This patient is likely experiencing an acute coronary syndrome, possibly a non-ST-elevation myocardial infarction (NSTEMI) or unstable angina. The troponin test will help confirm the diagnosis. The patient’s ECG showed ST depression in the inferior leads, but this normalized after treatment with GTN and morphine, ruling out a ST-elevation myocardial infarction (STEMI).

Immediate pain relief should be provided. GTN (sublingual or buccal) can be used, but intravenous opioids like morphine should be considered, especially if a heart attack is suspected.

Aspirin should be given to all patients with unstable angina or NSTEMI as soon as possible and continued indefinitely, unless there are contraindications like bleeding risk or aspirin hypersensitivity. A loading dose of 300 mg should be administered right after presentation.

Fondaparinux should be given to patients without a high bleeding risk, unless coronary angiography is planned within 24 hours of admission. Unfractionated heparin can be an alternative to fondaparinux for patients who will undergo coronary angiography within 24 hours. For patients with significant renal impairment, unfractionated heparin can also be considered, with dose adjustment based on clotting function monitoring.

Routine administration of oxygen is no longer recommended, but oxygen saturation should be monitored using pulse oximetry as soon as possible, preferably before hospital admission. Supplemental oxygen should only be offered to individuals with oxygen saturation (SpO2) below 94% who are not at risk of hypercapnic respiratory failure, aiming for a SpO2 of 94-98%. For individuals with chronic obstructive pulmonary disease at risk of hypercapnic respiratory failure, a target SpO2 of 88-92% should be achieved until blood gas analysis is available.

Bivalirudin, a specific and reversible direct thrombin inhibitor (DTI), is recommended by NICE as a possible treatment for adults with STEMI undergoing percutaneous coronary intervention.

For more information, refer to the NICE guidelines on the assessment and diagnosis of chest pain of recent onset.

Malaria is a contagious illness that is spread by female mosquitoes of the Anopheles genus. It is caused by a parasitic infection from the Plasmodium genus. There are five species of Plasmodium that can cause disease in humans: Plasmodium falciparum, Plasmodium ovale, Plasmodium vivax, Plasmodium malariae, and Plasmodium knowlesi.

The main symptom of malaria is the malarial paroxysm, which is a recurring cycle of cold, hot, and sweating stages. During the cold stage, the patient experiences intense chills, followed by an extremely hot stage, and finally a stage of profuse sweating. Upon examination, the patient may show signs of anemia, jaundice, and have an enlarged liver and spleen, but no signs of swollen lymph nodes.

Plasmodium falciparum is the most severe form of malaria and is responsible for the majority of deaths. Severe or complicated malaria is indicated by impaired consciousness, seizures, low blood sugar, anemia, kidney damage, difficulty breathing, and spontaneous bleeding. Given the presentation, it is likely that this case involves Plasmodium falciparum.

Currently, artemisinin-based combination therapy (ACT) is recommended for treating P. falciparum malaria. This involves combining fast-acting artemisinin-based compounds with a drug from a different class. Companion drugs include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives include dihydroartemisinin, artesunate, and artemether.

If ACT is not available, oral quinine or atovaquone with proguanil hydrochloride can be used. Quinine is highly effective but not well tolerated for long-term treatment, so it should be combined with another drug, usually oral doxycycline (or clindamycin for pregnant women and young children).

Severe or complicated falciparum malaria should be managed in a high dependency unit or intensive care setting. Intravenous artesunate is recommended for all patients with severe or complicated falciparum malaria, or those at high risk of developing severe disease (such as if more than 2% of red blood cells are infected), or

Glandular fever is typically treated with conservative management. It is a self-limiting illness that usually resolves within 2-4 weeks and can be effectively managed with over-the-counter pain relievers. Patients should also be informed about the expected duration of the illness, ways to minimize transmission, precautions to prevent complications like splenic rupture, and provided with appropriate support and guidance. These measures are outlined in the following notes.

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.

Transfusion transmitted bacterial infection is a rare complication that can occur during blood transfusion. It is more commonly associated with platelet transfusion, as platelets are stored at room temperature. Additionally, previously frozen components that are thawed using a water bath and red cell components stored for several weeks are also at a higher risk for bacterial infection.

Both Gram-positive and Gram-negative bacteria have been implicated in transfusion-transmitted bacterial infection, but Gram-negative bacteria are known to cause more severe illness and have higher rates of morbidity and mortality. Among the bacterial organisms, Yersinia enterocolitica is the most commonly associated with this type of infection. This particular organism is able to multiply at low temperatures and utilizes iron as a nutrient, making it well-suited for proliferation in blood stores.

The clinical features of transfusion-transmitted bacterial infection typically manifest shortly after the transfusion begins. These features include a high fever, chills and rigors, nausea and vomiting, tachycardia, hypotension, and even circulatory collapse.

If there is suspicion of a transfusion-transmitted bacterial infection, it is crucial to immediately stop the transfusion. Blood cultures and a Gram-stain should be requested to identify the specific bacteria causing the infection. Broad-spectrum antibiotics should be initiated promptly. Furthermore, the blood pack should be returned to the blood bank urgently for culture and Gram-stain analysis.

During Bier’s block, the cuff is inflated to a pressure that is 100 mmHg higher than the patient’s systolic blood pressure. For example, if the systolic blood pressure is 150 mmHg, the cuff would be inflated to 250 mmHg. It is important to note that Bier’s block should not be performed if the systolic blood pressure is greater than 200 mmHg, as this is considered a contraindication. Therefore, the maximum pressure ever used during Bier’s block is 300mmHg.

Further Reading:

Bier’s block is a regional intravenous anesthesia technique commonly used for minor surgical procedures of the forearm or for reducing distal radius fractures in the emergency department (ED). It is recommended by NICE as the preferred anesthesia block for adults requiring manipulation of distal forearm fractures in the ED.

Before performing the procedure, a pre-procedure checklist should be completed, including obtaining consent, recording the patient’s weight, ensuring the resuscitative equipment is available, and monitoring the patient’s vital signs throughout the procedure. The air cylinder should be checked if not using an electronic machine, and the cuff should be checked for leaks.

During the procedure, a double cuff tourniquet is placed on the upper arm, and the arm is elevated to exsanguinate the limb. The proximal cuff is inflated to a pressure 100 mmHg above the systolic blood pressure, up to a maximum of 300 mmHg. The time of inflation and pressure should be recorded, and the absence of the radial pulse should be confirmed. 0.5% plain prilocaine is then injected slowly, and the time of injection is recorded. The patient should be warned about the potential cold/hot sensation and mottled appearance of the arm. After injection, the cannula is removed and pressure is applied to the venipuncture site to prevent bleeding. After approximately 10 minutes, the patient should have anesthesia and should not feel pain during manipulation. If anesthesia is successful, the manipulation can be performed, and a plaster can be applied by a second staff member. A check x-ray should be obtained with the arm lowered onto a pillow. The tourniquet should be monitored at all times, and the cuff should be inflated for a minimum of 20 minutes and a maximum of 45 minutes. If rotation of the cuff is required, it should be done after the manipulation and plaster application. After the post-reduction x-ray is satisfactory, the cuff can be deflated while observing the patient and monitors. Limb circulation should be checked prior to discharge, and appropriate follow-up and analgesia should be arranged.

There are several contraindications to performing Bier’s block, including allergy to local anesthetic, hypertension over 200 mm Hg, infection in the limb, lymphedema, methemoglobinemia, morbid obesity, peripheral vascular disease, procedures needed in both arms, Raynaud’s phenomenon, scleroderma, severe hypertension and sickle cell disease.

According to NICE guidelines, when evaluating patients with acute upper GI bleeding, it is recommended to use the Blatchford score during the initial assessment and the full Rockall score after endoscopy. The Rockall score is specifically designed to assess the risk of re-bleeding or death in these patients. If a patient’s post-endoscopic Rockall score is less than 3, they are considered to have a low risk of re-bleeding or death and may be eligible for early discharge.

Further Reading:

Upper gastrointestinal bleeding (UGIB) refers to the loss of blood from the gastrointestinal tract, occurring in the upper part of the digestive system. It can present as haematemesis (vomiting blood), coffee-ground emesis, bright red blood in the nasogastric tube, or melaena (black, tarry stools). UGIB can lead to significant hemodynamic compromise and is a major health burden, accounting for approximately 70,000 hospital admissions each year in the UK with a mortality rate of 10%.

The causes of UGIB vary, with peptic ulcer disease being the most common cause, followed by gastritis/erosions, esophagitis, and other less common causes such as varices, Mallory Weiss tears, and malignancy. Swift assessment, hemodynamic resuscitation, and appropriate interventions are essential for the management of UGIB.

Assessment of patients with UGIB should follow an ABCDE approach, and scoring systems such as the Glasgow-Blatchford bleeding score (GBS) and the Rockall score are recommended to risk stratify patients and determine the urgency of endoscopy. Transfusion may be necessary for patients with massive hemorrhage, and platelet transfusion, fresh frozen plasma (FFP), and prothrombin complex concentrate may be offered based on specific criteria.

Endoscopy plays a crucial role in the management of UGIB. Unstable patients with severe acute UGIB should undergo endoscopy immediately after resuscitation, while all other patients should undergo endoscopy within 24 hours of admission. Endoscopic treatment of non-variceal bleeding may involve mechanical methods of hemostasis, thermal coagulation, or the use of fibrin or thrombin with adrenaline. Proton pump inhibitors should only be used after endoscopy.

