When a patient is suspected to have ischaemic stroke based on clinical assessment and CT scan results, further investigations are necessary to confirm the diagnosis and determine the underlying cause. The most effective method for identifying an acute ischaemic stroke is through MRI using diffusion-weighted imaging (DWI). However, if MRI is not available or the patient is not eligible, a serial CT scan may be used to show changes consistent with an evolving stroke.

Additional investigations should focus on localizing the source of the thrombus or atheroma that caused the stroke. However, it is important to only request investigations that will lead to a change in management. These may include a carotid duplex study and/or CT carotid angiogram, a transthoracic echocardiogram (TTE), and cardiac telemetry. These tests can identify significant stenosis requiring carotid endarterectomy, intraventricular thrombus, valvular pathology, or atrial fibrillation requiring anticoagulation.

It is also recommended to measure fasting lipids, glucose, and/or HbA1c in TIA/stroke patients. While a thrombophilia screen or TOE may be requested in certain cases, they are not routinely required. A CT cerebral angiogram may be necessary in some circumstances, but it is not currently part of the routine investigation for ischaemic stroke.

The Royal College of Physicians (RCP) and NICE have published guidelines on the diagnosis and management of patients following a stroke. The guidelines provide recommendations for the management of acute stroke, including maintaining normal levels of blood glucose, hydration, oxygen saturation, and temperature. Blood pressure should not be lowered in the acute phase unless there are complications. Aspirin should be given as soon as possible if a haemorrhagic stroke has been excluded. Anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke. If the cholesterol is > 3.5 mmol/l, patients should be commenced on a statin.

Thrombolysis with alteplase should only be given if it is administered within 4.5 hours of onset of stroke symptoms and haemorrhage has been definitively excluded. There are absolute and relative contraindications to thrombolysis, including previous intracranial haemorrhage, intracranial neoplasm, and active bleeding. Mechanical thrombectomy is a new treatment option for patients with an acute ischaemic stroke. NICE recommends considering thrombectomy together with intravenous thrombolysis for people last known to be well up to 24 hours previously.

Secondary prevention recommendations from NICE include the use of clopidogrel and dipyridamole. Clopidogrel is recommended ahead of combination use of aspirin plus modified-release dipyridamole in people who have had an ischaemic stroke. Aspirin plus MR dipyridamole is recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated. MR dipyridamole alone is recommended after an ischaemic stroke only if aspirin or clopidogrel are contraindicated or not tolerated. Carotid artery endarterectomy should only be considered if carotid stenosis is greater than 70% according to ECST criteria or greater than 50% according to NASCET criteria.

Management of a Patient with Injection-Related Tetanus

The patient in question presents with increased tone and muscle spasms, along with a history of IV drug abuse, indicating injection-related tetanus. The elevated white count and CRP levels further support this diagnosis. However, the abnormal liver function tests may be related to viral hepatitis. Given the high risk of rapid deterioration, prophylactic intubation and ventilation may be necessary.

The first step in management should be the administration of IM Anti-tetanus immunoglobulin to prevent further spread of the tetanus toxin. Debridement of any abscess should be delayed until after the immunoglobulin has been given to avoid increasing the toxin load in the peripheral circulation.

IV immunoglobulin is not appropriate in this case, as it is used for Guillain Barré syndrome, which presents with flaccid paralysis, not the spastic paralysis seen in tetanus. Similarly, IV Methylprednisolone is not recommended due to the underlying tetanus infection. Corticosteroids are also ineffective in managing GBS.

IV Metronidazole may be used to reduce the duration of tetanus symptoms, but it should be used in conjunction with tetanus immunoglobulin and debridement of any abscess. Overall, prompt administration of IM Anti-tetanus immunoglobulin is crucial in managing this patient with injection-related tetanus.

Diagnosing a patient can be challenging, especially when they are unable to fully participate in the examination. In this case, the patient is experiencing a fever and a clouded consciousness, which could indicate encephalitis. However, other potential diagnoses such as cerebral abscess or Parkinson’s dementia can be ruled out based on the lack of focal neurology or gradual onset. Additionally, a CT scan would typically reveal an old subdural in the case of subdural empyema.

Encephalitis: Symptoms, Causes, Diagnosis, and Treatment

Encephalitis is a condition characterized by inflammation of the brain. It can cause a range of symptoms, including fever, headache, psychiatric symptoms, seizures, and vomiting. In some cases, patients may also experience focal features such as aphasia. While peripheral lesions like cold sores are not related to the presence of HSV encephalitis, HSV-1 is responsible for 95% of cases in adults. The condition typically affects the temporal and inferior frontal lobes.

