ankle fracture, one must consider both the fracture and the patient. Diabetic patients and smokers are at greater risk of post-operative complication, especially wound problems and infection. Likewise, the long term outcome of post-traumatic arthritis from a malunited ankle fracture is extremely important for a young patient, but not as relevant in the elderly. Unimalleolar Weber type A fractures, by definition, are stable and therefore, can be mobilised fully in an ankle boot.

Answer: Osteopetrosis

Osteopetrosis is a clinical syndrome characterized by the failure of osteoclasts to resorb bone. As a consequence, bone modelling and remodelling are impaired. The defect in bone turnover characteristically results in skeletal fragility despite increased bone mass, and it may also cause hematopoietic insufficiency, disturbed tooth eruption, nerve entrapment syndromes, and growth impairment.
Many patients have bone pains. Bony defects are common and include neuropathies due to cranial nerve entrapment (e.g., with deafness, with facial palsy), carpal tunnel syndrome, and osteoarthritis. Bones are fragile and may fracture easily. Approximately 40% of patients have recurrent fractures. Osteomyelitis of the mandible occurs in 10% of patients.

Other manifestations include visual impairment due to retinal degeneration and psychomotor retardation. Bone marrow function is not compromised.

Osteogenesis imperfecta (OI), also known as brittle bone disease, is a group of genetic disorders that mainly affect the bones. It results in bones that break easily. The severity may be mild to severe. Other symptoms may include a blue tinge to the whites of the eye, short height, loose joints, hearing loss, breathing problems and problems with the teeth. Complications may include cervical artery dissection and aortic dissection.

The underlying mechanism is usually a problem with connective tissue due to a lack of type I collagen. This occurs in more than 90% of cases due to mutations in the COL1A1 or COL1A2 genes. These genetic problems are often inherited from a person’s parents in an autosomal dominant manner or occur via a new mutation. There are at least eight main types, with type I being the least severe and type II the most severe.

Osteomalacia it is the disease in which softening of the bones caused by impaired bone metabolism primarily due to inadequate levels of available phosphate, calcium, and vitamin D, or because of resorption of calcium. The impairment of bone metabolism causes inadequate bone mineralization. Osteomalacia in children is known as rickets, and because of this, use of the term Osteomalacia is often restricted to the milder, adult form of the disease. Signs and symptoms can include diffuse body pains, muscle weakness, and fragility of the bones. In addition to low systemic levels of circulating mineral ions necessary for bone and tooth mineralization, accumulation of mineralization-inhibiting proteins and peptides (such as osteopontin and ASARM peptides) occurs in the extracellular matrix of bones and teeth, likely contributing locally to cause matrix hypomineralization (Osteomalacia).

The presence of blown right pupil is a sign of the third cranial nerve compression. The most likely cause is an extradural bleed. However, since this option is not listed, transtentorial herniation would be the most applicable answer. Intraventricular bleeds are typically more common in premature neonates and deterioration due to hydrocephalus is more chronic. Subdural haematoma has a slower onset of symptoms.

Transtentorial herniation is a type of cerebral herniaton. It is further divided into two types with the uncal herniation being the most common.
1. Descending transtentorial herniation: more frequently known as uncal herniation
2. Ascending transtentorial herniation: less common than uncal herniation

Uncal (transtentorial) herniation is herniation of the medial temporal lobe from the middle into the posterior fossa, across the tentorial opening. The cardinal signs are an acute loss of consciousness associated with ipsilateral oculomotor nerve palsy with a fixed and dilated pupil (blown pupil) and contralateral hemiparesis.

Answer: Stress fracture

A stress fracture is caused by repetitive and submaximal loading of the bone, which eventually becomes fatigued and leads to a true fracture. The typical presentation is a complaint of increasing pain in the lower extremity during exercise or activity. The patient’s history usually reveals a recent increase in either training volume or intensity. Stress fractures result from recurrent and repetitive loading of bone. The stress fracture differs from other types of fractures in that in most cases, no acute traumatic event precedes the symptoms.

Normal bone remodelling occurs secondary to increased compressive or tensile loads or increased load frequency. In the normal physiologic response, minor microdamage of the bone occurs. This is repaired through remodelling. Stress fractures develop when extensive microdamage occurs before the bone can be adequately remodelled.
Common findings on physical examination may include tenderness or pain on palpation or percussion of the bone. Erythema or oedema may be present at the site of the stress fracture. Loading or stress of the affected bone may also produce symptoms.