Variceal bleeding requires specific management, including the use of terlipressin and prophylactic antibiotics. Oesophageal varices can be treated with band ligation or transjugular intrahepatic portosystemic shunts (TIPS), while gastric varices may be treated with endoscopic injection of N-butyl-2-cyanoacrylate or TIPS if bleeding is not controlled.

For patients taking NSAIDs, aspirin, or clopidogrel, low-dose aspirin can be continued once hemostasis is achieved, NSAIDs should be stopped in patients presenting with UGIB.

Digoxin is a medication used to manage heart failure and atrial fibrillation. It works by inhibiting the Na+/K+ ATPase in the myocardium, which slows down the ventricular response and has a positive effect on the heart’s contraction. Although less commonly used nowadays, digoxin still plays a role in certain cases.

One advantage of digoxin is its long half-life, allowing for once-daily maintenance doses. However, it is important to monitor the dosage to ensure it is correct and to watch out for factors that may lead to toxicity, such as renal dysfunction and hypokalemia. Once a steady state has been achieved, regular monitoring of plasma digoxin concentrations is not necessary unless there are concerns.

In atrial fibrillation, the effectiveness of digoxin treatment is best assessed by monitoring the ventricular rate. The target range for plasma digoxin concentration is 1.0-1.5 nmol/L, although higher levels of up to 2 nmol/L may be needed in some cases. It is important to note that the plasma concentration alone cannot reliably indicate toxicity, but levels above 2 nmol/L significantly increase the risk. To manage hypokalemia, which can increase the risk of digoxin toxicity, a potassium-sparing diuretic or potassium supplementation may be prescribed.

ACE inhibitors should not be used in individuals with HAE because they can enhance the effects of bradykinin. This can lead to drug-induced angioedema, which is a known side effect of ACE inhibitors. In individuals with HAE, ACE inhibitors can trigger attacks of angioedema.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

In order to gain a comprehensive understanding of AF management, it is crucial to familiarize oneself with the terminology used to describe its various subtypes. These terms help categorize different episodes of AF based on their characteristics and outcomes.

Acute AF refers to any episode that occurs within the previous 48 hours. It can manifest with or without symptoms and may or may not recur. On the other hand, paroxysmal AF describes episodes that spontaneously end within 7 days, typically within 48 hours. While these episodes are often recurrent, they can progress into a sustained form of AF.

Recurrent AF is defined as experiencing two or more episodes of AF. If the episodes self-terminate, they are classified as paroxysmal AF. However, if the episodes do not self-terminate, they are categorized as persistent AF. Persistent AF lasts longer than 7 days or has occurred after a previous cardioversion. To terminate persistent AF, electrical or pharmacological intervention is required. In some cases, persistent AF can progress into permanent AF.

Permanent AF, also known as Accepted AF, refers to episodes that cannot be successfully terminated, have relapsed after termination, or where cardioversion is not pursued. This subtype signifies a more chronic and ongoing form of AF.

By understanding and utilizing these terms, healthcare professionals can effectively communicate and manage the different subtypes of AF.

The current guidelines from NICE recommend that the first-line treatment for confirmed deep-vein thrombosis (DVT) or pulmonary embolus (PE) should be either apixaban or rivaroxaban, which are direct oral anticoagulants.

If neither of these options is suitable, the following alternatives should be considered:

1. LMWH (low molecular weight heparin) should be administered for at least 5 days, followed by dabigatran or edoxaban.

2. LMWH should be combined with a vitamin K antagonist (VKA), such as warfarin, for at least 5 days or until the international normalized ratio (INR) reaches at least 2.0 on 2 consecutive readings. Afterward, the VKA can be continued alone.

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.

The NICE guidelines for suspected DVT state that if a person scores two points or more on the DVT Wells score, they are likely to have DVT. On the other hand, if a person scores one point or less, it is unlikely that they have DVT.

For individuals who are likely to have DVT, it is recommended to offer a proximal leg vein ultrasound scan with the results available within 4 hours if possible. However, if the ultrasound scan cannot be done within 4 hours, the following steps should be taken: a D-dimer test should be offered, followed by interim therapeutic anticoagulation. It is preferable to choose an anticoagulant that can be continued if DVT is confirmed. Additionally, a proximal leg vein ultrasound scan should be conducted with the results available within 24 hours.

For individuals who are unlikely to have DVT, it is advised to offer a D-dimer test with the results available within 4 hours. If obtaining the results within 4 hours is not possible, interim therapeutic anticoagulation should be provided while awaiting the result. If feasible, an anticoagulant that can be continued if DVT is confirmed should be chosen.

For more information, you can refer to the NICE Clinical Knowledge Summary on deep vein thrombosis.

Clostridium difficile is a type of bacteria that is Gram-positive, anaerobic, and capable of forming spores. It is commonly associated with diarrhoea, which occurs after the use of broad-spectrum antibiotics. These antibiotics disrupt the normal bacteria flora in the bowel, allowing Clostridium difficile to multiply. As a result, the mucosa of the large intestine becomes inflamed and bleeds, leading to a distinct ‘pseudomembranous appearance’. The main symptoms of Clostridium difficile infection include abdominal cramps, bloody and/or watery diarrhoea, and fever. It is worth noting that over 80% of Clostridium difficile infections are reported in individuals aged 65 and above.

The cytotoxin assay is currently considered the gold standard for diagnosing Clostridium difficile colitis. However, this test has its drawbacks, as it can be challenging to perform and the results may take up to 48 hours to be available. An alternative laboratory test commonly used for diagnosis is an enzyme-mediated immunoassay that detects toxins A and B. This test has a specificity ranging from 93% to 100% and a sensitivity ranging from 63% to 99%.

It is important to note that alcohol hand gel is ineffective against Clostridium difficile spores. Therefore, healthcare providers who come into contact with this bacteria must wash their hands with soap and water to ensure proper hygiene.

Lastly, it is estimated that approximately 3% of healthy adults carry Clostridium difficile in their gut, according to the 2012 UK HPA estimates.

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. Shock can occur when there is a loss of 20 ml/kg from the intravascular space, whereas clinical dehydration is only noticeable after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children based on their body weight:

Bodyweight:
– First 10 kg: Daily fluid requirement of 100 ml/kg, hourly fluid requirement of 4 ml/kg
– Second 10 kg: Daily fluid requirement of 50 ml/kg, hourly fluid requirement of 2 ml/kg
– Subsequent kg: Daily fluid requirement of 20 ml/kg, hourly fluid requirement of 1 ml/kg

In general, a child showing clinical signs of dehydration without shock is assumed to be 5% dehydrated. If shock is also present, it is assumed that the child is 10% dehydrated or more. 5% dehydration means the body has lost 5 g per 100 g body weight, which is equivalent to 50 ml/kg of fluid. Therefore, 10% dehydration implies a loss of 100 ml/kg of fluid.

In this case, the child is in shock and should receive a 20 ml/kg fluid bolus. The initial volume of fluid to administer should be 20 x 25% ml = 500 ml.

Following this, the child requires:
– 100 ml/kg replacement for the 10% dehydration = 100 x 25 = 2500 ml
– 1st 10 kg = 100 ml/kg for daily maintenance fluid = 100 x 10 = 1000 ml
– 2nd 10kg = 50 ml/kg for daily maintenance fluid = 50 x 10 = 500 ml
– Subsequent kg = 20 ml/kg for daily maintenance fluid = 20 x 5 = 100 ml

The total fluid needed for rehydration and maintenance is 2500 + 1600 = 4100 ml over a 24-hour period.

The clinical features of dehydration are summarized below:

Dehydration (5%):
– Appears ‘unwell’
– Normal heart rate or tachycardia
– Normal respiratory rate or tachypnea
– Normal peripheral pulses
– Normal or mildly prolonged

Distinguishing between unstable angina and other acute coronary syndromes can be done by looking at normal troponin results. If serial troponin tests come back negative, it can rule out a diagnosis of myocardial infarction. Unstable angina is characterized by myocardial ischemia occurring at rest or with minimal exertion, without any acute damage or death of heart muscle cells. The patient in question shows ECG and biochemical features that align with this definition. Vincent’s angina, on the other hand, refers to an infection in the throat accompanied by ulcerative gingivitis.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

To measure blood pressure while standing, you will need to take repeated measurements for a duration of 3 minutes. This involves measuring both lying and standing blood pressure.

Further Reading:

Blackouts, also known as syncope, are defined as a spontaneous transient loss of consciousness with complete recovery. They are most commonly caused by transient inadequate cerebral blood flow, although epileptic seizures can also result in blackouts. There are several different causes of blackouts, including neurally-mediated reflex syncope (such as vasovagal syncope or fainting), orthostatic hypotension (a drop in blood pressure upon standing), cardiovascular abnormalities, and epilepsy.

When evaluating a patient with blackouts, several key investigations should be performed. These include an electrocardiogram (ECG), heart auscultation, neurological examination, vital signs assessment, lying and standing blood pressure measurements, and blood tests such as a full blood count and glucose level. Additional investigations may be necessary depending on the suspected cause, such as ultrasound or CT scans for aortic dissection or other abdominal and thoracic pathology, chest X-ray for heart failure or pneumothorax, and CT pulmonary angiography for pulmonary embolism.

During the assessment, it is important to screen for red flags and signs of any underlying serious life-threatening condition. Red flags for blackouts include ECG abnormalities, clinical signs of heart failure, a heart murmur, blackouts occurring during exertion, a family history of sudden cardiac death at a young age, an inherited cardiac condition, new or unexplained breathlessness, and blackouts in individuals over the age of 65 without a prodrome. These red flags indicate the need for urgent assessment by an appropriate specialist.

