Management of Acute Asthma

Acute asthma is classified by the British Thoracic Society (BTS) into three categories: moderate, severe, and life-threatening. Patients with any of the life-threatening features should be treated as having a life-threatening attack. A fourth category, Near-fatal asthma, is also recognized. Further assessment may include arterial blood gases for patients with oxygen saturation levels below 92%. A chest x-ray is not routinely recommended unless the patient has life-threatening asthma, suspected pneumothorax, or failure to respond to treatment.

Admission criteria include a previous near-fatal asthma attack, pregnancy, an attack occurring despite already using oral corticosteroid, and presentation at night. All patients with life-threatening asthma should be admitted to the hospital, and patients with features of severe acute asthma should also be admitted if they fail to respond to initial treatment. Oxygen therapy should be started for hypoxaemic patients. Bronchodilation with short-acting beta₂-agonists (SABA) is recommended, and all patients should be given 40-50mg of prednisolone orally daily. Ipratropium bromide and IV magnesium sulphate may also be considered for severe or life-threatening asthma. Patients who fail to respond require senior critical care support and should be treated in an appropriate ITU/HDU setting. Criteria for discharge include stability on discharge medication, checked and recorded inhaler technique, and PEF levels above 75% of best or predicted.

Non-typhi salmonella (NTS) is known to cause blood and bone infections, particularly in children with sickle cell disease and malaria. The exact reason for this susceptibility is not fully understood, but it may be due to the bacteria’s affinity for iron, which is made available through haemolysis. Other bacteria such as E.coli and P. aeruginosa are not commonly associated with sickle cell disease, and Staphylococcus aureus is a gram-positive coccus. Aplastic anaemia and parvovirus can be ruled out as causes, as the child’s haemoglobin level is normal and parvovirus does not cause osteomyelitis.

Understanding Osteomyelitis: Types, Causes, and Treatment

Osteomyelitis is a bone infection that can be classified into two types: haematogenous and non-haematogenous. Haematogenous osteomyelitis is caused by bacteria that enter the bloodstream and is usually monomicrobial. It is more common in children, with vertebral osteomyelitis being the most common form in adults. Risk factors include sickle cell anaemia, intravenous drug use, immunosuppression, and infective endocarditis. On the other hand, non-haematogenous osteomyelitis results from the spread of infection from adjacent soft tissues or direct injury to the bone. It is often polymicrobial and more common in adults, with risk factors such as diabetic foot ulcers, pressure sores, diabetes mellitus, and peripheral arterial disease.

Staphylococcus aureus is the most common cause of osteomyelitis, except in patients with sickle-cell anaemia where Salmonella species predominate. To diagnose osteomyelitis, MRI is the imaging modality of choice, with a sensitivity of 90-100%. Treatment for osteomyelitis involves a six-week course of flucloxacillin. Clindamycin is an alternative for patients who are allergic to penicillin.

In summary, osteomyelitis is a bone infection that can be caused by bacteria entering the bloodstream or spreading from adjacent soft tissues or direct injury to the bone. It is more common in children and adults with certain risk factors. Staphylococcus aureus is the most common cause, and MRI is the preferred imaging modality for diagnosis. Treatment involves a six-week course of flucloxacillin or clindamycin for penicillin-allergic patients.

Vesicoureteral reflux (VUR) is a likely cause of recurrent urinary tract infections (UTIs) in children under 6 years old. The family history, age of the patient, and abnormal ultrasound findings suggest VUR as the underlying issue. To determine the severity of VUR, a voiding cystourethrogram (micturating cystography) is necessary. This test involves injecting dye into the bladder via a catheter and taking x-ray images while the child urinates. Early detection of VUR is crucial to prevent kidney scarring (reflux nephropathy).

Bladder ultrasound is not an appropriate method for grading VUR severity. While ultrasound imaging of the urinary tract, including the kidneys, can be useful, it cannot grade VUR severity.

A CT abdomen is not necessary and would expose the child to unnecessary radiation.

A dimercaptosuccinic acid (DMSA) scan can assess renal parenchymal defects resulting from VUR and is typically performed within six months of an acute infection in children with recurrent UTIs. However, it cannot grade the severity of VUR.