A stress fracture can be difficult to see on an X-ray, because the bone often appears normal in the X-ray, and the small cracks can’t be seen. X-rays may not help diagnose a stress fracture unless it has started to heal. When the bone starts to heal, it creates a callus, or lump, that can be seen on X-rays. The doctors may recommend a bone scan or magnetic resonance imaging (MRI), which is more sensitive than an X-ray and can spot stress fractures early.

Freiberg disease is a degenerative process involving the epiphyses resulting in osteonecrosis of subchondral cancellous bone. If the process is altered in such a way as to restore normal physiology, this may be followed by regeneration or recalcification. If not, the process continues to subchondral collapse and eventual fragmentation of the joint surface.
Patients who have Freiberg disease typically present with complaints of activity-related forefoot pain. Walking alone is often sufficient to cause pain. Some patients describe an extended (months to years) history of chronic forefoot pain with episodic exacerbation, whereas others present with pain of recent onset that is related to a specific injury or event. A history of trauma may not be noted. Patients may present with stiffness and a limp. The pain is often vague and poorly localized to the forefoot. Some patients describe the sensation of a small, hard object under the foot.

Physical examination typically reveals a limited range of motion (ROM), swelling, and tenderness with direct palpation of the metatarsophalangeal (MTP) joint. In early stages of the disease, MTP tenderness may be the only finding. In later stages, crepitus or deformity may be present. A skin callus may be seen on the plantar surface of the affected metatarsal head.

Radiography
Depending on the stage of the disease, radiographs may show only sclerosis and widening of the joint space (early), with complete collapse of the metatarsal head and fragmentation later. Osteochondral loose bodies may be seen late in the disease as well. Oblique views may be especially useful for achieving a full appreciation of subtle changes early in the disease. One study advocated the use of radiographs to assess musculoskeletal foot conditions in women related to poorly fitting shoes.
Occasionally, patients are completely asymptomatic, with changes noted on radiographs taken for other reasons. Whether these patients later develop symptomatic Freiberg disease is not known.

Answer: Transposition of the great arteries

Transposition of the great arteries (TGA) is the most common cyanotic congenital heart lesion that presents in neonates. The hallmark of transposition of the great arteries is ventriculoarterial discordance, in which the aorta arises from the morphologic right ventricle and the pulmonary artery arises from the morphologic left ventricle.

Infants with transposition of the great arteries (TGA) are usually born at term, with cyanosis apparent within hours of birth.

The clinical course and manifestations depend on the extent of intercirculatory mixing and the presence of associated anatomic lesions. Note the following:

Transposition of the great arteries with intact ventricular septum: Prominent and progressive cyanosis within the first 24 hours of life is the usual finding in infants if no significant mixing at the atrial level is evident.

Transposition of the great arteries with large ventricular septal defect: Infants may not initially manifest symptoms of heart disease, although mild cyanosis (particularly when crying) is often noted. Signs of congestive heart failure (tachypnoea, tachycardia, diaphoresis, and failure to gain weight) may become evident over the first 3-6 weeks as pulmonary blood flow increases.

Transposition of the great arteries with ventricular septal defect and left ventricular outflow tract obstruction: Infants often present with extreme cyanosis at birth, proportional to the degree of left ventricular (pulmonary) outflow tract obstruction. The clinical history may be similar to that of an infant with tetralogy of Fallot.

Transposition of the great arteries with ventricular septal defect and pulmonary vascular obstructive disease: Progressively advancing pulmonary vascular obstructive disease can prevent this rare subgroup of patients from developing symptoms of congestive heart failure, despite a large ventricular septal defect. Most often, patients present with progressive cyanosis, despite an early successful palliative procedure.

Adductor canal compression syndrome most commonly presents in young males, and it is important to differentiate it from acute limb ischaemia on exertion. Of the listed options, popliteal fossa entrapment is the main differential diagnosis. However, the popliteal pulse disappears when the knee is fully extended in popliteal fossa entrapment.

Adductor canal compression syndrome is caused by compression of the femoral artery by the musculotendinous band of adductor magnus muscle. The treatment consists of division of the abnormal band and restoration of the arterial circulation.