There are several serious conditions that may be suggested by certain features. For example, myocardial infarction or ischemia may be indicated by a history of coronary artery disease, preceding chest pain, and ECG signs such as ST elevation or arrhythmia. Pulmonary embolism may be suggested by dizziness, acute shortness of breath, pleuritic chest pain, and risk factors for venous thromboembolism. Aortic dissection may be indicated by chest and back pain, abnormal ECG findings, and signs of cardiac tamponade include low systolic blood pressure, elevated jugular venous pressure, and muffled heart sounds. Other conditions that may cause blackouts include severe hypoglycemia, Addisonian crisis, and electrolyte abnormalities.

Malaria is a contagious illness that is spread by female mosquitoes of the Anopheles genus. It is a parasitic infection caused by the Plasmodium genus. There are five species of Plasmodium that are known to cause disease in humans: Plasmodium falciparum, Plasmodium ovale, Plasmodium vivax, Plasmodium malariae, and Plasmodium knowlesi.

The main symptom of malaria is the malarial paroxysm, which is a recurring pattern of symptoms. It begins with a cold phase, during which the patient experiences intense chills. This is followed by a hot stage, where the patient feels extremely hot. Finally, there is a sweating stage, during which the fever subsides and the patient sweats profusely. Upon examination, the patient may exhibit signs of anemia, jaundice, and have an enlarged liver and spleen, but there is no evidence of swollen lymph nodes.

If a patient develops haemoglobinuria (the presence of hemoglobin in the urine) and renal failure after treatment, it may indicate a condition called blackwater fever, which is caused by Plasmodium falciparum. In this condition, an autoimmune reaction occurs between the parasite and quinine, leading to the destruction of red blood cells, hemoglobinuria, jaundice, and renal failure. Blackwater fever can be life-threatening.

The patient has presented with a facial palsy that affects only the left side and involves the lower motor neurons. This can be distinguished from an upper motor neuron lesion because the patient is unable to raise their eyebrow and the upper facial muscles are also affected. Additionally, the patient demonstrates a phenomenon known as Bell’s phenomenon, where the eye on the affected side rolls upwards and outwards when attempting to close the eye and bare the teeth.

Approximately 80% of sudden onset lower motor neuron facial palsies are attributed to Bell’s palsy. It is believed that this condition is caused by swelling of the facial nerve within the petrous temporal bone, which is secondary to a latent herpesvirus, specifically HSV-1 and HZV.

There are other potential causes for an isolated lower motor neuron facial nerve palsy, including Ramsay-Hunt syndrome (caused by the herpes zoster virus), trauma, parotid gland tumor, cerebellopontine angle tumor (such as an acoustic neuroma), middle ear infection, cholesteatoma, and sarcoidosis.

However, Ramsay-Hunt syndrome is unlikely in this case since there is no presence of pain or pustular lesions in and around the ear. An acoustic neuroma is also less likely, especially without any symptoms of sensorineural deafness or tinnitus. Furthermore, there are no clinical features consistent with an inner ear infection.

The recommended treatment for this patient is the administration of steroids, and appropriate follow-up should be organized.

ELISA and other antibody tests are highly sensitive methods for detecting the presence of HIV. However, they cannot be used in the early stages of the disease. There is usually a window period of 6-12 weeks before antibodies are produced, and these tests will yield negative results during a seroconversion illness.

The p24 antigen, which is the viral protein that forms the majority of the HIV core, is present in high concentrations in the first few weeks after infection. Therefore, the p24 antigen test is a valuable tool for diagnosing very early infections, such as those occurring during a seroconversion illness.

During the early stages of HIV infection, CD4 and CD8 counts are typically within the normal range and cannot be used for diagnosis in such cases.

The ‘rapid HIV test’ is an antibody test for HIV. Consequently, it will also yield negative results during the early ‘window period’. This test is referred to as ‘rapid’ because it can detect antibodies in blood or saliva much faster than other antibody tests, with results often available within 20 minutes.

The subtraction of serial 7s is included in the 30-point Folstein mini-mental state examination (MMSE), but it is not included in the AMTS. The AMTS consists of ten questions that assess various cognitive abilities. These questions include asking about age, the nearest hour, the current year, the name of the hospital or location, the ability to recognize two people, date of birth, knowledge of historical events, knowledge of the present monarch or prime minister, counting backwards from 20 to 1, and recalling an address given earlier in the test. The AMTS is referenced in the RCEM syllabus under the topic of memory loss.

The maximum safe dose of plain lidocaine is 3 mg per kilogram of body weight, with a maximum limit of 200 mg. However, when lidocaine is administered with adrenaline in a 1:200,000 ratio, the maximum safe dose increases to 7 mg per kilogram of body weight, with a maximum limit of 500 mg.

In this particular case, the patient weighs 60 kg, so the maximum safe dose of lidocaine hydrochloride would be 60 multiplied by 7 mg, resulting in a total of 420 mg.

For more detailed information on lidocaine hydrochloride, you can refer to the BNF section dedicated to this topic.

A phaeochromocytoma is an uncommon functional tumor that develops from chromaffin cells in the adrenal medulla. Extra-adrenal paragangliomas, also known as extra-adrenal pheochromocytomas, are closely associated but less prevalent tumors that originate in the ganglia of the sympathetic nervous system. These tumors release catecholamines and result in a range of symptoms and indications linked to hyperactivity of the sympathetic nervous system.

This individual has presented with haemoptysis and a purpuric rash, alongside a history of asthma and allergic rhinitis. Blood tests have revealed elevated inflammatory markers, pronounced eosinophilia, and acute renal failure. The most likely diagnosis in this case is Churg-Strauss syndrome.

Churg-Strauss syndrome is a rare autoimmune vasculitis that affects small and medium-sized blood vessels. The American College of Rheumatology has established six criteria for diagnosing Churg-Strauss syndrome. The presence of at least four of these criteria is highly indicative of the condition:

1. Asthma (wheezing, expiratory rhonchi)
2. Eosinophilia of more than 10% in peripheral blood
3. Paranasal sinusitis
4. Pulmonary infiltrates (which may be transient)
5. Histological confirmation of vasculitis with extravascular eosinophils
6. Mononeuritis multiplex or polyneuropathy

Churg-Strauss syndrome can affect various organ systems, with the most common clinical features including:

– Constitutional symptoms: fever, fatigue, weight loss, and arthralgia
– Respiratory symptoms: asthma, haemoptysis, allergic rhinitis, and sinusitis
– Cardiovascular symptoms: heart failure, myocarditis, and myocardial infarction
– Gastrointestinal symptoms: gastrointestinal bleeding, bowel ischaemia, and appendicitis
– Dermatological symptoms: purpura, livedo reticularis, and skin nodules
– Renal symptoms: glomerulonephritis, renal failure, and hypertension
– Neurological symptoms: mononeuritis multiplex

Investigations often reveal eosinophilia, anaemia, elevated CRP and ESR, elevated creatinine, and elevated serum IgE levels. Approximately 70% of patients test positive for p-ANCA.

The mainstay of treatment for Churg-Strauss syndrome is high-dose steroids. In cases with life-threatening complications, cyclophosphamide and azathioprine are often administered.

Polyarteritis nodosa is another vasculitic disorder that affects small and medium-sized blood vessels. It can impact the gastrointestinal tract, kidneys, skin, and joints, but it is not typically associated with rhinitis or asthma.

Uveitis is the most prevalent eye complication that arises in individuals with ankylosing spondylitis (AS). Approximately one out of every three patients with AS will experience uveitis at some stage. The symptoms of uveitis include a red and painful eye, along with photophobia and blurred vision. Additionally, patients may notice the presence of floaters. The primary treatment for uveitis involves the use of corticosteroids, and it is crucial for patients to seek immediate attention from an ophthalmologist.

Myelodysplastic syndromes are a group of disorders affecting the haemopoietic stem cell, leading to ineffective production of myeloid blood cells. These conditions typically manifest between the ages of 60 and 75 and are more prevalent in men than women.

The clinical features of myelodysplastic syndromes include tiredness due to anaemia (the most common presentation), easy bruising, and a tendency to bleed. Laboratory findings often reveal anaemia (usually macrocytic or normocytic), neutropenia, thrombocytopenia, and abnormal cell morphology with oddly shaped macrocytes.

Chronic lymphocytic leukaemia (CLL) is the most common form of adult leukaemia, primarily affecting B-lymphocytes. It often presents asymptomatically in patients who undergo routine blood tests revealing elevated white cell counts and lymphocytosis. Men over the age of 50 account for over 75% of CLL cases. Blood films typically show a predominance of mature-looking lymphocytes and smear cells.

Iron deficiency anaemia is characterized by hypochromic microcytic anaemia and a reduced red blood cell count. Peripheral blood smears in iron deficiency anaemia may exhibit poikilocytosis (varying shapes) and anisocytosis (varying sizes). Pencil cells are also observed in this condition.

Vitamin B12 and folate deficiency can also cause macrocytic anaemia. However, the severity of anaemia and macrocytosis would generally need to be much more pronounced to result in neutropenia and thrombocytopenia. Therefore, a myelodysplastic syndrome is more likely in such cases.

Le Fort fractures are intricate fractures of the midface, which involve the maxillary bone and the surrounding structures. These fractures can occur in a horizontal, pyramidal, or transverse direction. The distinguishing feature of Le Fort fractures is the separation of the pterygomaxillary due to trauma. They make up approximately 10% to 20% of all facial fractures and can have severe consequences, both in terms of potential life-threatening situations and disfigurement.

