Motor Neuron Disease (MND) is a group of degenerative diseases that primarily involve the loss of specific neurons in the motor cortex, cranial nerve nuclei, and anterior horn cells. Both upper and lower motor neurons are affected in this condition. It is important to note that MND does not cause any sensory or sphincter disturbances, and it does not affect eye movements.

MND is relatively uncommon, with a prevalence of approximately 5-7 cases per 100,000 individuals. The median age of onset in the United Kingdom is 60 years, and unfortunately, it often leads to fatality within 2 to 4 years of diagnosis. The treatment for MND mainly focuses on providing supportive care through a multidisciplinary approach.

There are four distinct clinical patterns observed in MND. The first pattern, known as Amyotrophic Lateral Sclerosis (ALS), accounts for up to 50% of MND cases. It involves the loss of motor neurons in both the motor cortex and the anterior horn of the spinal cord. Clinically, individuals with ALS experience weakness and exhibit signs of both upper and lower motor neuron involvement.

The second pattern, called Progressive Bulbar Palsy, occurs in up to 10% of MND cases. This condition specifically affects cranial nerves IX-XII, resulting in Bulbar and pseudobulbar palsy.

Progressive Muscular Atrophy is the third pattern, also seen in up to 10% of MND cases. It primarily affects the anterior horn cells, leading to the presence of only lower motor neuron signs.

Lastly, Primary Lateral Sclerosis involves the loss of Betz cells in the motor cortex. Clinically, individuals with this pattern exhibit upper motor neuron signs, including marked spastic leg weakness and pseudobulbar palsy.

The human papillomavirus (HPV) is a viral infection that is primarily responsible for the development of genital warts. This virus is predominantly transmitted through sexual contact.

Eclampsia is the most likely diagnosis in this case. It is characterized by the occurrence of one or more convulsions on top of pre-eclampsia. To control seizures in eclampsia, the recommended treatment is magnesium sulphate. The Collaborative Eclampsia Trial regimen should be followed for administering magnesium sulphate. Initially, a loading dose of 4 g should be given intravenously over 5 to 15 minutes. This should be followed by a continuous infusion of 1 g per hour for 24 hours. If the woman experiences another eclamptic seizure, the infusion should be continued for an additional 24 hours after the last seizure. In case of recurrent seizures, a further dose of 2-4 g should be administered intravenously over 5 to 15 minutes. It is important to note that the only cure for eclampsia is the delivery of the fetus and placenta. Once the patient is stabilized, she should be prepared for an emergency caesarean section.

The BTS guidelines for managing acute asthma in children over the age of 2 recommend the following approaches:

Bronchodilator therapy is the first-line treatment for acute asthma. Inhaled β agonists are preferred, and a pmDI + spacer is the recommended option for children with mild to moderate asthma. It is important to individualize drug dosing based on the severity of the condition and adjust it according to the patient’s response. If initial β agonist treatment does not alleviate symptoms, ipratropium bromide can be added to the nebulized β2 agonist solution. In cases where children with a short duration of acute severe asthma symptoms have an oxygen saturation level below 92%, it is advisable to consider adding 150 mg of magnesium sulfate to each nebulized salbutamol and ipratropium within the first hour.

Long-acting β2 agonists should be discontinued if short-acting β2 agonists are required more frequently than every four hours.

Steroid therapy should be initiated early in the treatment of acute asthma attacks. For children aged 2-5 years, a dose of 20 mg prednisolone is recommended, while children over the age of 5 should receive a dose of 30-40 mg. Children already on maintenance steroid tablets should receive 2 mg/kg prednisolone, up to a maximum dose of 60 mg. If a child vomits after taking the initial dose of prednisolone, the dose should be repeated. In cases where a child is unable to retain orally ingested medication, intravenous steroids should be considered. Typically, treatment with oral steroids for up to three days is sufficient, but the duration of the course should be adjusted based on the time needed for recovery. Tapering is not necessary unless the course of steroids exceeds 14 days.

In cases where initial inhaled therapy does not yield a response in severe asthma attacks, the early addition of a single bolus dose of intravenous salbutamol (15 micrograms/kg over 10 minutes) should be considered. Aminophylline is not recommended for children with mild to moderate acute asthma, but it may be considered for those with severe or life-threatening asthma that is unresponsive to maximum doses of bronchodilators and steroids. The use of IV magnesium sulfate as a treatment for acute asthma in children is considered safe, although its role in management is not yet fully established.

According to NICE, one of the recommended treatments for mild-to-moderate Alzheimer’s disease is the use of acetylcholinesterase (AChE) inhibitors. These inhibitors include Donepezil (Aricept), Galantamine, and Rivastigmine. They work by inhibiting the enzyme that breaks down acetylcholine, a neurotransmitter involved in memory and cognitive function.

