Surgical referral for repair is necessary for femoral hernias, regardless of symptoms, due to the risk of strangulation. In this case, the patient’s history and examination suggest a hernia, potentially a femoral hernia, and surgical repair is necessary. The use of a support belt could increase the risk of strangulation, and a duplex scan, while a good idea, is not the most appropriate management for this patient. No action is unsafe, and antibiotics are not currently indicated.

Understanding Femoral Hernias

Femoral hernias occur when a part of the bowel or other abdominal organs pass through the femoral canal, which is a potential space in the anterior thigh. This can result in a lump in the groin area that is mildly painful and typically non-reducible. Femoral hernias are less common than inguinal hernias, accounting for only 5% of abdominal hernias, and are more prevalent in women, especially those who have had multiple pregnancies. Diagnosis is usually clinical, but ultrasound may be used to confirm the presence of a femoral hernia and exclude other possible causes of a lump in the groin area.

Complications of femoral hernias include incarceration, where the herniated tissue cannot be reduced, and strangulation, which is a surgical emergency. The risk of strangulation is higher with femoral hernias than with inguinal hernias and increases over time. Bowel obstruction and bowel ischaemia may also occur, leading to significant morbidity and mortality for the patient.

Surgical repair is necessary for femoral hernias, and it can be done laparoscopically or via a laparotomy. Hernia support belts or trusses should not be used for femoral hernias due to the risk of strangulation. In an emergency situation, a laparotomy may be the only option. It is essential to distinguish femoral hernias from inguinal hernias, as they have different locations and require different management approaches.

Cardiogenic shock is caused by conditions such as MI or valve abnormalities, leading to decreased cardiac output and blood pressure, with increased SVR and HR. Hypovolaemic shock is caused by blood volume depletion from sources such as haemorrhage or dehydration, also resulting in decreased cardiac output and blood pressure, with increased SVR and HR. Septic shock, as well as anaphylactic and neurogenic shock, is characterized by reduced SVR and increased HR, with normal or increased cardiac output and decreased blood pressure due to peripheral vascular dilation.

Understanding Shock: Aetiology and Management

Shock is a condition that occurs when there is inadequate tissue perfusion. It can be caused by various factors, including sepsis, haemorrhage, neurogenic injury, cardiogenic events, and anaphylaxis. Septic shock is a major concern, with a mortality rate of over 40% in patients with severe sepsis. Haemorrhagic shock is often seen in trauma patients, and the severity is classified based on the amount of blood loss and associated physiological changes. Neurogenic shock occurs following spinal cord injury, leading to decreased peripheral vascular resistance and cardiac output. Cardiogenic shock is commonly caused by ischaemic heart disease or direct myocardial trauma. Anaphylactic shock is a severe hypersensitivity reaction that can be life-threatening.

The management of shock depends on the underlying cause. In septic shock, prompt administration of antibiotics and haemodynamic stabilisation are crucial. In haemorrhagic shock, controlling bleeding and maintaining circulating volume are essential. In neurogenic shock, peripheral vasoconstrictors are used to restore vascular tone. In cardiogenic shock, supportive treatment and surgery may be required. In anaphylactic shock, adrenaline is the most important drug and should be given as soon as possible.

Understanding the aetiology and management of shock is crucial for healthcare professionals to provide timely and appropriate interventions to improve patient outcomes.

Erectile dysfunction (ED) is a condition where a person is unable to achieve or maintain an erection that is sufficient for satisfactory sexual performance. The causes of ED can be categorized into organic, psychogenic, or mixed, and can also be caused by certain medications. Symptoms that suggest a psychogenic cause include a sudden onset, early loss of erection, self-stimulated or waking erections, premature ejaculation or inability to ejaculate, problems or changes in a relationship, major life events, and psychological problems. On the other hand, symptoms that suggest an organic cause include a gradual onset, normal ejaculation, normal libido (except in hypogonadal men), risk factors in medical history (cardiovascular, endocrine or neurological), operations, radiotherapy, or trauma to the pelvis or scrotum, current use of drugs recognized as associated with ED, smoking, high alcohol consumption, and use of recreational or bodybuilding drugs.