Understanding Vesicoureteric Reflux

Vesicoureteric reflux (VUR) is a condition where urine flows back from the bladder into the ureter and kidney. This is a common urinary tract abnormality in children and can lead to urinary tract infections (UTIs). In fact, around 30% of children who present with a UTI have VUR. It is important to investigate for VUR in children following a UTI as around 35% of children develop renal scarring.

The pathophysiology of VUR involves the ureters being displaced laterally, which causes a shortened intramural course of the ureter. This means that the vesicoureteric junction cannot function properly. VUR can present in different ways, such as hydronephrosis on ultrasound during the antenatal period, recurrent childhood UTIs, and reflux nephropathy, which is chronic pyelonephritis secondary to VUR. Renal scarring can also produce increased quantities of renin, which can cause hypertension.

To diagnose VUR, a micturating cystourethrogram is usually performed. A DMSA scan may also be done to check for renal scarring. VUR is graded based on the severity of the condition, with Grade I being the mildest and Grade V being the most severe.

Overall, understanding VUR is important in preventing complications such as UTIs and renal scarring. Early diagnosis and management can help improve outcomes for children with this condition.

Acute mesenteric ischaemia (AMI) is a rare but potentially life-threatening condition caused by inadequate blood flow through the mesenteric vessels, leading to ischaemia and gangrene of the bowel wall. It can be classified as either arterial or venous, with embolic phenomena being the most common cause. Symptoms include sudden and severe abdominal pain, vomiting, and diarrhoea, with physical signs developing late in the disease process. Early and aggressive diagnosis and treatment are crucial to reduce mortality, but once bowel wall infarction has occurred, the mortality rate may be as high as 90%. Appendicitis, diverticulitis, pseudomembranous colitis, and ruptured AAA are important differential diagnoses to consider.

Abdominal wall hernias occur when an organ or the fascia of an organ protrudes through the wall of the cavity that normally contains it. Risk factors for developing these hernias include obesity, ascites, increasing age, and surgical wounds. Symptoms of abdominal wall hernias include a palpable lump, cough impulse, pain, obstruction (more common in femoral hernias), and strangulation (which can compromise the bowel blood supply and lead to infarction). There are several types of abdominal wall hernias, including inguinal hernias (which account for 75% of cases and are more common in men), femoral hernias (more common in women and have a high risk of obstruction and strangulation), umbilical hernias (symmetrical bulge under the umbilicus), paraumbilical hernias (asymmetrical bulge), epigastric hernias (lump in the midline between umbilicus and xiphisternum), incisional hernias (which may occur after abdominal surgery), Spigelian hernias (rare and seen in older patients), obturator hernias (more common in females and can cause bowel obstruction), and Richter hernias (a rare type of hernia that can present with strangulation without symptoms of obstruction). In children, congenital inguinal hernias and infantile umbilical hernias are the most common types, with surgical repair recommended for the former and most resolving on their own for the latter.

The ECG changes in this patient suggest pericarditis, given their young age, widespread ST-segment elevation, and normal troponin levels. While PR segment depression is typically seen in pericarditis, note that the PR segment may be elevated in aVR. Myocarditis would be a possible diagnosis if the troponin levels were elevated. Infective endocarditis is less likely due to the absence of fever and ECG changes consistent with pericarditis. Although cardiac tamponade is a potential complication of pericarditis, it is unlikely in this case as the patient’s blood pressure is normal and pulsus paradoxus is not present.

Understanding Acute Pericarditis

Acute pericarditis is a medical condition characterized by inflammation of the pericardial sac that lasts for less than 4-6 weeks. The condition can be caused by various factors such as viral infections, tuberculosis, uraemia, post-myocardial infarction, autoimmune pericarditis, radiotherapy, connective tissue disease, hypothyroidism, malignancy, and trauma. Symptoms of acute pericarditis include chest pain, non-productive cough, dyspnoea, and flu-like symptoms. Patients may also experience pericardial rub.

To diagnose acute pericarditis, doctors may perform an electrocardiogram (ECG) to check for changes in the heart’s electrical activity. Blood tests may also be conducted to check for inflammatory markers and troponin levels. Patients suspected of having acute pericarditis should undergo transthoracic echocardiography.