On the other hand, Memantine is a different type of medication that acts by blocking NMDA-type glutamate receptors. It is recommended for patients with moderate Alzheimer’s disease who cannot tolerate or have a contraindication to AChE inhibitors, or for those with severe Alzheimer’s disease.

The internal jugular vein is situated in the anterior triangle of the neck and is frequently utilized for the insertion of central lines. It is important for candidates to have a good understanding of the anatomy of the anterior triangle, including its contents, according to the RCEM.

Further Reading:

A central venous catheter (CVC) is a type of catheter that is inserted into a large vein in the body, typically in the neck, chest, or groin. It has several important uses, including CVP monitoring, pulmonary artery pressure monitoring, repeated blood sampling, IV access for large volumes of fluids or drugs, TPN administration, dialysis, pacing, and other procedures such as placement of IVC filters or venous stents.

When inserting a central line, it is ideal to use ultrasound guidance to ensure accurate placement. However, there are certain contraindications to central line insertion, including infection or injury to the planned access site, coagulopathy, thrombosis or stenosis of the intended vein, a combative patient, or raised intracranial pressure for jugular venous lines.

The most common approaches for central line insertion are the internal jugular, subclavian, femoral, and PICC (peripherally inserted central catheter) veins. The internal jugular vein is often chosen due to its proximity to the carotid artery, but variations in anatomy can occur. Ultrasound can be used to identify the vessels and guide catheter placement, with the IJV typically lying superficial and lateral to the carotid artery. Compression and Valsalva maneuvers can help distinguish between arterial and venous structures, and doppler color flow can highlight the direction of flow.

In terms of choosing a side for central line insertion, the right side is usually preferred to avoid the risk of injury to the thoracic duct and potential chylothorax. However, the left side can also be used depending on the clinical situation.

Femoral central lines are another option for central venous access, with the catheter being inserted into the femoral vein in the groin. Local anesthesia is typically used to establish a field block, with lidocaine being the most commonly used agent. Lidocaine works by blocking sodium channels and preventing the propagation of action potentials.

In summary, central venous catheters have various important uses and should ideally be inserted using ultrasound guidance. There are contraindications to their insertion, and different approaches can be used depending on the clinical situation. Local anesthesia is commonly used for central line insertion, with lidocaine being the preferred agent.

Patients with Parkinson’s disease (PD) typically exhibit the following clinical features:

– Hypokinesia (reduced movement)
– Bradykinesia (slow movement)
– Rest tremor (usually occurring at a rate of 4-6 cycles per second)
– Rigidity (increased muscle tone and ‘cogwheel rigidity’)

Other commonly observed clinical features include:

– Gait disturbance (characterized by a shuffling gait and loss of arm swing)
– Loss of facial expression
– Monotonous, slurred speech
– Micrographia (small, cramped handwriting)
– Increased salivation and dribbling
– Difficulty with fine movements

Initially, these signs are typically seen on one side of the body at the time of diagnosis, but they progressively worsen and may eventually affect both sides. In later stages of the disease, additional clinical features may become evident, including:

– Postural instability
– Cognitive impairment
– Orthostatic hypotension

Although PD primarily affects movement, patients often experience psychiatric issues such as depression and dementia. Autonomic disturbances and pain can also occur, leading to significant disability and reduced quality of life for the affected individual. Additionally, family members and caregivers may also be indirectly affected by the disease.

To remove contaminated material, it is recommended to remove and dispose of clothing. It is important to seal the clothing and treat it as hazardous waste. If wet decontamination is being utilized, patients should shower using warm water and detergent.

Further Reading:

Chemical incidents can occur as a result of leaks, spills, explosions, fires, terrorism, or the use of chemicals during wars. Industrial sites that use chemicals are required to conduct risk assessments and have accident plans in place for such incidents. Health services are responsible for decontamination, unless mass casualties are involved, and all acute health trusts must have major incident plans in place.

When responding to a chemical incident, hospitals prioritize containment of the incident and prevention of secondary contamination, triage with basic first aid, decontamination if not done at the scene, recognition and management of toxidromes (symptoms caused by exposure to specific toxins), appropriate supportive or antidotal treatment, transfer to definitive treatment, a safe end to the hospital response, and continuation of business after the event.

To obtain advice when dealing with chemical incidents, the two main bodies are Toxbase and the National Poisons Information Service. Signage on containers carrying chemicals and material safety data sheets (MSDS) accompanying chemicals also provide information on the chemical contents and their hazards.

Contamination in chemical incidents can occur in three phases: primary contamination from the initial incident, secondary contamination spread via contaminated people leaving the initial scene, and tertiary contamination spread to the environment, including becoming airborne and waterborne. The ideal personal protective equipment (PPE) for chemical incidents is an all-in-one chemical-resistant overall with integral head/visor and hands/feet worn with a mask, gloves, and boots.