The causes of Le Fort fractures vary depending on the type of fracture. Common mechanisms include motor vehicle accidents, sports injuries, assaults, and falls from significant heights. Patients with Le Fort fractures often have concurrent head and cervical spine injuries. Additionally, they frequently experience other facial fractures, as well as neuromuscular injuries and dental avulsions.

The specific type of fracture sustained is determined by the direction of the force applied to the face. Le Fort type I fractures typically occur when a force is directed downward against the upper teeth. Le Fort type II fractures are usually the result of a force applied to the lower or mid maxilla. Lastly, Le Fort type III fractures are typically caused by a force applied to the nasal bridge and upper part of the maxilla.

Public Health England advises that children with impetigo should not attend school, nursery, or be under the care of childminders until the sores have formed a crust or until 48 hours after starting antibiotic treatment. Antibiotics help accelerate the healing process and decrease the period of contagiousness.

For more information, please refer to the Guidance on Infection Control in Schools and other Childcare Settings.
https://www.publichealth.hscni.net/sites/default/files/Guidance_on_infection_control_in%20schools_poster.pdf

Bladder cancer ranks as the seventh most prevalent form of cancer in the United Kingdom, with men outnumbering women by a ratio of 3 to 1. The primary factors that increase the risk of bladder cancer are advancing age and smoking. It is estimated that around 50% of bladder cancer cases are caused by smoking, which is believed to be influenced by the presence of aromatic amines and polycyclic aromatic hydrocarbons that are eliminated through the kidneys. Smokers face a 2 to 6 times higher risk of developing bladder cancer compared to non-smokers.

Additional risk factors for bladder cancer include occupational exposure to aromatic amines found in dyes, paints, solvents, leather dust, combustion products, rubber, and textiles. Radiation therapy to the pelvic region is also considered a risk factor.

In developing nations, particularly in the Middle East, schistosomiasis is responsible for approximately 80% of bladder cancer cases.

The typical range for lactate levels in the body is 0.5-2.2 mmol/L, according to most UK trusts. However, it is important to mention that the RCEM sepsis guides consider a lactate level above 2 mmol/L to be abnormal.

Further Reading:

Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.

To reduce the risk of harm to the patient, it is important to test for collateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.

Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.

The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.

The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.

The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.

Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.

The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.

In the blood tests, certain findings can support a diagnosis of glandular fever. One of these findings is lymphocytosis, which refers to an increased number of lymphocytes in the blood. Lymphocytes are a type of white blood cell that plays a crucial role in the immune response. In glandular fever, the Epstein-Barr virus (EBV) is the most common cause, and it primarily infects and activates lymphocytes, leading to their increased numbers in the blood.

On the other hand, neutropenia (a decreased number of neutrophils) and neutrophilia (an increased number of neutrophils) are not typically associated with glandular fever. Neutrophils are another type of white blood cell that helps fight off bacterial infections. In glandular fever, the primary involvement is with lymphocytes rather than neutrophils.

Monocytosis, which refers to an increased number of monocytes, can also be seen in glandular fever. Monocytes are another type of white blood cell that plays a role in the immune response. Their increased numbers can be a result of the immune system’s response to the Epstein-Barr virus.

Eosinophilia, an increased number of eosinophils, is not commonly associated with glandular fever. Eosinophils are white blood cells involved in allergic reactions and parasitic infections, and their elevation is more commonly seen in those conditions.

In summary, the presence of lymphocytosis and possibly monocytosis in the blood tests would support a diagnosis of glandular fever, while neutropenia, neutrophilia, and eosinophilia are less likely to be associated with this condition.

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.

Veins and arteries can be differentiated on ultrasound based on their compressibility, response to valsalva, and shape. When compressed, veins are obliterated while arteries remain unaffected. Additionally, when a patient performs a valsalva maneuver, the neck veins expand. In transverse view, arteries appear circular with a muscular wall, whereas veins tend to have an oval shape. It is important to note that the overall size and internal diameter are not reliable indicators for distinguishing between arteries and veins.

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.

A recent audit conducted by the Royal College of Emergency Medicine (RCEM) in 2018 revealed a concerning decline in the standards of pain management for children with fractured limbs in Emergency Departments (EDs). The audit found that the majority of patients experienced longer waiting times for pain relief compared to previous years. Shockingly, more than 1 in 10 children who presented with significant pain due to a limb fracture did not receive any pain relief at all.

To address this issue, the Agency for Health Care Policy and Research (AHCPR) in the USA recommends following the ABCs of pain management for all patients, including children. This approach involves regularly asking about pain, systematically assessing it, believing the patient and their family in their reports of pain and what relieves it, choosing appropriate pain control options, delivering interventions in a timely and coordinated manner, and empowering patients and their families to have control over their pain management.

The RCEM has established standards that require a child’s pain to be assessed within 15 minutes of their arrival at the ED. This is considered a fundamental standard. Various rating scales are available for assessing pain in children, with the choice depending on the child’s age and ability to use the scale. These scales include the Wong-Baker Faces Pain Rating Scale, Numeric rating scale, and Behavioural scale.

To ensure timely administration of analgesia to children in acute pain, the RCEM has set specific standards. These standards state that 100% of patients in severe pain should receive appropriate analgesia within 60 minutes of their arrival or triage, whichever comes first. Additionally, 75% should receive analgesia within 30 minutes, and 50% within 20 minutes.

The first-rank symptoms of schizophrenia, as described by Kurt Schneider, include auditory hallucinations such as hearing 3rd person voices discussing the patient, experiencing thought echo, and receiving commentary on one’s actions. Additionally, passivity phenomena may occur, such as thought insertion, thought withdrawal, thought broadcast, and feelings of thoughts and actions being under external control. Delusions, which can be primary or secondary, are also common in schizophrenia.

On the other hand, chronic schizophrenia is characterized by negative symptoms. These include poor motivation and self-care, social withdrawal, depression, flat and blunted affect, emotional incongruity, decreased activity, and poverty of thought and speech. These symptoms are often present in individuals with chronic schizophrenia.

Currently, there are three beta-blockers that have been approved for the treatment of chronic heart failure. These medications include bisoprolol, carvedilol, and nebivolol.

Chronic HF is a common clinical syndrome resulting from coronary artery disease (CAD), HTN, valvular heart disease, and/or primary cardiomyopathy. There is now conclusive evidence that β-blockers, when added to ACE inhibitors, substantially reduce mortality, decrease sudden death, and improve symptoms in patients with HF. Despite the overwhelming evidence and guidelines that mandate the use of β-blockers in all HF patients without contraindications, many patients do not receive this treatment.

If you are conducting research or an audit that involves using patient identifiable information, you must submit a Caldicott request to the designated Caldicott guardian for the trust.

Further Reading:

Principles of Medical Ethics:

1. Autonomy: Competent adults have the right to make informed decisions about their own medical care.
2. Beneficence: Healthcare professionals should take actions that serve the best interests of patients.
3. Non-maleficence: Healthcare professionals should not take actions that may injure or harm patients.
4. Justice: Healthcare professionals should take actions that are fair and equitable to both the individual and society as a whole.

Confidentiality:

1. Use minimum necessary personal information and consider anonymizing information if possible.
2. Manage and protect personal information to prevent improper access, disclosure, or loss.
3. Understand and adhere to information governance appropriate to your role.
4. Comply with the law when handling personal information.
5. Share relevant information for direct care unless the patient objects.
6. Obtain explicit consent to disclose identifiable information for purposes other than care or local clinical audit, unless required by law or justified in the public interest.
7. Inform patients about disclosures of personal information they would not reasonably expect, unless not practicable or undermines the purpose of the disclosure.
8. Support patients in accessing their information and respecting their legal rights.

Obtaining Patient’s Consent for Disclosure:

– Consent should be obtained for disclosing personal information for purposes other than direct care or local clinical audit, unless required by law or not appropriate or practicable.

Situations Where Patient Consent is Not Required for Disclosure:

– Adults at risk of or suffering abuse or neglect, as required by law.
– Adults lacking capacity, if neglect or harm is suspected, unless not overall beneficial to the patient.
– When required by law or approved through a statutory process.
– When justified in the public interest, such as for the prevention, detection, or prosecution of serious crime, patient’s fitness to drive, serious communicable disease, or posing a serious risk to others through being unfit for work.

Confidentiality Following a Patient’s Death:

– Respect the patient’s confidentiality even after their death.
– If the patient previously requested not to share personal information with those close to them, abide by their wishes.
– Be considerate, sensitive, and responsive to those close to the patient, providing as much information as possible.

The Law & Caldicott Guardians:

Data Protection Act:
– Sets rules and standards for the use and handling of personal data by organizations.
– Personal data must be used fairly, lawfully, transparently, and for specified purposes.
– Individuals have rights

Activated charcoal is a commonly used substance for decontamination in cases of poisoning. Its main function is to adsorb the molecules of the ingested toxin onto its surface.

Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. It is produced by subjecting carbonaceous matter to high heat, a process known as pyrolysis, and then treating it with a zinc chloride solution to increase its concentration. This process creates a network of pores within the charcoal, giving it a large absorptive area of approximately 3,000 m2/g. This allows it to effectively inhibit the absorption of toxins by up to 50%.

The usual dose of activated charcoal is 50 grams for adults and 1 gram per kilogram of body weight for children. It can be administered orally or through a nasogastric tube. It is important to administer it within one hour of ingestion, and it may be repeated after one hour if necessary.