To diagnose encephalitis, doctors may perform a cerebrospinal fluid test to look for lymphocytosis and elevated protein levels. They may also use PCR to test for HSV, VZV, and enteroviruses. Neuroimaging can reveal medial temporal and inferior frontal changes, such as petechial hemorrhages, although it may be normal in one-third of patients. MRI is a better option, and EEG can show lateralized periodic discharges at 2 Hz.

The treatment for encephalitis involves starting intravenous aciclovir in all cases of suspected encephalitis. This antiviral medication can help reduce inflammation and prevent further damage to the brain. With prompt treatment, many patients can recover from encephalitis without any long-term complications.

Hypoadrenalism is a common complication in patients with HIV, often caused by necrotising adrenalitis related to cytomegalovirus (CMV). The weakened adaptive immune system in HIV and AIDS patients increases their vulnerability to CMV infection, which in turn increases the risk of adrenal failure.

The first step in managing hypoadrenalism is to quickly replace steroids, while also prioritizing fluid resuscitation.

There is no conclusive evidence to suggest a bacterial infection, and addressing the hypoadrenalism should resolve the hyperkalaemia.

Understanding Addisonian Crisis and Its Management

Addisonian crisis is a medical emergency that occurs when the adrenal glands suddenly stop functioning properly. This can be caused by various factors such as sepsis, surgery, adrenal haemorrhage, or steroid withdrawal. The condition is characterized by symptoms such as severe weakness, low blood pressure, dehydration, and electrolyte imbalances.

To manage Addisonian crisis, immediate medical attention is required. The first step is to administer hydrocortisone, either intravenously or intramuscularly, at a dose of 100 mg. This should be followed by the infusion of normal saline or dextrose if the patient is hypoglycaemic. Hydrocortisone should be continued every 6 hours until the patient is stable. Fludrocortisone is not required as high cortisol levels exert weak mineralocorticoid action.

After 24 hours, oral replacement therapy may begin and gradually reduced to maintenance over 3-4 days. It is important to monitor the patient’s electrolyte levels and blood pressure during this time. With prompt and appropriate management, most patients with Addisonian crisis can recover fully.

When a patient experiences refractory vomiting despite ondansetron, dexamethasone can be an effective second line antiemetic in chemotherapy-related nausea and vomiting. In this case, cyclizine is not the best option as it binds histamine receptors and is more useful in treating labyrinthitis and motion sickness. Potassium salt replacement may exacerbate vomiting, and delaying chemotherapy may be considered as a last resort. Surgery is not a viable solution in this scenario. Dexamethasone has been proven to be effective in preventing tumor lysis syndrome in lymphoma patients. Ensuring the patient can maintain fluids is crucial.

Managing Nausea and Vomiting as Side-Effects of Chemotherapy

Chemotherapy is a common treatment for cancer, but it often comes with side-effects such as nausea and vomiting. These symptoms can be triggered by various factors, including anxiety, age, concurrent use of opioids, and the type of chemotherapy used. Patients who are at low-risk of developing these symptoms may be prescribed drugs like metoclopramide as a first-line treatment. However, for high-risk patients, 5HT3 receptor antagonists like ondansetron are often more effective, especially when combined with dexamethasone.

To manage nausea and vomiting, it is important to identify the risk factors and choose the appropriate medication. Patients should also be advised to eat small, frequent meals and avoid foods that trigger their symptoms. Additionally, relaxation techniques such as deep breathing and meditation may help reduce anxiety and prevent nausea and vomiting. With proper management, patients can minimize the impact of these side-effects and focus on their recovery.

Bacterial Vaginosis: Symptoms, Risk Factors, and Treatment Options

Bacterial vaginosis is a common condition among women of childbearing age. It is characterized by a thin, milky white discharge with a distinct fishy odor that is not accompanied by itching. The odor can be intensified by adding 10% potassium hydroxide to the discharge, and the vaginal pH is typically higher than 4.5. Risk factors for bacterial vaginosis include the use of intrauterine coil devices, vaginal douching, and having multiple sexual partners.

If left untreated, bacterial vaginosis can lead to pelvic inflammatory disease, which can cause serious complications. While some patients may not experience any symptoms, those who do should seek treatment. In the UK, the first-line treatment for bacterial vaginosis is metronidazole 400 mg taken twice daily for seven days. Alternatively, a single dose of oral metronidazole 2 g may be given if adherence is a concern.