Decontamination of contaminated individuals involves the removal and disposal of contaminated clothing, followed by either dry or wet decontamination. Dry decontamination is suitable for patients contaminated with non-caustic chemicals and involves blotting and rubbing exposed skin gently with dry absorbent material. Wet decontamination is suitable for patients contaminated with caustic chemicals and involves a warm water shower while cleaning the body with simple detergent.

After decontamination, the focus shifts to assessing the extent of any possible poisoning and managing it. The patient’s history should establish the chemical the patient was exposed to, the volume and concentration of the chemical, the route of exposure, any protective measures in place, and any treatment given. Most chemical poisonings require supportive care using standard resuscitation principles, while some chemicals have specific antidotes. Identifying toxidromes can be useful in guiding treatment, and specific antidotes may be administered accordingly.

A common indication of a mandibular fracture is the presence of a haematoma in the sublingual space after trauma. If there are lacerations in the gum mucosa, it is highly likely that the mandible is fractured and it is an open fracture.

Further Reading:

Mandibular fractures are a common type of facial fracture that often present to the emergency department. The mandible, or lower jaw, is formed by the fusion of two hemimandibles and articulates with the temporomandibular joints. Fractures of the mandible are typically caused by direct lateral force and often involve multiple fracture sites, including the body, condylar head and neck, and ramus.

When assessing for mandibular fractures, clinicians should use a look, feel, move method similar to musculoskeletal examination. However, it is important to note that TMJ effusion, muscle spasm, and pain can make moving the mandible difficult. Key signs of mandibular fracture include malocclusion, trismus (limited mouth opening), pain with the mouth closed, broken teeth, step deformity, hematoma in the sublingual space, lacerations to the gum mucosa, and bleeding from the ear.

The Manchester Mandibular Fracture Decision Rule uses the absence of five exam findings (malocclusion, trismus, broken teeth, pain with closed mouth, and step deformity) to exclude mandibular fracture. This rule has been found to be 100% sensitive and 39% specific in detecting mandibular fractures. Imaging is an important tool in diagnosing mandibular fractures, with an OPG X-ray considered the best initial imaging for TMJ dislocation and mandibular fracture. CT may be used if the OPG is technically difficult or if a CT is being performed for other reasons, such as a head injury.

It is important to note that head injury often accompanies mandibular fractures, so a thorough head injury assessment should be performed. Additionally, about a quarter of patients with mandibular fractures will also have a fracture of at least one other facial bone.

This infant is displaying prolonged jaundice and failure to thrive. Prolonged jaundice is defined as jaundice that persists beyond the first 14 days of life. Neonatal jaundice can be divided into two categories: unconjugated hyperbilirubinemia, which can be either physiological or pathological, and conjugated hyperbilirubinemia, which is always pathological.

Causes of prolonged unconjugated hyperbilirubinemia include breast milk jaundice, infections (particularly urinary tract infections), haemolysis (most commonly rhesus haemolytic disease), hypothyroidism, hereditary disorders (such as Crigler-Najjar syndrome), and galactosemia.

Causes of prolonged conjugated hyperbilirubinemia include biliary atresia, choledochal cysts, and neonatal hepatitis. Conjugated hyperbilirubinemia often presents with symptoms such as failure to thrive, easy bruising or bleeding tendency, dark urine, and pale, chalky stools.

In this case, the jaundice is clearly conjugated, and the only cause of prolonged conjugated hyperbilirubinemia listed is biliary atresia. To evaluate conjugated hyperbilirubinemia, an ultrasound of the bile ducts and gallbladder should be performed. If dilatation is observed, it may indicate the presence of choledochal cysts, which should be further investigated with a cholangiogram. If the bile ducts and gallbladder appear normal or are not visualized, a radionuclide scan is often conducted. The absence of excretion on the scan is consistent with biliary atresia.

Biliary atresia is a condition characterized by progressive destruction or absence of the extrahepatic biliary tree and intrahepatic biliary ducts. It is a rare condition, occurring in approximately 1 in 10-15,000 live births in the western world. Infants with biliary atresia typically exhibit jaundice early on, and their stools are pale while their urine is dark starting from the second day of life. If left untreated, the condition will progress to chronic liver failure, leading to portal hypertension and hepatosplenomegaly. Without treatment, death is inevitable.

This patient has presented with acute closed-angle glaucoma, which is a medical emergency in the field of ophthalmology. It occurs when the iris bows forward and blocks the fluid access to the trabecular meshwork, which is located at the entrance to Schlemm’s canal. As a result, the intraocular pressure rises and leads to glaucomatous optic neuropathy.

The main clinical features of acute closed-angle glaucoma include severe eye pain, loss of vision or decreased visual acuity, congestion and redness around the cornea, corneal swelling, a fixed semi-dilated oval-shaped pupil, nausea and vomiting, and preceding episodes of blurred vision or seeing haloes.