However, there are certain situations where activated charcoal should not be used. These include cases where the patient is unconscious or in a coma, as there is a risk of aspiration. It should also be avoided if seizures are imminent, as there is a risk of aspiration. Additionally, if there is reduced gastrointestinal motility, activated charcoal should not be used to prevent the risk of obstruction.

Activated charcoal is effective in treating overdose with certain drugs and toxins, such as aspirin, paracetamol, barbiturates, tricyclic antidepressants, digoxin, amphetamines, morphine, cocaine, and phenothiazines. However, it is ineffective in cases of overdose with iron, lithium, boric acid, cyanide, ethanol, ethylene glycol, methanol, malathion, DDT, carbamate, hydrocarbon, strong acids, or alkalis.

There are potential adverse effects associated with the use of activated charcoal. These include nausea and vomiting, diarrhea, constipation, bezoar formation (a mass of undigested material that can cause blockages), bowel obstruction, pulmonary aspiration (inhalation of charcoal into the lungs), and impaired absorption of oral medications or antidotes.

Burn injuries can be classified based on their type (degree, partial thickness or full thickness), extent as a percentage of total body surface area (TBSA), and severity (minor, moderate, major/severe). Severe burns are defined as a >10% TBSA in a child and >15% TBSA in an adult.

When assessing a burn, it is important to consider airway injury, carbon monoxide poisoning, type of burn, extent of burn, special considerations, and fluid status. Special considerations may include head and neck burns, circumferential burns, thorax burns, electrical burns, hand burns, and burns to the genitalia.

Airway management is a priority in burn injuries. Inhalation of hot particles can cause damage to the respiratory epithelium and lead to airway compromise. Signs of inhalation injury include visible burns or erythema to the face, soot around the nostrils and mouth, burnt/singed nasal hairs, hoarse voice, wheeze or stridor, swollen tissues in the mouth or nostrils, and tachypnea and tachycardia. Supplemental oxygen should be provided, and endotracheal intubation may be necessary if there is airway obstruction or impending obstruction.

The initial management of a patient with burn injuries involves conserving body heat, covering burns with clean or sterile coverings, establishing IV access, providing pain relief, initiating fluid resuscitation, measuring urinary output with a catheter, maintaining nil by mouth status, closely monitoring vital signs and urine output, monitoring the airway, preparing for surgery if necessary, and administering medications.

Burns can be classified based on the depth of injury, ranging from simple erythema to full thickness burns that penetrate into subcutaneous tissue. The extent of a burn can be estimated using methods such as the rule of nines or the Lund and Browder chart, which takes into account age-specific body proportions.

Fluid management is crucial in burn injuries due to significant fluid losses. Evaporative fluid loss from burnt skin and increased permeability of blood vessels can lead to reduced intravascular volume and tissue perfusion. Fluid resuscitation should be aggressive in severe burns, while burns <15% in adults and <10% in children may not require immediate fluid resuscitation. The Parkland formula can be used to calculate the intravenous fluid requirements for someone with a significant burn injury.

When managing individuals with severe burns, the desired amount of urine output is 0.5 ml per kilogram of body weight per hour. For the average adult, this translates to a target urine output of 30-50 ml per hour.

Further Reading:

Burn injuries can be classified based on their type (degree, partial thickness or full thickness), extent as a percentage of total body surface area (TBSA), and severity (minor, moderate, major/severe). Severe burns are defined as a >10% TBSA in a child and >15% TBSA in an adult.

When assessing a burn, it is important to consider airway injury, carbon monoxide poisoning, type of burn, extent of burn, special considerations, and fluid status. Special considerations may include head and neck burns, circumferential burns, thorax burns, electrical burns, hand burns, and burns to the genitalia.

Airway management is a priority in burn injuries. Inhalation of hot particles can cause damage to the respiratory epithelium and lead to airway compromise. Signs of inhalation injury include visible burns or erythema to the face, soot around the nostrils and mouth, burnt/singed nasal hairs, hoarse voice, wheeze or stridor, swollen tissues in the mouth or nostrils, and tachypnea and tachycardia. Supplemental oxygen should be provided, and endotracheal intubation may be necessary if there is airway obstruction or impending obstruction.

The initial management of a patient with burn injuries involves conserving body heat, covering burns with clean or sterile coverings, establishing IV access, providing pain relief, initiating fluid resuscitation, measuring urinary output with a catheter, maintaining nil by mouth status, closely monitoring vital signs and urine output, monitoring the airway, preparing for surgery if necessary, and administering medications.

Burns can be classified based on the depth of injury, ranging from simple erythema to full thickness burns that penetrate into subcutaneous tissue. The extent of a burn can be estimated using methods such as the rule of nines or the Lund and Browder chart, which takes into account age-specific body proportions.

Fluid management is crucial in burn injuries due to significant fluid losses. Evaporative fluid loss from burnt skin and increased permeability of blood vessels can lead to reduced intravascular volume and tissue perfusion. Fluid resuscitation should be aggressive in severe burns, while burns <15% in adults and <10% in children may not require immediate fluid resuscitation. The Parkland formula can be used to calculate the intravenous fluid requirements for someone with a significant burn injury.

The duration of submersion is the most crucial factor in predicting the outcome of drowning incidents. If the submersion time is less than 10 minutes, it is considered a positive indicator for prognosis, while if it exceeds 25 minutes, it is considered a negative indicator. There are other factors that are associated with higher rates of illness and death, such as a low Glasgow Coma Score, absence of pupillary response, pH imbalance (acidosis), and low blood pressure (hypotension). However, it is important to note that these prognostic factors have not been consistently validated in studies and cannot reliably predict the outcome of drowning incidents.

Further Reading:

Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid. It can be classified as cold-water or warm-water drowning. Risk factors for drowning include young age and male sex. Drowning impairs lung function and gas exchange, leading to hypoxemia and acidosis. It also causes cardiovascular instability, which contributes to metabolic acidosis and cell death.

When someone is submerged or immersed, they will voluntarily hold their breath to prevent aspiration of water. However, continued breath holding causes progressive hypoxia and hypercapnia, leading to acidosis. Eventually, the respiratory center sends signals to the respiratory muscles, forcing the individual to take an involuntary breath and allowing water to be aspirated into the lungs. Water entering the lungs stimulates a reflex laryngospasm that prevents further penetration of water. Aspirated water can cause significant hypoxia and damage to the alveoli, leading to acute respiratory distress syndrome (ARDS).

Complications of drowning include cardiac ischemia and infarction, infection with waterborne pathogens, hypothermia, neurological damage, rhabdomyolysis, acute tubular necrosis, and disseminated intravascular coagulation (DIC).

In children, the diving reflex helps reduce hypoxic injury during submersion. It causes apnea, bradycardia, and peripheral vasoconstriction, reducing cardiac output and myocardial oxygen demand while maintaining perfusion of the brain and vital organs.

Associated injuries with drowning include head and cervical spine injuries in patients rescued from shallow water. Investigations for drowning include arterial blood gases, chest X-ray, ECG and cardiac monitoring, core temperature measurement, and blood and sputum cultures if secondary infection is suspected.

Management of drowning involves extricating the patient from water in a horizontal position with spinal precautions if possible. Cardiovascular considerations should be taken into account when removing patients from water to prevent hypotension and circulatory collapse. Airway management, supplemental oxygen, and ventilation strategies are important in maintaining oxygenation and preventing further lung injury. Correcting hypotension, electrolyte disturbances, and hypothermia is also necessary. Attempting to drain water from the lungs is ineffective.

Patients without associated physical injury who are asymptomatic and have no evidence of respiratory compromise after six hours can be safely discharged home. Ventilation strategies aim to maintain oxygenation while minimizing ventilator-associated lung injury.

Public Health England (PHE) has a primary goal of promptly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it is not the main focus. Since 1968, the clinical suspicion of a notifiable infection has been sufficient for reporting purposes.

Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) when they suspect cases of certain infectious diseases.

The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

It is worth noting that leptospirosis is not considered a notifiable disease, making it the least likely option among the diseases listed above.

The primary cause of roseola is the human herpesvirus 6B (HHV6B), with the human herpesvirus 7 (HHV7) being a less common cause.

Further Reading:

Roseola infantum, also known as roseola, exanthem subitum, or sixth disease, is a common disease that affects infants. It is primarily caused by the human herpesvirus 6B (HHV6B) and less commonly by human herpesvirus 7 (HHV7). Many cases of roseola are asymptomatic, and the disease is typically spread through saliva from an asymptomatic infected individual. The incubation period for roseola is around 10 days.

Roseola is most commonly seen in children between 6 months and 3 years of age, and studies have shown that as many as 85% of children will have had roseola by the age of 1 year. The clinical features of roseola include a high fever lasting for 2-5 days, accompanied by upper respiratory tract infection (URTI) signs such as rhinorrhea, sinus congestion, sore throat, and cough. After the fever subsides, a maculopapular rash appears, characterized by rose-pink papules on the trunk that may spread to the extremities. The rash is non-itchy and painless and can last from a few hours to a few days. Around 2/3 of patients may also have erythematous papules, known as Nagayama spots, on the soft palate and uvula. Febrile convulsions occur in approximately 10-15% of cases, and diarrhea is commonly seen.

Management of roseola is usually conservative, with rest, maintaining adequate fluid intake, and taking paracetamol for fever being the main recommendations. The disease is typically mild and self-limiting. However, complications can arise from HHV6 infection, including febrile convulsions, aseptic meningitis, and hepatitis.