In the US, the Centers for Disease Control and Prevention (CDC) updated their treatment recommendations for bacterial vaginosis in 2010. The recommended therapy is metronidazole 500 mg taken orally twice a day for seven days. Other options include several tinidazole regimens or clindamycin (oral or intravaginal). Additional regimens include metronidazole (750 mg extended-release tablets once daily for seven days) or a single dose of clindamycin intravaginal cream, although data on the effectiveness of these alternative treatments are limited. It is important for patients to seek medical attention if they suspect they have bacterial vaginosis to prevent potential complications.

Treatment Options for Familial Combined Hyperlipidaemia

Familial combined hyperlipidaemia is a common genetic disorder that increases the risk of premature cardiovascular disease. The first-line treatment for this condition is a statin, which can reduce LDL cholesterol levels and lower the risk of cardiovascular events. However, if triglyceride levels remain high, fenofibrate may be added to the treatment regimen. Dietary modifications may not have a significant impact on lipid parameters in individuals who already lead a healthy lifestyle. Ezetimibe is an option for individuals who cannot tolerate statin therapy or require additional lipid-lowering therapy. It is recommended to use ezetimibe in combination with a statin when serum cholesterol levels are not adequately controlled with the maximum tolerated dose of statin. It is important to identify and treat familial combined hyperlipidaemia early to prevent cardiovascular events.

The CT scan indicates the presence of a biconvex collection outside the brain, which is likely an extradural hematoma, and is associated with a fracture.

There are different types of traumatic brain injury, including focal (contusion/haematoma) or diffuse (diffuse axonal injury). Diffuse axonal injury occurs due to mechanical shearing following deceleration, causing disruption and tearing of axons. Intracranial haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact. Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury.

Understanding Histoplasmosis

Histoplasmosis is a fungal infection caused by Histoplasma capsulatum. This infection is commonly found in the Mississippi and Ohio River valleys. The symptoms of histoplasmosis include upper respiratory tract infection symptoms and retrosternal pain.

To manage histoplasmosis, pharmacological agents such as amphotericin or itraconazole are used. These agents are considered the best options for treating this infection.

Oral Hairy Leukoplakia and Other Related Conditions

Oral hairy leukoplakia is a condition that is commonly seen in individuals who are infected with HIV and have a CD4 count between 200 and 500/mm3. Unlike Candida, the lesions associated with this condition cannot be scraped off the tongue. Although it is painless, it is important to note that the diagnosis is a clinical one. As such, treatment is rarely required, especially since the condition is asymptomatic. However, it is worth noting that highly active antiretroviral therapy (HAART) can be used to manage the condition.

In addition to oral hairy leukoplakia, there are other conditions that are worth noting. For instance, Kaposi’s sarcoma is caused by the human herpes virus 8 (HHV8). On the other hand, tinea rubrum is responsible for causing fungal skin and nail infections. these conditions is important, especially for individuals who are at risk of developing them. By seeking medical attention early enough, it is possible to manage these conditions and prevent them from causing further complications.

Early Fluid Resuscitation for Prevention of Acute Kidney Injury in Rhabdomyolysis

Acute kidney injury (AKI) secondary to rhabdomyolysis can be prevented by early fluid resuscitation. This is because injured muscles sequester water, leading to large volume depletion. To prevent this, volumes of up to 10 liters in 24 hours may be required. The target urine output is 3 ml per kilogram per hour or >300 ml per hour.

Furosemide is not appropriate for AKI prevention as fluid resuscitation is the only proven benefit. Mannitol has theoretical benefits but has not been shown to improve outcomes in AKI. Renal replacement therapy is not biochemically indicated at this stage. Urinary alkalisation can be used alongside aggressive fluid resuscitation, but there is no level 1-3 evidence to support its use.

In summary, early fluid resuscitation is crucial in preventing AKI secondary to rhabdomyolysis. Other interventions such as furosemide, mannitol, renal replacement therapy, and urinary alkalisation may not be effective or indicated at this stage.

Stopping amphotericin is the best course of action to prevent contrast-induced acute kidney injury (CI-AKI). Although stopping metformin is also appropriate, it is done to avoid lactic acidosis when renal function is deteriorating. While n-acetylcysteine is still frequently prescribed, it is not currently recommended by guidelines, although this may change. There is no need to initiate an insulin sliding scale unless the patient is unable to eat or drink.

Contrast media nephrotoxicity is characterized by a 25% increase in creatinine levels within three days of receiving intravascular contrast media. This condition typically occurs between two to five days after administration and is more likely to affect patients with pre-existing renal impairment, dehydration, cardiac failure, or those taking nephrotoxic drugs like NSAIDs. Procedures that may cause contrast-induced nephropathy include CT scans with contrast and coronary angiography or percutaneous coronary intervention (PCI). Around 5% of patients who undergo PCI experience a temporary increase in plasma creatinine levels of more than 88 µmol/L.