The diagnosis can be confirmed by tonometry, which measures the pressure inside the eye. The normal range of intraocular pressure is 10-21 mmHg, but in acute closed-angle glaucoma, it is often higher than 30 mmHg. Goldmann’s applanation tonometer is commonly used in hospitals for this purpose.

Management of acute closed-angle glaucoma should include providing pain relief, such as morphine, and antiemetics if the patient is experiencing vomiting. Intravenous administration of acetazolamide 500 mg is recommended to reduce intraocular pressure. Treatment with a topical miotic, like pilocarpine 1% or 2%, should be initiated approximately one hour after starting other measures, as the pupil may initially be paralyzed and unresponsive.

On the other hand, chronic open-angle glaucoma is a more common presentation than acute closed-angle glaucoma. It affects approximately 1 in 50 people over the age of 40 and 1 in 10 people over the age of 75. In this condition, there is a partial blockage within the trabecular meshwork, which hinders the drainage of aqueous humor and gradually increases intraocular pressure, leading to optic neuropathy. Unlike acute closed-angle glaucoma, chronic open-angle glaucoma does not cause eye pain or redness. It presents gradually with a progressive loss of peripheral vision, while central vision is relatively preserved.

Naseptin, a topical antiseptic cream containing chlorhexidine and neomycin, has been found to be just as effective as silver nitrate cautery in treating recurrent nosebleeds in children. This means that using Naseptin can help prevent future nosebleeds in children with this condition. It is important to note that silver nitrate cautery can cause more pain and should only be used if a specific bleeding vessel can be identified.

Further Reading:

Epistaxis, or nosebleed, is a common condition that can occur in both children and older adults. It is classified as either anterior or posterior, depending on the location of the bleeding. Anterior epistaxis usually occurs in younger individuals and arises from the nostril, most commonly from an area called Little’s area. These bleeds are usually not severe and account for the majority of nosebleeds seen in hospitals. Posterior nosebleeds, on the other hand, occur in older patients with conditions such as hypertension and atherosclerosis. The bleeding in posterior nosebleeds is likely to come from both nostrils and originates from the superior or posterior parts of the nasal cavity or nasopharynx.

The management of epistaxis involves assessing the patient for signs of instability and implementing measures to control the bleeding. Initial measures include sitting the patient upright with their upper body tilted forward and their mouth open. Firmly pinching the cartilaginous part of the nose for 10-15 minutes without releasing the pressure can also help stop the bleeding. If these measures are successful, a cream called Naseptin or mupirocin nasal ointment can be prescribed for further treatment.

If bleeding persists after the initial measures, nasal cautery or nasal packing may be necessary. Nasal cautery involves using a silver nitrate stick to cauterize the bleeding point, while nasal packing involves inserting nasal tampons or inflatable nasal packs to stop the bleeding. In cases of posterior bleeding, posterior nasal packing or surgery to tie off the bleeding vessel may be considered.

Complications of epistaxis can include nasal bleeding, hypovolemia, anemia, aspiration, and even death. Complications specific to nasal packing include sinusitis, septal hematoma or abscess, pressure necrosis, toxic shock syndrome, and apneic episodes. Nasal cautery can lead to complications such as septal perforation and caustic injury to the surrounding skin.

In children under the age of 2 presenting with epistaxis, it is important to refer them for further investigation as an underlying cause is more likely in this age group.

This woman is displaying symptoms and signs that are in line with a diagnosis of meningococcal septicaemia. In the United Kingdom, the majority of cases of meningococcal septicaemia are caused by Neisseria meningitidis group B.

The implementation of a vaccination program for Neisseria meningitidis group C has significantly reduced the prevalence of this particular type. However, a vaccine for group B disease is currently undergoing clinical trials and is not yet accessible for widespread use.

The tricuspid valve is the most commonly affected valve in cases of infective endocarditis among intravenous drug users. This means that when IV drug users develop infective endocarditis, it is most likely to affect the tricuspid valve. On the other hand, in cases of native valve endocarditis and prosthetic valve endocarditis, the mitral valve is the valve that is most commonly affected.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

This patient’s symptoms are consistent with a diagnosis of oesophageal candidiasis, which is commonly seen in patients undergoing treatment for haematopoietic or lymphatic malignancies.

The classic combination of symptoms associated with oesophageal candidiasis includes dysphagia, odynophagia, and retrosternal pain. This infection can be life-threatening and often requires hospital admission.

The recommended treatment for oesophageal candidiasis is as follows:

– First-line treatment involves taking oral fluconazole at a daily dose of 200-400 mg.
– If the patient is unable to tolerate oral treatment, intravenous fluconazole can be used instead.
– Second-line treatment options include oral itraconazole, oral posaconazole, or intravenous or oral voriconazole.