Erectile dysfunction (ED) is a condition where a man is unable to achieve or maintain an erection that is sufficient for sexual activity. It is not a disease but a symptom that can be caused by organic, psychogenic, or mixed factors. It is important to differentiate between the causes of ED, with gradual onset of symptoms, lack of tumescence, and normal libido favoring an organic cause, while sudden onset of symptoms, decreased libido, and major life events favoring a psychogenic cause. Risk factors for ED include cardiovascular disease, alcohol use, and certain medications.

To assess for ED, it is recommended to measure lipid and fasting glucose serum levels to calculate cardiovascular risk, as well as free testosterone levels in the morning. If free testosterone is low or borderline, further assessment may be needed. PDE-5 inhibitors, such as sildenafil, are the first-line treatment for ED and should be prescribed to all patients regardless of the cause. Vacuum erection devices can be used as an alternative for those who cannot or will not take PDE-5 inhibitors.

For young men who have always had difficulty achieving an erection, referral to urology is appropriate. Additionally, people with ED who cycle for more than three hours per week should be advised to stop. Overall, ED is a common condition that can be effectively managed with appropriate treatment.

To detect bowel perforation, an erect chest x-ray is commonly used. This is particularly useful in cases of suspected perforated diverticulitis, as it can reveal the presence of pneumoperitoneum (air under the diaphragm). A supine chest x-ray is not as effective in detecting this. While an abdominal x-ray can also suggest pneumoperitoneum, it is less sensitive than an erect chest x-ray. An intravenous urogram is not necessary in this case, as the patient’s symptoms do not align with those of ureteric colic, which is the most likely diagnosis. Ultrasound may also reveal air in the abdominal cavity, but its accuracy and image quality can vary greatly, making it a less optimal choice.

An erect chest x-ray is a useful tool for diagnosing an acute abdomen, as it can reveal the presence of free air in the abdomen, also known as pneumoperitoneum. This abnormal finding is indicative of a perforated abdominal viscus, such as a perforated duodenal ulcer. On an abdominal film, Rigler’s sign, also known as the double wall sign, may be visible. However, CT scans are now the preferred method for detecting free air in the abdomen.

The image used on license from Radiopaedia shows an erect chest x-ray with air visible under the diaphragm on both sides. Another image from Radiopaedia demonstrates an abdominal x-ray with numerous loops of small bowel outlined by gas, both within the lumen and free within the peritoneal cavity. Ascites, or fluid in the abdomen, is also visible, with mottled gas densities over bilateral paracolic gutters. In a normal x-ray, only the luminal surface should be visible outlined by gas, while the serosal surface should not be visible as it is normally in contact with other intra-abdominal content of similar density. However, in this case, gas abuts the serosal surface, making it visible. As this film was obtained supine, ascites pools in the paracolic gutters, with fluid mixed in with gas bubbles.

Atrial fibrillation is a known risk factor for embolic acute limb ischaemia, as it increases the likelihood of thromboembolic disease. This occurs when thrombi form in the atrium and migrate, resulting in an embolism that can cause acute limb ischaemia. The patient’s alcohol intake is within recommended limits and is unlikely to be the cause of her condition, although excessive alcohol consumption can increase the risk of bleeding and cardiovascular disease. Hormone replacement therapy (HRT) is generally considered to prevent arterial disease progression, but it can increase the risk of venous thrombosis such as deep vein thrombosis or pulmonary embolism. Reduced mobility can increase the risk of venous thromboembolic disease, but it is not typically associated with acute limb ischaemia. While hyperglycaemia in type 2 diabetes can damage blood vessels, the patient’s diabetes is well controlled and is unlikely to be the primary cause of her presentation. However, diabetes is associated with atherosclerosis, which can lead to arterial occlusion, and patients with diabetic neuropathy may present late and have an increased risk of developing gangrene requiring amputation.