Thyroid storm is a rare condition that affects only 1-2% of patients with hyperthyroidism. However, it is crucial to diagnose it promptly because it has a high mortality rate of approximately 10%. Thyroid storm is often triggered by a physiological stressor, such as stopping antithyroid therapy prematurely, recent surgery or radio-iodine treatment, infections (especially chest infections), trauma, diabetic ketoacidosis or hyperosmolar diabetic crisis, thyroid hormone overdose, pre-eclampsia. It typically occurs in patients with Graves’ disease or toxic multinodular goitre and presents with sudden and severe hyperthyroidism. Symptoms include high fever (over 41°C), dehydration, rapid heart rate (greater than 140 beats per minute) with or without irregular heart rhythms, low blood pressure, congestive heart failure, nausea, jaundice, vomiting, diarrhea, abdominal pain, confusion, agitation, delirium, psychosis, seizures, or coma.

To diagnose thyroid storm, various blood tests should be conducted, including a full blood count, urea and electrolytes, blood glucose, coagulation screen, CRP, and thyroid profile (T4/T3 and TSH). A bone profile/calcium test should also be done as 10% of patients develop hypocalcemia. Blood cultures should be taken as well. Other important investigations include a urine dipstick/MC&S, chest X-ray, and ECG.

The management of thyroid storm involves several steps. Intravenous fluids, such as 1-2 liters of 0.9% saline, should be administered. Airway support and management should be provided as necessary. A nasogastric tube should be inserted if the patient is vomiting. Urgent referral for inpatient management is essential. Paracetamol (1 g PO/IV) can be given to reduce fever. Benzodiazepines, such as diazepam (5-20 mg PO/IV), can be used for sedation. Steroids, like hydrocortisone (100 mg IV), may be necessary if there is co-existing adrenal suppression. Antibiotics should be prescribed if there is an intercurrent infection. Beta-blockers, such as propranolol (80 mg PO), can help control heart rate. High-dose carbimazole (45-60 mg/day) is recommended.

This patient is experiencing a reactionary haemorrhage following their recent dental extraction.

There are three types of haemorrhage that can occur after a dental extraction. The first is immediate haemorrhage, which happens at the time of extraction. The second is reactionary haemorrhage, which occurs 2-3 hours after the extraction when the vasoconstrictor effects of the local anaesthetic wear off. The third is secondary haemorrhage, which typically happens at 48-72 hours and occurs if the clot becomes infected.

To manage this situation, the first step is to clean and rinse the mouth, removing any excessive clot. Then, a square of gauze should be rolled up into a pledgelet that is approximately twice the size of the bleeding socket and inserted. The patient should be instructed to bite down on it to apply pressure for about 10-20 minutes.

If the bleeding continues after this initial management, the area should be anaesthetised using lidocaine with adrenaline. Following the anaesthesia, a horizontal mattress suture should be inserted, pulling the gum over the bone edges tightly enough to blanch them. It is important to refer the patient to the on-call dental surgeon at this point.

There are several risk factors for dental haemorrhage, including hypertension, the use of anticoagulants such as warfarin, and hereditary bleeding disorders like von Willebrand disease or haemophilia.

Consent for individuals who lack capacity can be given by the person with lasting power of attorney, a court-appointed deputy, or doctors. Since the patient is an adult (>18), parental consent is not applicable. However, parents or family members can consent on behalf of an adult if they have been granted lasting power of attorney (LPA). The authorized individuals who can provide consent are the person with lasting power of attorney, court-appointed deputies, and doctors in cases involving treatment under best interests or mental health legislation. It is important to note that parental consent is only appropriate if they have LPA.

Further Reading:

Patients have the right to determine what happens to their own bodies, and for consent to be valid, certain criteria must be met. These criteria include the person being informed about the intervention, having the capacity to consent, and giving consent voluntarily and freely without any pressure or undue influence.

In order for a person to be deemed to have capacity to make a decision on a medical intervention, they must be able to understand the decision and the information provided, retain that information, weigh up the pros and cons, and communicate their decision.

Valid consent can only be provided by adults, either by the patient themselves, a person authorized under a Lasting Power of Attorney, or someone with the authority to make treatment decisions, such as a court-appointed deputy or a guardian with welfare powers.

In the UK, patients aged 16 and over are assumed to have the capacity to consent. If a patient is under 18 and appears to lack capacity, parental consent may be accepted. However, a young person of any age may consent to treatment if they are considered competent to make the decision, known as Gillick competence. Parental consent may also be given by those with parental responsibility.

The Fraser guidelines apply to the prescription of contraception to under 16’s without parental involvement. These guidelines allow doctors to provide contraceptive advice and treatment without parental consent if certain criteria are met, including the young person understanding the advice, being unable to be persuaded to inform their parents, and their best interests requiring them to receive contraceptive advice or treatment.

Competent adults have the right to refuse consent, even if it is deemed unwise or likely to result in harm. However, there are exceptions to this, such as compulsory treatment authorized by the mental health act or if the patient is under 18 and refusing treatment would put their health at serious risk.

In emergency situations where a patient is unable to give consent, treatment may be provided without consent if it is immediately necessary to save their life or prevent a serious deterioration of their condition. Any treatment decision made without consent must be in the patient’s best interests, and if a decision is time-critical and the patient is unlikely to regain capacity in time, a best interest decision should be made. The treatment provided should be the least restrictive on the patient’s future choices.

Alteplase (rt-pA) is recommended for the treatment of acute ischaemic stroke in adults if it is administered as soon as possible within 4.5 hours of the onset of stroke symptoms. It is important to exclude intracranial haemorrhage through appropriate imaging techniques before starting the treatment. The initial dose of alteplase is 0.9 mg/kg, with a maximum dose of 90 mg. This dose should be given intravenously over 60 minutes, with the initial 10% administered by intravenous injection and the remainder by intravenous infusion. In the case of a patient weighing 120 kg, the maximum dose of 90 mg should be administered. For more information, please refer to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old.

This patient is displaying symptoms that are characteristic of normal-pressure hydrocephalus (NPH). NPH is a type of communicating hydrocephalus where the pressure inside the skull, as measured through lumbar puncture, is either normal or occasionally elevated. It primarily affects elderly individuals, and the likelihood of developing NPH increases with age.

Around 50% of NPH cases are idiopathic, meaning that no clear cause can be identified. The remaining cases are secondary to various conditions such as head injury, meningitis, subarachnoid hemorrhage, central nervous system tumors, and radiotherapy.

The typical presentation of NPH includes a classic triad of symptoms: gait disturbance (often characterized by a broad-based and shuffling gait), sphincter disturbance leading to incontinence (usually urinary incontinence), and progressive dementia with memory loss, inattention, inertia, and bradyphrenia.

Diagnosing NPH primarily relies on identifying the classic clinical triad mentioned above. Additional investigations can provide supportive evidence and may involve CT and MRI scans, which reveal enlarged ventricles and periventricular lucency. Lumbar puncture can also be performed to assess cerebrospinal fluid (CSF) levels, which are typically normal or intermittently elevated. Intraventricular monitoring may show beta waves present for more than 5% of a 24-hour period.

NPH is one of the few reversible causes of dementia, making early recognition and treatment crucial. Medical treatment options include the use of carbonic anhydrase inhibitors (such as acetazolamide) and repeated lumbar punctures as temporary measures. However, the definitive treatment for NPH involves surgically inserting a cerebrospinal fluid (CSF) shunt. This procedure provides lasting clinical benefits for 70% to 90% of patients compared to their pre-operative state.

Children with gastroenteritis who exhibit jittery movements, increased muscle tone, hyper-reflexia, or convulsions should be suspected of having hypernatraemic dehydration. This condition occurs when there is an excessive amount of sodium in the body. In this case, the patient’s history aligns with gastroenteritis, which puts them at risk for hypernatraemia. The presence of jittery movements, increased muscle tone, and hyper-reflexia further support this suspicion. To confirm the diagnosis, it is recommended to send a sample for urea and electrolyte testing to assess the patient’s sodium levels.

Further Reading:

Gastroenteritis is a common condition in children, particularly those under the age of 5. It is characterized by the sudden onset of diarrhea, with or without vomiting. The most common cause of gastroenteritis in infants and young children is rotavirus, although other viruses, bacteria, and parasites can also be responsible. Prior to the introduction of the rotavirus vaccine in 2013, rotavirus was the leading cause of gastroenteritis in children under 5 in the UK. However, the vaccine has led to a significant decrease in cases, with a drop of over 70% in subsequent years.

Norovirus is the most common cause of gastroenteritis in adults, but it also accounts for a significant number of cases in children. In England & Wales, there are approximately 8,000 cases of norovirus each year, with 15-20% of these cases occurring in children under 9.

When assessing a child with gastroenteritis, it is important to consider whether there may be another more serious underlying cause for their symptoms. Dehydration assessment is also crucial, as some children may require intravenous fluids. The NICE traffic light system can be used to identify the risk of serious illness in children under 5.

In terms of investigations, stool microbiological testing may be indicated in certain cases, such as when the patient has been abroad, if diarrhea lasts for more than 7 days, or if there is uncertainty over the diagnosis. U&Es may be necessary if intravenous fluid therapy is required or if there are symptoms and/or signs suggestive of hypernatremia. Blood cultures may be indicated if sepsis is suspected or if antibiotic therapy is planned.