It is important to seek medical attention promptly for oesophageal candidiasis, as timely treatment is crucial in managing this potentially serious infection.

In the UK, the classification of pressure ulcers is done using the international NPUAP-EPUAP system. This particular description refers to a pressure ulcer of grade 2. Please refer to the notes below for more information on the classification of pressure ulcers.

Further Reading:

Pressure ulcers, also known as bedsores, are localized damage to the skin and underlying tissues caused by pressure or pressure combined with shear force. They most commonly occur over bony prominences but can develop on any part of the body. Pressure ulcers develop due to five main factors: pressure, shear, friction, moisture, and circulation and tissue perfusion. Pressure is the most important factor, with intensity and duration playing key roles in the development of pressure ulcers.

Assessment of pressure ulcers in adults should be done using a validated classification tool. The International NPUAP-EPUAP pressure ulcer classification system is preferred in the UK. This system categorizes pressure ulcers into four stages. Stage I is characterized by non-blanchable erythema, which is non-blanchable redness of the skin. Stage II involves partial thickness loss of the dermis, presenting as a shallow open ulcer with a red pink wound bed. Stage III is full thickness skin loss, with subcutaneous fat visible but no exposure of bone, tendon, or muscle. Stage IV is also full thickness tissue loss, but with exposed bone, tendon, or muscle. In addition, some pressure ulcers may be classified as suspected deep tissue injury or unstageable.

Management of pressure ulcers involves general measures such as pressure reducing aids, repositioning, hygiene, cleansing, dressings, analgesia, and dietary optimization. It is also important to optimize or treat underlying health conditions, such as diabetes. For grade 3 and 4 ulcers, additional measures to consider include antibiotics and surgical debridement with or without skin flap coverage.

Type I hypersensitivity reactions are allergic reactions that occur when a person is exposed again to a particular antigen, known as an allergen. These reactions are triggered by IgE and typically happen within 15 to 30 minutes after exposure to the allergen.

A rapid onset of an urticarial rash, which occurs shortly after being exposed to an allergen (such as latex), is highly likely to be caused by a type I hypersensitivity reaction.

Septic arthritis occurs when an infectious agent invades a joint, causing it to become purulent. The main symptoms of septic arthritis include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty moving the joint. Patients may also experience fever and systemic upset. The most common cause of septic arthritis is Staphylococcus aureus, but other bacteria such as Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea, and Escherichia coli can also be responsible.

According to the current recommendations by NICE and the BNF, the initial treatment for septic arthritis is flucloxacillin. However, if a patient is allergic to penicillin, clindamycin can be used instead. If there is a suspicion of MRSA infection, vancomycin is the recommended choice. In cases where gonococcal arthritis or a Gram-negative infection is suspected, cefotaxime is the preferred treatment. The suggested duration of treatment is typically 4-6 weeks, although it may be longer if the infection is complicated.

In this case, a 70-year-old male who recently underwent aortic valve replacement is presenting with symptoms of fever, fatigue, and overall malaise. Upon examination, splinter hemorrhages are observed on the patient’s fingernails, which raises suspicion of infective endocarditis. Given the patient’s history and symptoms, the most likely causative organism in this particular case is Staphylococcus.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

The intravascular volume of an infant is approximately 80 ml/kg, while in older children it is around 70 ml/kg. Dehydration itself does not lead to death, but shock can occur when there is a loss of 20 ml/kg from the intravascular space. Clinical dehydration becomes evident only after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children: Bodyweight:

– First 10 kg: Daily fluid requirement of 100 ml/kg and hourly fluid requirement of 4 ml/kg.

– Second 10 kg: Daily fluid requirement of 50 ml/kg and hourly fluid requirement of 2 ml/kg.

– Subsequent kg: Daily fluid requirement of 20 ml/kg and hourly fluid requirement of 1 ml/kg.

Based on this information, the hourly maintenance fluid requirements for this child can be calculated as follows:

– First 10 kg: 4 ml/kg = 40 ml

– Second 10 kg: 2 ml/kg = 20 ml

– Subsequent kg: 1 ml/kg = 5 ml

Therefore, the total hourly maintenance fluid requirement for this child is 65 ml.

Haloperidol should not be used in patients with Parkinson’s, Lewy body dementia, or prolonged QT syndrome. It is the first choice for controlling aggressive behavior in most patients with delirium, but lorazepam is preferred for patients with Parkinson’s, Lewy body dementia, prolonged QT syndrome, extrapyramidal side effects, or delirium due to alcohol withdrawal. Haloperidol can reduce the effectiveness of levodopa in Parkinson’s disease by blocking dopamine receptors in the corpus striatum, which can lead to worsened motor function, psychosis, or a combination of both.