Peripheral arterial disease can present in three main ways: intermittent claudication, critical limb ischaemia, and acute limb-threatening ischaemia. The latter is characterized by one or more of the 6 P’s: pale, pulseless, painful, paralysed, paraesthetic, and perishing with cold. Initial investigations include a handheld arterial Doppler examination and an ankle-brachial pressure index (ABI) if Doppler signals are present. It is important to determine whether the ischaemia is due to a thrombus or embolus, as this will guide management. Thrombus is suggested by pre-existing claudication with sudden deterioration, reduced or absent pulses in the contralateral limb, and evidence of widespread vascular disease. Embolus is suggested by a sudden onset of painful leg (<24 hours), no history of claudication, clinically obvious source of embolus, and no evidence of peripheral vascular disease. Initial management includes an ABC approach, analgesia, intravenous unfractionated heparin, and vascular review. Definitive management options include intra-arterial thrombolysis, surgical embolectomy, angioplasty, bypass surgery, or amputation for irreversible ischaemia.

Manifestations of Gallstone Disease

All options for gallstone disease can be seen in different manifestations. However, the combination of pyrexia, an elevated white cell count, and local peritonism (Murphy’s sign) is a classic symptom of acute cholecystitis. Pancreatitis can be eliminated with normal amylase levels, while jaundice and cholangitis (which are usually associated with fever and tenderness: Charcot’s triad) can be ruled out with normal bilirubin levels. Biliary colic, on the other hand, would not exhibit peritonism and an elevated white cell count. It is important to note that these symptoms can help in the diagnosis and treatment of gallstone disease.

The most likely cause of bilious vomiting on the first day of life is intestinal atresia. This is because the presence of bilious vomiting in early life suggests a bowel obstruction, and the fact that it has occurred on the first day of life indicates an underlying structural issue. Children with Down’s syndrome are at a higher risk of developing this condition, especially at the duodenum. The diagnosis of intestinal/duodenal atresia is further supported by the presence of the ‘double bubble’ on the x-ray.

Biliary atresia is an incorrect answer as it would not cause the clinical picture described above. This condition results in neonatal jaundice beyond 14 days of life, with dark urine and pale stools.

Malrotation with volvulus is also an incorrect answer. While it can cause bilious vomiting, it tends to present around 3 to 7 days following birth.

Necrotising enterocolitis is another incorrect answer. Although it can cause bilious vomiting, it typically does not occur so early following birth. Additionally, it is usually a condition of prematurity and is rarely seen in infants born at term.

Causes and Treatments for Bilious Vomiting in Neonates

Bilious vomiting in neonates can be caused by various disorders, including duodenal atresia, malrotation with volvulus, jejunal/ileal atresia, meconium ileus, and necrotising enterocolitis. Duodenal atresia occurs in 1 in 5000 births and is more common in babies with Down syndrome. It typically presents a few hours after birth and can be diagnosed through an abdominal X-ray that shows a double bubble sign. Treatment involves duodenoduodenostomy. Malrotation with volvulus is usually caused by incomplete rotation during embryogenesis and presents between 3-7 days after birth. An upper GI contrast study or ultrasound can confirm the diagnosis, and treatment involves Ladd’s procedure. Jejunal/ileal atresia is caused by vascular insufficiency in utero and occurs in 1 in 3000 births. It presents within 24 hours of birth and can be diagnosed through an abdominal X-ray that shows air-fluid levels. Treatment involves laparotomy with primary resection and anastomosis. Meconium ileus occurs in 15-20% of babies with cystic fibrosis and presents in the first 24-48 hours of life with abdominal distension and bilious vomiting. Diagnosis involves an abdominal X-ray that shows air-fluid levels, and a sweat test can confirm cystic fibrosis. Treatment involves surgical decompression, and segmental resection may be necessary for serosal damage. Necrotising enterocolitis occurs in up to 2.4 per 1000 births, with increased risks in prematurity and inter-current illness. It typically presents in the second week of life and can be diagnosed through an abdominal X-ray that shows dilated bowel loops, pneumatosis, and portal venous air. Treatment involves conservative and supportive measures for non-perforated cases, while laparotomy and resection are necessary for perforated cases or ongoing clinical deterioration.

A subarachnoid haemorrhage (SAH) is a type of bleeding that occurs within the subarachnoid space of the meninges in the brain. It can be caused by head injury or occur spontaneously. Spontaneous SAH is often caused by an intracranial aneurysm, which accounts for around 85% of cases. Other causes include arteriovenous malformation, pituitary apoplexy, and mycotic aneurysms. The classic symptoms of SAH include a sudden and severe headache, nausea and vomiting, meningism, coma, seizures, and ECG changes.