To prevent contrast-induced nephropathy, intravenous 0.9% sodium chloride should be administered at a rate of 1 mL/kg/hour for 12 hours before and after the procedure. Isotonic sodium bicarbonate may also be used. While N-acetylcysteine was previously used, recent evidence suggests it is not effective. Patients at high risk for contrast-induced nephropathy should have metformin withheld for at least 48 hours and until their renal function returns to normal to avoid the risk of lactic acidosis.

Mesalazine and sulfasalazine are both known to cause drug-induced pancreatitis, but mesalazine carries a higher risk. Therefore, sulfasalazine may be the safer option. On the other hand, NSAIDs like naproxen and ibuprofen can increase the likelihood of gastric ulceration, but the patient’s symptoms are more indicative of pancreatitis rather than peptic ulcer disease.

Acute pancreatitis is a condition that is primarily caused by gallstones and alcohol consumption in the UK. However, there are other factors that can contribute to the development of this condition. A popular mnemonic used to remember these factors is GET SMASHED, which stands for gallstones, ethanol, trauma, steroids, mumps, autoimmune diseases, scorpion venom, hypertriglyceridaemia, hyperchylomicronaemia, hypercalcaemia, hypothermia, ERCP, and certain drugs. It is important to note that pancreatitis is seven times more common in patients taking mesalazine than sulfasalazine. CT scans can show diffuse parenchymal enlargement with oedema and indistinct margins in patients with acute pancreatitis.

Treatment options for Ramsay-Hunt syndrome

Ramsay-Hunt syndrome is a condition caused by the reactivation of the varicella-zoster virus, which can lead to facial paralysis and other symptoms. Early treatment is crucial for a better recovery. The recommended treatment for patients presenting within 72 hours of symptom onset is a combination of oral antiviral agent (aciclovir/valaciclovir) and glucocorticoid (oral prednisolone 1 mg/kg body weight). Physiotherapy and facial nerve stimulation may have a role in rehabilitation, but the primary focus should be on early initiation of antiviral and glucocorticoid therapy. Monotherapy with either antiviral or prednisolone is not as effective as combination therapy. Topical antiviral therapy is also not as effective as oral therapy. Therefore, early initiation of combination therapy is the best approach for the management of Ramsay-Hunt syndrome.

Nocturnal Retro-Orbital Pain with Autonomic Features: Cluster Headache

This patient is experiencing episodes of retro-orbital pain at night accompanied by autonomic symptoms such as tearing, Horner’s syndrome, and facial flushing. These symptoms are consistent with a diagnosis of cluster headache, which is more common in males with a male-to-female ratio of 9:1 and an average onset age of 30 years. The attacks often occur at night and are associated with increased parasympathetic activity.

The recommended treatment for acute attacks includes subcutaneous or intranasal sumatriptan and high-flow oxygen. Prophylactic treatment options include lithium, verapamil, sodium valproate, prednisolone, and ergotamines. There is no indication of temporal arteritis or optic neuritis based on the patient’s history and clinical findings, so further investigations are not necessary.

Understanding Trimethoprim: Mechanism of Action, Adverse Effects, and Use in Pregnancy

Trimethoprim is an antibiotic that is commonly used to treat urinary tract infections. Its mechanism of action involves interfering with DNA synthesis by inhibiting dihydrofolate reductase. This may cause an interaction with methotrexate, which also inhibits dihydrofolate reductase. However, the use of trimethoprim may also lead to adverse effects such as myelosuppression and a transient rise in creatinine. The drug competitively inhibits the tubular secretion of creatinine, resulting in a temporary increase that reverses upon stopping the medication. Additionally, trimethoprim blocks the ENaC channel in the distal nephron, causing a hyperkalaemic distal RTA (type 4). It also inhibits creatinine secretion, which often leads to an increase in creatinine by around 40 points, but not necessarily causing AKI.

When it comes to the use of trimethoprim in pregnancy, caution is advised. The British National Formulary (BNF) warns of a teratogenic risk in the first trimester due to its folate antagonist properties. Manufacturers advise avoiding the use of trimethoprim during pregnancy. It is important to consult with a healthcare provider before taking any medication, especially during pregnancy, to ensure the safety of both the mother and the developing fetus.

A Case of MERRF Syndrome

This patient exhibits a range of symptoms and signs that are consistent with MERRF syndrome, which stands for myoclonic epilepsy and red ragged fibers. She experiences generalised myoclonus, ataxia, cognitive decline, and encephalopathy, as well as epilepsy. Additionally, she has short stature, optic atrophy, right sensorineural hearing loss, and impaired glucose tolerance. The patient’s EEG findings show generalised slow waves.