Treatment for acute pericarditis depends on the underlying cause. Patients with high-risk features such as fever or elevated troponin levels may need to be hospitalized. However, most patients with pericarditis secondary to viral infection can be managed as outpatients. Strenuous physical activity should be avoided until symptoms resolve and inflammatory markers normalize. A combination of nonsteroidal anti-inflammatory drugs (NSAIDs) and colchicine is typically used as first-line treatment for patients with acute idiopathic or viral pericarditis. The medication is usually tapered off over 1-2 weeks.

Overall, understanding acute pericarditis is important for prompt diagnosis and appropriate management of the condition.

Vagal manoeuvres, such as carotid sinus massage or the Valsalva manoeuvre, are the initial treatment for supraventricular tachycardia. Adenosine should only be administered if these manoeuvres are ineffective. According to the ALS guidelines, direct current cardioversion is not recommended for this condition.

Understanding Supraventricular Tachycardia

Supraventricular tachycardia (SVT) is a type of tachycardia that originates above the ventricles. It is commonly associated with paroxysmal SVT, which is characterized by sudden onset of a narrow complex tachycardia, usually an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.

When it comes to acute management, vagal maneuvers such as the Valsalva maneuver or carotid sinus massage can be used. Intravenous adenosine is also an option, with a rapid IV bolus of 6mg given initially, followed by 12mg and then 18mg if necessary. However, adenosine is contraindicated in asthmatics, and verapamil may be a better option for them. Electrical cardioversion is another option.

To prevent episodes of SVT, beta-blockers can be used. Radio-frequency ablation is also an option. It is important to work with a healthcare provider to determine the best course of treatment for each individual case.

Overall, understanding SVT and its management options can help individuals with this condition better manage their symptoms and improve their quality of life.

The HbA1c is a reliable indicator of good glycaemic control and should be used to determine any necessary changes to diabetes medications. It reflects average glucose levels over a period of 2-3 months, rather than a single reading. It is possible that the recent use of steroids has temporarily worsened glycaemic control in this case.

NICE updated its guidance on the management of type 2 diabetes mellitus (T2DM) in 2022, reflecting advances in drug therapy and improved evidence regarding newer therapies such as SGLT-2 inhibitors. The first-line drug of choice remains metformin, which should be titrated up slowly to minimize gastrointestinal upset. HbA1c targets should be agreed upon with patients and checked every 3-6 months until stable, with consideration for relaxing targets on a case-by-case basis. Dietary advice includes encouraging high fiber, low glycemic index sources of carbohydrates and controlling intake of foods containing saturated fats and trans fatty acids. Blood pressure targets are the same as for patients without type 2 diabetes, and antiplatelets should not be offered unless a patient has existing cardiovascular disease. Only patients with a 10-year cardiovascular risk > 10% should be offered a statin, with atorvastatin 20mg as the first-line choice.

An umbilical granuloma is a growth of tissue that can occur during the healing process of the umbilicus, typically within the first few weeks of life. It appears as a small, red growth in the center of the umbilicus that may leak clear or yellow fluid. Treatment involves applying salt to the wound or cauterizing the granuloma with silver nitrate if necessary.

Omphalitis, also known as umbilical cellulitis, is a bacterial infection that affects the umbilical stump. It typically presents as a superficial cellulitis a few days after birth.

Umbilical hernias are common in newborns, occurring in approximately 1 in 5 children. They usually resolve on their own by the age of 2.

The umbilicus has two arteries and one vein during development, which later dessicates and separates after birth. Umbilical hernias are common in neonates and may resolve spontaneously. Paraumbilical hernias have more defined edges and are less likely to resolve on their own. Omphalitis is a potentially serious infection of the umbilicus that requires antibiotics. Umbilical granulomas can be treated with silver nitrate. Persistent urachus and vitello-intestinal ducts are rare conditions that require imaging and surgical closure.