Further Reading:

Delirium is an acute syndrome that causes disturbances in consciousness, attention, cognition, and perception. It is also known as an acute confusional state. The DSM-IV criteria for diagnosing delirium include recent onset of fluctuating awareness, impairment of memory and attention, and disorganized thinking. Delirium typically develops over hours to days and may be accompanied by behavioral changes, personality changes, and psychotic features. It often occurs in individuals with predisposing factors, such as advanced age or multiple comorbidities, when exposed to new precipitating factors, such as medications or infection. Symptoms of delirium fluctuate throughout the day, with lucid intervals occurring during the day and worse disturbances at night. Falling and loss of appetite are often warning signs of delirium.

Delirium can be classified into three subtypes based on the person’s symptoms. Hyperactive delirium is characterized by inappropriate behavior, hallucinations, and agitation. Restlessness and wandering are common in this subtype. Hypoactive delirium is characterized by lethargy, reduced concentration, and appetite. The person may appear quiet or withdrawn. Mixed delirium presents with signs and symptoms of both hyperactive and hypoactive subtypes.

The exact pathophysiology of delirium is not fully understood, but it is believed to involve multiple mechanisms, including cholinergic deficiency, dopaminergic excess, and inflammation. The cause of delirium is usually multifactorial, with predisposing factors and precipitating factors playing a role. Predisposing factors include older age, cognitive impairment, frailty, significant injuries, and iatrogenic events. Precipitating factors include infection, metabolic or electrolyte disturbances, cardiovascular disorders, respiratory disorders, neurological disorders, endocrine disorders, urological disorders, gastrointestinal disorders, severe uncontrolled pain, alcohol intoxication or withdrawal, medication use, and psychosocial factors.

Delirium is highly prevalent in hospital settings, affecting up to 50% of inpatients aged over 65 and occurring in 30% of people aged over 65 presenting to the emergency department. Complications of delirium include increased risk of death, high in-hospital mortality rates, higher mortality rates following hospital discharge, increased length of stay in hospital, nosocomial infections, increased risk of admission to long-term care or re-admission to hospital, increased incidence of dementia, increased risk of falls and associated injuries and pressure sores.

Febrile convulsions are harmless, generalized seizures that occur in otherwise healthy children who have a fever due to an infection outside the brain. To diagnose febrile convulsions, the child must be developing normally, the seizure should last less than 20 minutes, have no complex features, and not cause any lasting abnormalities.

The prognosis for febrile convulsions is generally positive. There is a 30 to 50% chance of experiencing recurrent febrile convulsions, with a 10% risk of recurrence within the first 24 hours. The likelihood of developing long-term epilepsy is around 6%.

Complex febrile convulsions are characterized by certain factors. These include focal seizures, seizures lasting longer than 15 minutes, experiencing more than one convulsion during a single fever episode, or the child being left with a focal neurological deficit.

Overall, febrile convulsions are typically harmless and do not cause any lasting damage.

Enterotoxigenic E.coli is a strain that does not invade the body and does not lead to inflammation or bloody diarrhea. On the other hand, enterogenic strains result in excessive watery diarrhea and are typically not accompanied by abdominal cramping.

There are several infectious causes of bloody diarrhea, including Campylobacter spp., Shigella spp., Salmonella spp., Clostridium difficile, Enterohaemorrhagic Escherichia coli, Yersinia spp., Schistosomiasis, and Amoebiasis (Entamoeba histolytica).

This patient has developed Wernicke’s encephalopathy, a condition that is associated with alcohol abuse and other causes of thiamine deficiency. It is important to note that the infusion of glucose-containing intravenous fluids without thiamine in a patient with chronic thiamine deficiency can trigger Wernicke’s encephalopathy. In this particular case, it seems that this is what has occurred.

Wernicke’s encephalopathy is typically characterized by a triad of symptoms, which include acute confusion, ophthalmoplegia, and ataxia. Additionally, other possible features of this condition may include papilloedema, hearing loss, apathy, dysphagia, memory impairment, and hypothermia. It is also common for peripheral neuropathy, primarily affecting the legs, to occur in the majority of cases.

This condition is characterized by the presence of acute capillary haemorrhages, astrocytosis, and neuronal death in the upper brainstem and diencephalon. These abnormalities can be visualized through MRI scanning, although CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will go on to develop a Korsakoff psychosis. This condition is characterized by retrograde amnesia, an inability to form new memories, disordered time perception, and confabulation.

Patients who are suspected to have Wernicke’s encephalopathy should be promptly treated with parenteral thiamine (such as Pabrinex) for a minimum of 5 days. Following the parenteral therapy, oral thiamine should be administered.

Based on his symptoms, the most likely diagnosis is benign paroxysmal positional vertigo. The most suitable initial treatment option for this condition would be the Epley maneuver.