Answer: Undertake a laparotomy

Intussusception, which is defined as the telescoping or invagination of a proximal portion of intestine (intussusceptum) into a more distal portion (intussuscipiens), is one of the most common causes of bowel obstruction in infants and toddlers.
Intussusception may be ileoileal, colocolic, ileoileocolic, or ileocolic (the most common type).
Most infants with intussusception have a history of intermittent severe cramping
or colicky abdominal pain, occurring every 5-30 minutes. During these attacks, the infant screams and flexes at the waist, draws the legs up to the abdomen, and may appear pale. These episodes may last for only a few seconds and are separated by periods of calm normal appearance and activity. However, some infants become quite lethargic and somnolent between attacks.
Infants with intussusception require surgical correction. Prompt laparotomy following diagnosis is crucial for achieving better outcomes. Primary anastomosis can be performed successfully, and stomas can be created in the critically ill patients or those with late detection and septicaemia.

Answer: Sickle cell disease

An anal fissure is a painful linear tear or crack in the distal anal canal, which, in the short term, usually involves only the epithelium and, in the long term, involves the full thickness of the anal mucosa. Anal fissures develop with equal frequency in both sexes; they tend to occur in younger and middle-aged persons.

The exact aetiology of anal fissures is unknown, but the initiating factor is thought to be trauma from the passage of a particularly hard or painful bowel movement. Low-fibre diets (e.g., those lacking in raw fruits and vegetables) are associated with the development of anal fissures. No occupations are associated with a higher risk for the development of anal fissures. Prior anal surgery is a predisposing factor because scarring from the surgery may cause either stenosis or tethering of the anal canal, which makes it more susceptible to trauma from hard stool.

In rare cases, an anal fissure may develop due to:
-anal cancer
-HIV
-tuberculosis
-syphilis
-herpes

A study showed that a patient may exhibit severe, disabling, anorectal symptoms which are disproportionate to physical findings. Rarely leukaemia may be the cause, and the first signs of blood dyscrasia may appear in the anorectum. The diagnosis may not be suggested by the history, physical examination or routine laboratory data.

Crohn’s disease can also cause problems around the anus. These may include tiny but painful cracks in the skin known as anal fissures. Tunnelling sores called fistulas cause abnormal connections between the bowel and the skin; or an abscess, a pocket of inflamed or dead tissue that is usually very painful.

Answer: Lanz

The Lanz and Gridiron incisions are two incisions that can be used to access the appendix, predominantly for appendectomy.

Both incisions are made at McBurney’s point (two-thirds from the umbilicus to the anterior superior iliac spine). They involve passing through all of the abdominal muscles, transversalis fascia, and then the peritoneum, before entering the abdominal cavity.

The Lanz incision is a transverse incision, whilst the Gridiron incision is oblique (superolateral to inferomedial). Due to its continuation with Langer’s lines, the Lanz incision produces much more aesthetically pleasing results with reduced scarring.

Answer: Ankylosing spondylitis

Ankylosing spondylitis (AS), a spondyloarthropathy, is a chronic, multisystem inflammatory disorder involving primarily the sacroiliac (SI) joints and the axial skeleton. Key components of the patient history that suggest AS include the following:
Insidious onset of low back pain – The most common symptom
Onset of symptoms before age 40 years
Presence of symptoms for more than 3 months
Symptoms worse in the morning or with inactivity
Improvement of symptoms with exercise

General symptoms of AS include the following:

Those related to inflammatory back pain – Stiffness of the spine and kyphosis resulting in a stooped posture are characteristic of advanced-stage AS.
Peripheral enthesitis and arthritis
Constitutional and organ-specific extra-articular manifestations
Fatigue is another common complaint, occurring in approximately 65% of patients with AS. Increased levels of fatigue are associated with increased pain and stiffness and decreased functional capacity.
Pharmacologic therapy

Agents used in the treatment of AS include the following:

Nonsteroidal anti-inflammatory drugs (NSAIDs)
Sulfasalazine
Tumour necrosis factor-α (TNF-α) antagonists
Corticosteroids

AS is the prototype of the spondyloarthropathies, a family of related disorders that also includes reactive arthritis (ReA), psoriatic arthritis (PsA), spondyloarthropathy associated with inflammatory bowel disease (IBD), undifferentiated spondyloarthropathy (USpA), and, possibly, Whipple disease and Behçet disease (see the image below). The spondyloarthropathies are linked by common genetics (the human leukocyte antigen [HLA] class-I gene HLA-B27) and a common pathology (enthesitis). The aetiology of AS is not understood completely; however, a strong genetic predisposition exists. A direct relationship between AS and the HLA-B27 gene has been determined. The precise role of HLA-B27 in precipitating AS remains unknown; however, it is believed that HLA-B27 may resemble or act as a receptor for an inciting antigen (e.g., a bacterial antigen).