Understanding ECG Findings in Acute Pericarditis

Acute pericarditis is a condition that commonly presents with central pleuritic chest pain, relieved on leaning forward. One of the main ECG findings in acute pericarditis is widespread concave ST-segment elevations with PR-segment depression, which is 85% specific for the condition. Absent P waves are not typically caused by acute pericarditis, and ST-segment elevation in the anterior leads is more suggestive of anterior myocardial infarction. U waves are not characteristic ECG findings in acute pericarditis and are associated with other conditions. Other clinical features of acute pericarditis are largely dependent on the underlying cause. It is important to understand these ECG findings to aid in the diagnosis and management of acute pericarditis.

Common Medications and Their Side Effects

Furosemide: A loop diuretic that carries the risk of ototoxicity, especially in patients with renal impairment or given a rapid intravenous infusion. Hearing loss and tinnitus are potential side effects.

Ciprofloxacin: A broad-spectrum quinolone antibiotic that is not commonly associated with ototoxicity, but has an increased risk of Clostridium difficile infection. Rupture of the Achilles tendon is a known side effect.

Amlodipine: A calcium channel blocker used to treat hypertension. Common side effects include flushing, headaches, and ankle swelling due to vasodilation.

Indapamide: A thiazide-like diuretic that is not associated with ototoxicity. Possible side effects include electrolyte imbalances, dry mouth, and gastrointestinal disturbance.

Paracetamol: Not associated with ototoxicity and has few side effects listed in the British National Formulary. Non-steroidal anti-inflammatory drugs, which have similar indications for use, can cause ototoxicity.

Understanding the Side Effects of Common Medications

Misconceptions about the Pathophysiology of Allograft Rejection

There are several misconceptions about the pathophysiology of allograft rejection. One of them is that hyper-acute allograft rejection is solely caused by class I HLA antibody activation, granulocyte adhesion, and thrombosis. While these factors do play a role, the ultimate result of hyper-acute rejection is thrombosis of the vessels and graft ischaemia, which presents itself as graft swelling once perfusion is reinstated.

Another misconception is that donor MHC I antigens react with host CD8 resulting in direct cytotoxic damage, which is a sequence in the pathophysiology of acute rejection response, not hyper-acute rejection.

Class II HLA antibodies are often thought to be the primary source of activation of the coagulation cascade, but this is not the case. Monocytes are also not activated in this process.

Interstitial fibrosis is often thought to be a mechanism of acute rejection, but it is actually the end-stage mechanism of chronic graft rejection.

Lastly, lymphocyte, killer T-cell, and cytokine activation are often thought to be part of the mechanism of hyper-acute allograft rejection, but they are actually part of the mechanism of action in acute allograft rejection.

It is important to have a clear understanding of the pathophysiology of allograft rejection to properly diagnose and treat patients.

Management of Otitis Externa: Recommended Actions and Guidelines

Otitis externa is a common condition that affects the outer ear canal. The management of this condition depends on the severity of the inflammation and the presence of other symptoms. Here are some recommended actions and guidelines for managing otitis externa:

1. Start topical antibiotic and steroid: This is recommended for patients with acute otitis externa who present with more severe inflammation. The treatment should last for seven days.

2. Start topical acetic acid 2% spray: This is recommended for patients with mild otitis externa who do not have hearing loss or discharge.

3. Refer to ENT urgently: This is not part of initial management but should be considered for patients with chronic diffuse otitis externa when treatment is prolonged beyond two to three months.

4. Start oral amoxicillin: Oral antibiotics are rarely indicated for otitis externa. They should only be considered for patients with severe infection or at high risk of severe infection.

5. Take an ear swab and start topical antibiotic: Ear swab is not recommended as first-line management. It should only be done if there is no response to initial treatment or in recurrent infections.

In summary, the management of otitis externa depends on the severity of the inflammation and the presence of other symptoms. Following these recommended actions and guidelines can help improve patient outcomes.

BPPV can be diagnosed using the Dix-Hallpike manoeuvre, while the Epley manoeuvre is used for treatment.

Understanding Benign Paroxysmal Positional Vertigo

Benign paroxysmal positional vertigo (BPPV) is a common condition that causes sudden dizziness and vertigo triggered by changes in head position. It typically affects individuals over the age of 55 and is less common in younger patients. Symptoms include vertigo triggered by movements such as rolling over in bed or looking upwards, and may be accompanied by nausea. Each episode usually lasts between 10-20 seconds and can be diagnosed through a positive Dix-Hallpike manoeuvre, which involves the patient experiencing vertigo and rotatory nystagmus.