Fluid management is a key aspect of treating children with gastroenteritis. In children without clinical dehydration, normal oral fluid intake should be encouraged, and oral rehydration solution (ORS) supplements may be considered. For children with dehydration, ORS solution is the preferred method of rehydration, unless intravenous fluid therapy is necessary. Intravenous fluids may be required for children with shock or those who are unable to tolerate ORS solution.

Antibiotics are generally not required for gastroenteritis in children, as most cases are viral or self-limiting. However, there are some exceptions, such as suspected or confirmed sepsis, Extraintestinal spread of bacterial infection, or specific infections like Clostridium difficile-associated pseudomembranous enterocolitis or giardiasis.

Hyperventilation leads to the constriction of blood vessels in the brain, which in turn reduces the flow and volume of blood in the brain, ultimately decreasing intracranial pressure (ICP). This is because hyperventilation lowers the levels of carbon dioxide (PaCO2) in the blood, resulting in an increase in pH and causing the arteries in the brain to constrict and reduce blood flow. As a result, cerebral blood volume and ICP decrease. The effects of hyperventilation are immediate, but they gradually diminish over a period of 6-24 hours as the brain adjusts its bicarbonate levels to normalize pH. However, caution must be exercised when discontinuing hyperventilation after a prolonged period, as the sudden increase in PaCO2 can lead to a rapid rise in cerebral blood flow and a detrimental increase in ICP.

Further Reading:

Intracranial pressure (ICP) refers to the pressure within the craniospinal compartment, which includes neural tissue, blood, and cerebrospinal fluid (CSF). Normal ICP for a supine adult is 5-15 mmHg. The body maintains ICP within a narrow range through shifts in CSF production and absorption. If ICP rises, it can lead to decreased cerebral perfusion pressure, resulting in cerebral hypoperfusion, ischemia, and potentially brain herniation.

The cranium, which houses the brain, is a closed rigid box in adults and cannot expand. It is made up of 8 bones and contains three main components: brain tissue, cerebral blood, and CSF. Brain tissue accounts for about 80% of the intracranial volume, while CSF and blood each account for about 10%. The Monro-Kellie doctrine states that the sum of intracranial volumes is constant, so an increase in one component must be offset by a decrease in the others.

There are various causes of raised ICP, including hematomas, neoplasms, brain abscesses, edema, CSF circulation disorders, venous sinus obstruction, and accelerated hypertension. Symptoms of raised ICP include headache, vomiting, pupillary changes, reduced cognition and consciousness, neurological signs, abnormal fundoscopy, cranial nerve palsy, hemiparesis, bradycardia, high blood pressure, irregular breathing, focal neurological deficits, seizures, stupor, coma, and death.

Measuring ICP typically requires invasive procedures, such as inserting a sensor through the skull. Management of raised ICP involves a multi-faceted approach, including antipyretics to maintain normothermia, seizure control, positioning the patient with a 30º head up tilt, maintaining normal blood pressure, providing analgesia, using drugs to lower ICP (such as mannitol or saline), and inducing hypocapnoeic vasoconstriction through hyperventilation. If these measures are ineffective, second-line therapies like barbiturate coma, optimised hyperventilation, controlled hypothermia, or decompressive craniectomy may be considered.

Le Fort fractures are complex fractures of the midface that involve the maxillary bone and surrounding structures. These fractures can occur in a horizontal, pyramidal, or transverse direction. The distinguishing feature of Le Fort fractures is the traumatic separation of the pterygomaxillary region. They make up approximately 10% to 20% of all facial fractures and can have severe consequences, both in terms of potential life-threatening injuries and disfigurement.

The Le Fort classification system categorizes midface fractures into three groups based on the plane of injury. As the classification level increases, the location of the maxillary fracture moves from inferior to superior within the maxilla.

Le Fort I fractures are horizontal fractures that occur across the lower aspect of the maxilla. These fractures cause the teeth to separate from the upper face and extend through the lower nasal septum, the lateral wall of the maxillary sinus, and into the palatine bones and pterygoid plates. They are sometimes referred to as a floating palate because they often result in the mobility of the hard palate from the midface. Common accompanying symptoms include facial swelling, loose teeth, dental fractures, and misalignment of the teeth.

Le Fort II fractures are pyramidal-shaped fractures, with the base of the pyramid located at the level of the teeth and the apex at the nasofrontal suture. The fracture line extends from the nasal bridge and passes through the superior wall of the maxilla, the lacrimal bones, the inferior orbital floor and rim, and the anterior wall of the maxillary sinus. These fractures are sometimes called a floating maxilla because they typically result in the mobility of the maxilla from the midface. Common symptoms include facial swelling, nosebleeds, subconjunctival hemorrhage, cerebrospinal fluid leakage from the nose, and widening and flattening of the nasal bridge.

Le Fort III fractures are transverse fractures of the midface. The fracture line passes through the nasofrontal suture, the maxillo frontal suture, the orbital wall, and the zygomatic arch and zygomaticofrontal suture. These fractures cause separation of all facial bones from the cranial base, earning them the nickname craniofacial disjunction or floating face fractures. They are the rarest and most severe type of Le Fort fracture. Common symptoms include significant facial swelling, bruising around the eyes, facial flattening, and the entire face can be shifted.

Neisseria gonorrhoeae is a type of bacteria that is shaped like two spheres and stains pink when tested. It is responsible for causing the sexually transmitted infection known as gonorrhoea. This infection is most commonly seen in individuals between the ages of 15 and 35, and it is primarily transmitted through sexual contact. One important thing to note is that the gonococcal pili, which are hair-like structures on the bacteria, can change their appearance. This means that even if someone has recovered from a previous infection, they can still be reinfected due to the bacteria’s ability to change.

In men, the clinical signs of gonorrhoea include inflammation of the urethra, which is seen in approximately 80% of cases. Around 50% of men experience pain or discomfort during urination, and a mucopurulent discharge may also be present. Rectal infection is possible, although it is usually asymptomatic. In some cases, it can cause anal discharge. Pharyngitis, or inflammation of the throat, is also possible but typically does not cause any noticeable symptoms.

Women with gonorrhoea may experience a vaginal discharge, which is seen in about 50% of cases. Lower abdominal pain is reported in approximately 25% of women, and dysuria, or painful urination, is seen in 10-15% of cases. Pelvic or lower abdominal tenderness is less common, occurring in less than 5% of women. Additionally, women may have an endocervical discharge and/or bleeding. Similar to men, rectal infection is usually asymptomatic but can cause anal discharge. Pharyngitis is also possible in women, but it is typically asymptomatic.

In patients with pre-existing hypovolaemia, the amount of sodium thiopentone administered should be reduced by half. This is because sodium thiopentone can cause venodilation and myocardial depression, which can result in significant hypovolaemia. Alternatively, an induction agent that does not cause hypotension, such as Etomidate, can be used instead. It is important to note that both propofol and thiopentone are known to cause hypotension.

Further Reading:

There are four commonly used induction agents in the UK: propofol, ketamine, thiopentone, and etomidate.

Propofol is a 1% solution that produces significant venodilation and myocardial depression. It can also reduce cerebral perfusion pressure. The typical dose for propofol is 1.5-2.5 mg/kg. However, it can cause side effects such as hypotension, respiratory depression, and pain at the site of injection.

Ketamine is another induction agent that produces a dissociative state. It does not display a dose-response continuum, meaning that the effects do not necessarily increase with higher doses. Ketamine can cause bronchodilation, which is useful in patients with asthma. The initial dose for ketamine is 0.5-2 mg/kg, with a typical IV dose of 1.5 mg/kg. Side effects of ketamine include tachycardia, hypertension, laryngospasm, unpleasant hallucinations, nausea and vomiting, hypersalivation, increased intracranial and intraocular pressure, nystagmus and diplopia, abnormal movements, and skin reactions.

Thiopentone is an ultra-short acting barbiturate that acts on the GABA receptor complex. It decreases cerebral metabolic oxygen and reduces cerebral blood flow and intracranial pressure. The adult dose for thiopentone is 3-5 mg/kg, while the child dose is 5-8 mg/kg. However, these doses should be halved in patients with hypovolemia. Side effects of thiopentone include venodilation, myocardial depression, and hypotension. It is contraindicated in patients with acute porphyrias and myotonic dystrophy.

Etomidate is the most haemodynamically stable induction agent and is useful in patients with hypovolemia, anaphylaxis, and asthma. It has similar cerebral effects to thiopentone. The dose for etomidate is 0.15-0.3 mg/kg. Side effects of etomidate include injection site pain, movement disorders, adrenal insufficiency, and apnoea. It is contraindicated in patients with sepsis due to adrenal suppression.

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.

Grade 2 shock is characterized by a pulse rate of 100 to 120 beats per minute and a respiratory rate of 20 to 30 breaths per minute. These clinical features align with the symptoms of grade 2 hypovolemic shock, as indicated in the below notes.

Further Reading:

Shock is a condition characterized by inadequate tissue perfusion due to circulatory insufficiency. It can be caused by fluid loss or redistribution, as well as impaired cardiac output. The main causes of shock include haemorrhage, diarrhoea and vomiting, burns, diuresis, sepsis, neurogenic shock, anaphylaxis, massive pulmonary embolism, tension pneumothorax, cardiac tamponade, myocardial infarction, and myocarditis.

One common cause of shock is haemorrhage, which is frequently encountered in the emergency department. Haemorrhagic shock can be classified into different types based on the amount of blood loss. Type 1 haemorrhagic shock involves a blood loss of 15% or less, with less than 750 ml of blood loss. Patients with type 1 shock may have normal blood pressure and heart rate, with a respiratory rate of 12 to 20 breaths per minute.