The first-line investigation for SAH is a non-contrast CT head, which can detect acute blood in the basal cisterns, sulci, and ventricular system. If the CT is normal within 6 hours of symptom onset, a lumbar puncture is not recommended. However, if the CT is normal after 6 hours, a lumbar puncture should be performed at least 12 hours after symptom onset to check for xanthochromia and other CSF findings consistent with SAH. If SAH is confirmed, referral to neurosurgery is necessary to identify the underlying cause and provide urgent treatment.

Management of aneurysmal SAH involves supportive care, such as bed rest, analgesia, and venous thromboembolism prophylaxis. Vasospasm is prevented with oral nimodipine, and intracranial aneurysms require prompt intervention to prevent rebleeding. Most aneurysms are treated with a coil by interventional neuroradiologists, but some require a craniotomy and clipping by a neurosurgeon. Complications of aneurysmal SAH include re-bleeding, hydrocephalus, vasospasm, and hyponatraemia. Predictive factors for SAH include conscious level on admission, age, and amount of blood visible on CT head.

The patient’s symptoms and observations suggest that they are suffering from ureteric colic caused by urinary calculi, which may be accompanied by an infection leading to sepsis. In such cases, urgent renal decompression and IV antibiotics are necessary. While fluid resuscitation may help manage ureteric colic, it is not sufficient when there are signs of infection, and inpatient management is required. Although oral fluids, IV antibiotics, and analgesia may provide some relief, urgent renal decompression is the definitive treatment. While NSAIDs may be helpful in managing ureteric colic, they cannot be the sole treatment when there is an infection. Rectal diclofenac is often the preferred NSAID. An urgent nephrectomy is not necessary for this condition.

The management of renal stones involves initial medication and investigations, including an NSAID for analgesia and a non-contrast CT KUB for imaging. Stones less than 5mm may pass spontaneously, but more intensive treatment is needed for ureteric obstruction or renal abnormalities. Treatment options include shockwave lithotripsy, ureteroscopy, and percutaneous nephrolithotomy. Prevention strategies include high fluid intake, low animal protein and salt diet, and medication such as thiazides diuretics for hypercalciuria and allopurinol for uric acid stones.

When a man presents with typical urinary symptoms of prostate cancer, such as hesitancy, nocturia, and post-void dribbling, along with back pain and unintentional weight loss, it may indicate metastatic disease. Even if the PSA level is normal, the presence of findings consistent with prostate cancer on examination warrants further assessment through the suspected cancer pathway. Nowadays, multiparametric MRI is the preferred first-line investigation for suspected prostate cancer, even if metastasis is suspected. Depending on the results, an MRI-guided biopsy may or may not be recommended. While CT chest, abdomen, and pelvis can detect metastasis, it is not the primary investigation for prostate cancer. Transrectal ultrasound-guided biopsy used to be the traditional first-line investigation for prostate cancer, but due to the risk of complications such as sepsis or long-term pain, it is no longer the preferred option. Repeating PSA levels is unnecessary in suspected prostate cancer, as a single elevated level is sufficient to warrant further investigation.

Investigation for Prostate Cancer

Prostate cancer is a common type of cancer that affects men. The traditional investigation for suspected prostate cancer was a transrectal ultrasound-guided (TRUS) biopsy. However, recent guidelines from NICE have now recommended the increasing use of multiparametric MRI as a first-line investigation. This is because TRUS biopsy can lead to complications such as sepsis, pain, fever, haematuria, and rectal bleeding.

Multiparametric MRI is now the first-line investigation for people with suspected clinically localised prostate cancer. The results of the MRI are reported using a 5-point Likert scale. If the Likert scale is 3 or higher, a multiparametric MRI-influenced prostate biopsy is offered. If the Likert scale is 1-2, then NICE recommends discussing with the patient the pros and cons of having a biopsy. This approach helps to reduce the risk of complications associated with TRUS biopsy and ensures that patients receive the most appropriate investigation for their condition.