Fortunately, BPPV has a good prognosis and often resolves on its own within a few weeks to months. Treatment options include the Epley manoeuvre, which is successful in around 80% of cases, and vestibular rehabilitation exercises such as the Brandt-Daroff exercises. While medication such as Betahistine may be prescribed, it tends to have limited value. However, it is important to note that around half of people with BPPV will experience a recurrence of symptoms 3-5 years after their initial diagnosis.

Overall, understanding BPPV and its symptoms can help individuals seek appropriate treatment and manage their condition effectively.

Syphilis, Lymphogranuloma venereum (LGV), and donovanosis (granuloma inguinal) can all lead to the development of genital ulcers that are not accompanied by pain. However, in the case of the patient who has recently changed sexual partners and is not experiencing any other symptoms, herpes simplex is the more probable cause of the painful genital ulcers. Behcets may also cause painful genital ulcers.

STI Ulcers: Causes and Symptoms

Genital ulcers are a common symptom of several sexually transmitted infections (STIs). One of the most common causes of genital ulcers is the herpes simplex virus (HSV) type 2, which is responsible for genital herpes. The primary attack of genital herpes is usually severe and accompanied by fever, while subsequent attacks are less severe and localized to one site. The ulcers caused by genital herpes are multiple and painful.

Syphilis is another STI that can cause genital ulcers. It is caused by the spirochaete Treponema pallidum and is characterized by primary, secondary, and tertiary stages. The primary stage of syphilis is marked by the appearance of a painless ulcer, known as a chancre. The incubation period for syphilis is between 9-90 days.

Chancroid is a tropical disease caused by Haemophilus ducreyi. It causes painful genital ulcers that are associated with unilateral, painful inguinal lymph node enlargement. The ulcers typically have a sharply defined, ragged, undermined border.

Lymphogranuloma venereum (LGV) is caused by Chlamydia trachomatis and typically occurs in three stages. The first stage is marked by a small, painless pustule that later forms an ulcer. The second stage is characterized by painful inguinal lymphadenopathy, while the third stage is proctocolitis. LGV is treated using doxycycline.

Other causes of genital ulcers include Behcet’s disease, carcinoma, and granuloma inguinale, which is caused by Klebsiella granulomatis (previously called Calymmatobacterium granulomatis).

Fluid retention may be caused by pioglitazone.

Thiazolidinediones: A Class of Diabetes Medications

Thiazolidinediones are a type of medication used to treat type 2 diabetes. They work by activating the PPAR-gamma receptor, which reduces insulin resistance in the body. However, one medication in this class, rosiglitazone, was withdrawn in 2010 due to concerns about its cardiovascular side effects.

The PPAR-gamma receptor is a nuclear receptor found inside cells. It is naturally activated by free fatty acids and is involved in regulating the differentiation and function of adipocytes (fat cells).

While thiazolidinediones can be effective in treating diabetes, they can also have adverse effects. Patients may experience weight gain, liver impairment (which requires monitoring of liver function tests), and fluid retention. Thiazolidinediones are contraindicated in patients with heart failure due to the increased risk of fluid retention, especially if the patient is also taking insulin. Recent studies have also shown an increased risk of fractures and bladder cancer in patients taking pioglitazone, another medication in this class.

An urgent referral to a breast clinic is necessary for women over the age of 30 who have an unexplained breast lump, using a suspected cancer pathway referral. This is in accordance with NICE guidelines, as the lump may represent cancerous pathology and should be investigated promptly. Conservative management or routine referral to breast clinic is not appropriate in this case, as the potential for cancerous pathology requires urgent attention.

In 2015, NICE released guidelines for referring individuals suspected of having breast cancer. If a person is 30 years or older and has an unexplained breast lump with or without pain, or if they are 50 years or older and have discharge, retraction, or other concerning changes in one nipple only, they should be referred using a suspected cancer pathway referral for an appointment within two weeks. If a person has skin changes that suggest breast cancer or is 30 years or older with an unexplained lump in the axilla, a suspected cancer pathway referral should also be considered. For individuals under 30 years old with an unexplained breast lump with or without pain, non-urgent referral should be considered.