Further Reading:

Benign paroxysmal positional vertigo (BPPV) is a common cause of vertigo, characterized by 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. BPPV is caused by dysfunction in the inner ear, specifically the detachment of otoliths (calcium carbonate particles) from the utricular otolithic membrane. These loose otoliths move through the semicircular canals, triggering a sensation of movement and resulting in conflicting sensory inputs that cause vertigo.

The majority of BPPV cases involve otoliths in the posterior semicircular canal, followed by the inferior semicircular canal. BPPV in the anterior semicircular canals is rare. Clinical features of BPPV include vertigo triggered by head position changes, such as rolling over in bed or looking upwards, accompanied by nausea. Episodes of vertigo typically last 10-20 seconds and can be diagnosed through positional nystagmus, which is a specific eye movement, observed during diagnostic maneuvers like the Dix-Hallpike maneuver.

Hearing loss and tinnitus are not associated with BPPV. The prognosis for BPPV is generally good, with spontaneous resolution occurring within a few weeks to months. Symptomatic relief can be achieved through the Epley maneuver, which is successful in around 80% of cases, or patient home exercises like the Brandt-Daroff exercises. Medications like Betahistine may be prescribed but have limited effectiveness in treating BPPV.

Femoral shaft fractures are quite common among children and have a significant impact on both the child and their family. It is important to carefully examine children with these fractures for any associated injuries, such as soft-tissue injury, head trauma, or additional fractures. In fact, up to 40% of children who experience a femoral shaft fracture due to high-energy trauma may have these associated injuries. Additionally, a thorough neurovascular examination should be conducted.

Rapidly immobilizing the limb is crucial for managing pain and limiting further blood loss from the fracture. For distal femoral shaft fractures, well-padded long leg splints with split plaster casts can be applied. However, for more proximal shaft fractures, long leg splints alone may not provide adequate control. In these cases, skin traction is a better option. Skin traction involves attaching a large foam pad to the patient’s lower leg using spray adhesive. A weight, approximately 10% of the child’s body weight, is then applied to the foam pad and allowed to hang over the foot of the bed. This constant longitudinal traction helps keep the bone fragments aligned.

When children experience severe pain, it is important to manage it aggressively yet safely. Immobilizing the fracture can provide significant relief. The Royal College of Emergency Medicine recommends other pain control measures for children, such as intranasal diamorphine (0.1 mg/kg in 0.2 ml sterile water), intravenous morphine (0.1-0.2 mg/kg), and oral analgesia (e.g., paracetamol 20 mg/kg, max 1 g, and ibuprofen 10 mg/kg, max 400 mg).

Thiopental sodium is a barbiturate with a very short duration of action. It is primarily used to induce anesthesia. Barbiturates are believed to primarily affect synapses by reducing the sensitivity of postsynaptic receptors to neurotransmitters and by interfering with the release of neurotransmitters from presynaptic neurons.

Thiopental sodium specifically binds to a unique site associated with a chloride ionophore at the GABAA receptor, which is responsible for the opening of chloride ion channels. This binding increases the length of time that the chloride ionophore remains open. As a result, the inhibitory effect of GABA on postsynaptic neurons in the thalamus is prolonged.

In summary, thiopental sodium acts as a short-acting barbiturate that is commonly used to induce anesthesia. It affects synapses by reducing postsynaptic receptor sensitivity and interfering with neurotransmitter release. By binding to a specific site at the GABAA receptor, thiopental sodium prolongs the inhibitory effect of GABA in the thalamus.

The administration of nitrous oxide increases the amount of inhaled anaesthetic gases in the body through a phenomenon called the ‘second gas effect’. Nitrous oxide is much more soluble than nitrogen, with a solubility that is 20 to 30 times higher. When nitrous oxide is given, it causes a decrease in the volume of air in the alveoli. Additionally, nitrous oxide can enhance the absorption of other inhaled anaesthetic agents through the second gas effect. However, it is important to note that nitrous oxide alone cannot be used as the sole maintenance agent in anaesthesia.

Further Reading:

Entonox® is a mixture of 50% nitrous oxide and 50% oxygen that can be used for self-administration to reduce anxiety. It can also be used alongside other anesthesia agents. However, its mechanism of action for anxiety reduction is not fully understood. The Entonox bottles are typically identified by blue and white color-coded collars, but a new standard will replace these with dark blue shoulders in the future. It is important to note that Entonox alone cannot be used as the sole maintenance agent in anesthesia.

One of the effects of nitrous oxide is the second-gas effect, where it speeds up the absorption of other inhaled anesthesia agents. Nitrous oxide enters the alveoli and diffuses into the blood, displacing nitrogen. This displacement causes the remaining alveolar gases to become more concentrated, increasing the fractional content of inhaled anesthesia gases and accelerating the uptake of volatile agents into the blood.