It is important to differentiate MERRF syndrome from other conditions that may present with similar symptoms. For example, Huntington’s disease typically presents in middle age with dementia and choreiform movement disorder. Neuronal ceroid-lipofuscinosis is a lysosomal storage disorder that typically presents in infancy and childhood, and can present with epilepsy and ataxia. Patients with this condition may also develop lipomata and retinal degeneration. Genetic testing is available for this condition.

NvCJD, on the other hand, typically presents with psychiatric and sensory disturbances. Sporadic CJD presents later in life, typically in the 60s, with dementia, myoclonus, and cerebellar dysfunction. By the unique characteristics of each condition, healthcare providers can make an accurate diagnosis and provide appropriate treatment.

It is highly unusual for a patient with type 1 diabetes to have such tight control of their blood sugar levels while experiencing hypoglycemia. Additionally, the patient’s symptoms of easy tanning, nausea, vomiting, and a drop in blood pressure upon standing strongly suggest the possibility of Addison’s disease. The slight increase in eosinophil count, anemia, hyponatremia, and high potassium levels also support this diagnosis.

In order to effectively treat this condition, corticosteroid replacement is essential. Simply administering normal saline will not address the hypotension or hyponatremia. Anti-emetics may also be necessary.

Addison’s disease is the most common cause of primary hypoadrenalism in the UK, with autoimmune destruction of the adrenal glands being the main culprit, accounting for 80% of cases. This results in reduced production of cortisol and aldosterone. Symptoms of Addison’s disease include lethargy, weakness, anorexia, nausea and vomiting, weight loss, and salt-craving. Hyperpigmentation, especially in palmar creases, vitiligo, loss of pubic hair in women, hypotension, hypoglycemia, and hyponatremia and hyperkalemia may also be observed. In severe cases, a crisis may occur, leading to collapse, shock, and pyrexia.

Other primary causes of hypoadrenalism include tuberculosis, metastases (such as bronchial carcinoma), meningococcal septicaemia (Waterhouse-Friderichsen syndrome), HIV, and antiphospholipid syndrome. Secondary causes include pituitary disorders, such as tumours, irradiation, and infiltration. Exogenous glucocorticoid therapy can also lead to hypoadrenalism.

It is important to note that primary Addison’s disease is associated with hyperpigmentation, while secondary adrenal insufficiency is not.

The patient is experiencing right heart failure due to an infero-posterior infarct, resulting in poor cardiac output despite adequate filling. Inotropic support, such as β1 agonists, dopamine, or dobutamine, is the appropriate next step instead of further crystalloid loading. Urgent cardiological consultation should be sought to consider acute mitral regurgitation from papillary muscle rupture. Intravenous furosemide is not recommended due to the patient’s current blood pressure. Normal saline is not necessary as the patient is not underfilled. Atropine is the first-line treatment for bradycardia, but given the lack of response and clinical features of cardiogenic shock, vasopressors are the optimal next treatment. Digoxin toxicity is unlikely given the regular pulse rate, lack of response to atropine, and absence of a history of heart failure. Treatment for digoxin toxicity includes withdrawing its use, treating underlying electrolyte imbalances, administering Digibind, and cardiac pacing if necessary.

Diagnosis of Oesophageal Stricture

When a patient presents with rapidly progressive dysphagia symptoms, a likely diagnosis is a malignant oesophageal stricture. Endoscopy is the best investigation for this case as it allows tissue diagnosis through biopsies and brushings with a 98% detection rate in oesophageal carcinoma. Additionally, endoscopy permits dilatation and/or stent placement where dysphagia is severe or the stricture is impassable. It also allows for the diagnosis of many of the differential causes of dysphagia. On the other hand, a barium swallow may be the initial investigation where dysphagia is not severe or if the patient has previously been diagnosed with a stricture and the site is known. It is also likely to be more helpful where a motility disorder is suspected. However, it does not have the benefit of allowing a histological diagnosis which is key in this case. A chest x-ray is helpful in identifying mediastinal lymphadenopathy or aspiration, but endoscopy is the investigation of choice in making the diagnosis. An air-fluid level may also be seen on chest x-ray, but its presence indicates obstruction rather than a specific underlying cause. After the diagnosis is made, a staging CT scan will be required, with endoscopy being more important in obtaining histology. Endoscopic ultrasound (EUS) is better than CT or MRI for assessing lymphadenopathy, staging mural invasion, and assessing suitability for surgery in patients with oesophageal carcinoma.