Common Sites of Metastatic Spread in Bone

Metastatic spread to the bone is a common occurrence in many types of cancer. The following are some of the most common sites of metastases in bone:

Spine: The spine is the most common site for bony metastases, with spread often found from a range of solid and haematological cancers, as well as infectious diseases such as tuberculosis.

Ribs: While breast cancer is known to spread to the ribs, this is not the case for many other cancers.

Pelvis: The pelvis is a prevalent site of metastatic spread occurring mostly from the prostate, breast, kidney, lung, and thyroid cancer.

Skull: Skull metastases are seen in 15-25% of all cancer patients and tend to include those from the breast, lungs, prostate, and thyroid, as well as melanoma.

Long bones: Localised bone pain is a red flag for metastatic spread to any of the long bones such as the femur and humerus. Breast, prostate, renal, thyroid, and lung cancers frequently metastasize to these areas.

Overall, understanding the common sites of metastatic spread in bone can help with early detection and treatment of cancer.

Pleural plaques are benign and do not develop into cancerous growths, so there is no need for any follow-up. These plaques are the most common form of lung disease caused by asbestos exposure, but they do not increase the risk of lung cancer or mesothelioma. While ongoing monitoring of the patient’s lung disease is recommended, there is no need to specifically monitor the pleural plaques. It is important to note that pleural plaques are a sign of past asbestos exposure, which could increase the risk of mesothelioma, but the plaques themselves are not a cause for concern. Therefore, the patient does not require a specialist referral for the pleural plaques alone. However, if the patient experiences worsening shortness of breath or frequent exacerbations, a specialist referral may be necessary to assess for disease progression or malignancy.

Asbestos-Related Lung Diseases

Asbestos exposure can lead to various lung diseases, ranging from benign pleural plaques to malignant mesothelioma. Pleural plaques are non-cancerous and do not require any follow-up, but they are the most common form of asbestos-related lung disease and typically appear after a latent period of 20-40 years. Asbestos exposure may also cause diffuse pleural thickening, which is similar to the pattern seen after an empyema or haemothorax, but the underlying pathophysiology is not fully understood.

Asbestosis is a lung disease that is related to the length of exposure to asbestos. It causes lower lobe fibrosis and is typically characterized by dyspnea, reduced exercise tolerance, clubbing, bilateral end-inspiratory crackles, and a restrictive pattern with reduced gas transfer on lung function tests. Asbestosis is treated conservatively, as no interventions offer significant benefits. The latent period for asbestosis is typically 15-30 years.

Mesothelioma is a malignant disease of the pleura that is caused by asbestos exposure, with crocidolite (blue) asbestos being the most dangerous form. Possible features of mesothelioma include progressive shortness-of-breath, chest pain, and pleural effusion. Patients are usually offered palliative chemotherapy, and there is a limited role for surgery and radiotherapy. Unfortunately, the prognosis for mesothelioma is very poor, with a median survival from diagnosis of 8-14 months.

Although mesothelioma is often associated with asbestos exposure, lung cancer is actually the most common form of cancer related to asbestos exposure. It has a synergistic effect with cigarette smoke, which increases the risk of developing lung cancer.

Misconceptions about Dementia: Debunking Common Myths

Dementia is a complex and often misunderstood condition. Here are some common misconceptions about dementia that need to be debunked:

1. In Creutzfeldt-Jakob disease an EEG may be characteristic: An EEG is abnormal in approximately 90% of cases of Creutzfeldt-Jakob disease, showing characteristic changes (i.e. periodic sharp wave complexes).

2. A multi-infarct aetiology is more common than the Alzheimer disease type: Multi-infarct dementia is the second most common type of dementia in people aged over 65 years.

3. A CT scan will reliably distinguish between Alzheimer disease and multi-infarct dementia: The diagnosis of both AD and multi-infarct dementia remains essentially a clinical one (and can only be definitively confirmed at autopsy).

4. In Alzheimer disease a gait disorder is seen at an early stage: Gait disturbances are usually a late sign of AD.

5. Visual hallucinations are typical of Alzheimer’s disease: Visual hallucinations, often very vivid and colourful, are typical of dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), not of AD.