However, when nitrous oxide administration is stopped, it can cause diffusion hypoxia. Nitrous oxide exits the blood and diffuses back into the alveoli, while nitrogen diffuses in the opposite direction. Nitrous oxide enters the alveoli much faster than nitrogen leaves, resulting in the dilution of oxygen within the alveoli. This can lead to diffusion hypoxia, where the oxygen concentration in the alveoli is diluted, potentially causing oxygen deprivation in patients breathing air.

There are certain contraindications for using nitrous oxide, as it can expand in air-filled spaces. It should be avoided in conditions such as head injuries with intracranial air, pneumothorax, recent intraocular gas injection, and entrapped air following a recent underwater dive.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In this case, the patient has already received two doses of benzodiazepine and is currently on a phenytoin infusion. However, despite these treatments, the seizures persist, and it has been 20 minutes since the infusion started. At this point, the preferred treatment option is to induce general anesthesia. The induction agents that can be considered include thiopental sodium, propofol, and midazolam. There is no need to administer intravenous thiamine in this situation.

The management of status epilepticus involves several general measures, which are outlined in the following table:

1st stage (Early status, 0-10 minutes):
– Secure the airway and provide resuscitation
– Administer oxygen
– Assess cardiorespiratory function
– Establish intravenous access

2nd stage (0-30 minutes):
– Implement regular monitoring
– Consider the possibility of non-epileptic status
– Initiate emergency antiepileptic drug (AED) therapy
– Perform emergency investigations
– Administer glucose or intravenous thiamine if alcohol abuse or impaired nutrition is suspected
– Treat severe acidosis if present

3rd stage (0-60 minutes):
– Determine the underlying cause of status epilepticus
– Notify the anesthetist and intensive care unit (ITU)
– Identify and treat any medical complications
– Consider pressor therapy if necessary

4th stage (30-90 minutes):
– Transfer the patient to the intensive care unit
– Establish intensive care and EEG monitoring
– Initiate long-term maintenance AED therapy
– Perform further investigations as needed, such as brain imaging or lumbar puncture

Emergency investigations include blood tests for gases, glucose, renal and liver function, calcium and magnesium levels, full blood count (including platelets), blood clotting, and AED drug levels. Serum and urine samples should be saved for future analysis, including toxicology if the cause of convulsive status epilepticus is uncertain. A chest radiograph may be done to evaluate the possibility of aspiration. Additional investigations depend on the clinical circumstances and may include brain imaging or lumbar puncture.

Monitoring during the management of status epilepticus involves regular neurological observations and measurements of pulse, blood pressure, and temperature.

The most suitable approach for investigation in this case would be to send a blood test for Epstein-Barr virus (EBV) viral serology. Glandular fever, also known as infectious mononucleosis, is commonly caused by the Epstein-Barr virus. The symptoms described by the patient, including a sore throat, fever, and feeling unwell, are consistent with this condition. To confirm the diagnosis, a blood test for EBV viral serology can be performed. This test detects antibodies produced by the body in response to the virus. It is important to note that the Monospot test, which is another blood test for infectious mononucleosis, may not be as accurate in younger children. Therefore, the most appropriate option would be to send a blood test for EBV viral serology in 2-3 days time. This will allow for the detection of specific antibodies and provide a more accurate diagnosis.

Further Reading:

Glandular fever, also known as infectious mononucleosis or mono, is a clinical syndrome characterized by symptoms such as sore throat, fever, and swollen lymph nodes. It is primarily caused by the Epstein-Barr virus (EBV), with other viruses and infections accounting for the remaining cases. Glandular fever is transmitted through infected saliva and primarily affects adolescents and young adults. The incubation period is 4-8 weeks.

The majority of EBV infections are asymptomatic, with over 95% of adults worldwide having evidence of prior infection. Clinical features of glandular fever include fever, sore throat, exudative tonsillitis, lymphadenopathy, and prodromal symptoms such as fatigue and headache. Splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may also be present, and a non-pruritic macular rash can sometimes occur.

Glandular fever can lead to complications such as splenic rupture, which increases the risk of rupture in the spleen. Approximately 50% of splenic ruptures associated with glandular fever are spontaneous, while the other 50% follow trauma. Diagnosis of glandular fever involves various investigations, including viral serology for EBV, monospot test, and liver function tests. Additional serology tests may be conducted if EBV testing is negative.

Management of glandular fever involves supportive care and symptomatic relief with simple analgesia. Antiviral medication has not been shown to be beneficial. It is important to identify patients at risk of serious complications, such as airway obstruction, splenic rupture, and dehydration, and provide appropriate management. Patients can be advised to return to normal activities as soon as possible, avoiding heavy lifting and contact sports for the first month to reduce the risk of splenic rupture.

Rare but serious complications associated with glandular fever include hepatitis, upper airway obstruction, cardiac complications, renal complications, neurological complications, haematological complications, chronic fatigue, and an increased risk of lymphoproliferative cancers and multiple sclerosis.