Type 2 haemorrhagic shock involves a blood loss of 15 to 30%, with 750 to 1500 ml of blood loss. Patients with type 2 shock may have a pulse rate of 100 to 120 beats per minute and a respiratory rate of 20 to 30 breaths per minute. Blood pressure is typically normal in type 2 shock.

Type 3 haemorrhagic shock involves a blood loss of 30 to 40%, with 1.5 to 2 litres of blood loss. Patients with type 3 shock may have a pulse rate of 120 to 140 beats per minute and a respiratory rate of more than 30 breaths per minute. Urine output is decreased to 5-15 mls per hour.

Type 4 haemorrhagic shock involves a blood loss of more than 40%, with more than 2 litres of blood loss. Patients with type 4 shock may have a pulse rate of more than 140 beats per minute and a respiratory rate of more than 35 breaths per minute. They may also be drowsy, confused, and possibly experience loss of consciousness. Urine output may be minimal or absent.

In summary, shock is a condition characterized by inadequate tissue perfusion. Haemorrhage is a common cause of shock, and it can be classified into different types based on the amount of blood loss. Prompt recognition and management of shock are crucial in order to prevent further complications and improve patient outcomes

In an adult patient, a Glasgow Coma Scale (GCS) score of 13 or lower necessitates an urgent CT scan of the head. The GCS is a neurological assessment tool that evaluates a patient’s level of consciousness and neurological functioning. It consists of three components: eye opening, verbal response, and motor response. Each component is assigned a score ranging from 1 to 4 or 5, with a higher score indicating a higher level of consciousness.

A GCS score of 15 is considered normal and indicates that the patient is fully conscious. A score of 14 or 13 suggests a mild impairment in consciousness, but it may not necessarily require an urgent CT scan unless there are other concerning symptoms or signs. However, a GCS score of 11 or 9 indicates a moderate to severe impairment in consciousness, which raises concerns for a potentially serious head injury. In these cases, an urgent CT scan of the head is necessary to assess for any structural brain abnormalities or bleeding that may require immediate intervention.

Therefore, in this case, the minimum GCS score that necessitates an urgent CT scan of the head is 13.

Further Reading:

Indications for CT Scanning in Head Injuries (Adults):
– CT head scan should be performed within 1 hour if any of the following features are present:
– GCS < 13 on initial assessment in the ED
– GCS < 15 at 2 hours after the injury on assessment in the ED
– Suspected open or depressed skull fracture
– Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)
– Post-traumatic seizure
– New focal neurological deficit
– > 1 episode of vomiting

Indications for CT Scanning in Head Injuries (Children):
– CT head scan should be performed within 1 hour if any of the features in List 1 are present:
– Suspicion of non-accidental injury
– Post-traumatic seizure but no history of epilepsy
– GCS < 14 on initial assessment in the ED for children more than 1 year of age
– Paediatric GCS < 15 on initial assessment in the ED for children under 1 year of age
– At 2 hours after the injury, GCS < 15
– Suspected open or depressed skull fracture or tense fontanelle
– Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)
– New focal neurological deficit
– For children under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head

– CT head scan should be performed within 1 hour if none of the above features are present but two or more of the features in List 2 are present:
– Loss of consciousness lasting more than 5 minutes (witnessed)
– Abnormal drowsiness
– Three or more discrete episodes of vomiting
– Dangerous mechanism of injury (high-speed road traffic accident, fall from a height of

Patients who have suffered burns should receive high-flow oxygen (15 L) through a reservoir bag while their breathing is being evaluated. If intubation is necessary, it is crucial to use an appropriately sized endotracheal tube (ETT). Using a tube that is too small can make it difficult or even impossible to ventilate the patient, clear secretions, or perform bronchoscopy.

According to the ATLS guidelines, adults should be intubated using an ETT with an internal diameter (ID) of at least 7.5 mm or larger. Children, on the other hand, should have an ETT with an ID of at least 4.5 mm. Once a patient has been intubated, it is important to continue administering 100% oxygen until their carboxyhemoglobin levels drop to less than 5%.

To protect the lungs, it is recommended to use lung protective ventilation techniques. This involves using low tidal volumes (4-8 mL/kg) and ensuring that peak inspiratory pressures do not exceed 30 cmH2O.

Homonymous quadrantanopia occur when there are lesions in the optic radiation. The optic tract passes through the posterolateral angle of the optic chiasm, running alongside the cerebral peduncle and inside the uncus of the temporal lobe. Eventually, it reaches the lateral geniculate body (LGN) in the thalamus. Acting as a relay center, the LGN sends axons through the optic radiation to the primary visual cortex in the occipital lobe. The upper optic radiation carries fibers from the superior retinal quadrants (which corresponds to the lower half of the visual field) and travels through the parietal lobe. On the other hand, the lower optic radiation carries fibers from the inferior retinal quadrants (which corresponds to the upper half of the visual field) and travels through the temporal lobe. Consequently, lesions in the temporal lobe can lead to superior homonymous quadrantanopia, while lesions in the parietal lobe can cause inferior homonymous quadrantanopia. The diagram below provides a summary of the different visual field defects resulting from lesions at various points in the visual pathway.

In the treatment of diabetic ketoacidosis (DKA), it is important to continue the infusion of insulin until certain criteria are met. These criteria include ketone levels being less than 0.3 mmol/L and the pH of the blood being above 7.3 or the bicarbonate levels being above 18 mmol/L. Additionally, the patient should feel comfortable enough to eat at this point. It is crucial not to stop the intravenous insulin infusion until at least 30 minutes after administering subcutaneous short-acting insulin.

Further Reading:

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

This patient presents with a classic case of temporal arteritis, also known as giant cell arteritis (GCA). Temporal arteritis is a chronic condition characterized by inflammation in the walls of medium and large arteries, specifically granulomatous inflammation. It typically affects individuals who are over 50 years old.

The clinical features of temporal arteritis include headache, tenderness in the scalp, jaw claudication, and episodes of sudden blindness or amaurosis fugax (usually occurring in one eye). Some patients may also experience systemic symptoms such as fever, fatigue, loss of appetite, weight loss, and depression.

Temporal arteritis is often associated with polymyalgia rheumatica (PMR) in about 50% of cases. PMR is characterized by stiffness, aching, and tenderness in the upper arms (bilateral) and pain in the pelvic girdle.

Visual loss is an early and significant complication of temporal arteritis, and once it occurs, it rarely improves. Therefore, early treatment with high-dose corticosteroids is crucial to prevent further visual loss and other ischemic complications. If temporal arteritis is suspected, immediate initiation of high-dose glucocorticosteroid treatment (40 – 60 mg prednisolone daily) is necessary. It is also important to arrange an urgent referral for specialist evaluation, including a same-day ophthalmology assessment for those with visual symptoms, and a temporal artery biopsy.

The correct answer is 10-15%. This means that out of all phaeochromocytoma cases, approximately 10-15% occur outside of the adrenal glands.

Further Reading:

Phaeochromocytoma is a rare neuroendocrine tumor that secretes catecholamines. It typically arises from chromaffin tissue in the adrenal medulla, but can also occur in extra-adrenal chromaffin tissue. The majority of cases are spontaneous and occur in individuals aged 40-50 years. However, up to 30% of cases are hereditary and associated with genetic mutations. About 10% of phaeochromocytomas are metastatic, with extra-adrenal tumors more likely to be metastatic.

The clinical features of phaeochromocytoma are a result of excessive catecholamine production. Symptoms are typically paroxysmal and include hypertension, headaches, palpitations, sweating, anxiety, tremor, abdominal and flank pain, and nausea. Catecholamines have various metabolic effects, including glycogenolysis, mobilization of free fatty acids, increased serum lactate, increased metabolic rate, increased myocardial force and rate of contraction, and decreased systemic vascular resistance.

Diagnosis of phaeochromocytoma involves measuring plasma and urine levels of metanephrines, catecholamines, and urine vanillylmandelic acid. Imaging studies such as abdominal CT or MRI are used to determine the location of the tumor. If these fail to find the site, a scan with metaiodobenzylguanidine (MIBG) labeled with radioactive iodine is performed. The highest sensitivity and specificity for diagnosis is achieved with plasma metanephrine assay.

The definitive treatment for phaeochromocytoma is surgery. However, before surgery, the patient must be stabilized with medical management. This typically involves alpha-blockade with medications such as phenoxybenzamine or phentolamine, followed by beta-blockade with medications like propranolol. Alpha blockade is started before beta blockade to allow for expansion of blood volume and to prevent a hypertensive crisis.

The risk of primary spontaneous pneumothorax is associated with smoking tobacco and increases as the duration of exposure and daily consumption rise. The changes caused by smoking in the small airways may contribute to the development of local emphysema, leading to the formation of bullae. In this case, the patient does not have any clinical features or significant risk factors for the other conditions mentioned. Therefore, primary spontaneous pneumothorax is the most probable diagnosis.

Cerebral edema is the most significant complication of diabetic ketoacidosis (DKA), leading to death in many cases. It occurs in approximately 0.2-1% of DKA cases. The high blood glucose levels cause an osmolar gradient, resulting in the movement of water from the intracellular fluid (ICF) to the extracellular fluid (ECF) space and a decrease in cell volume. When insulin and intravenous fluids are administered to correct the condition, the effective osmolarity decreases rapidly, causing a reversal of the fluid shift and the development of cerebral edema.

Cerebral edema is associated with a higher mortality rate and poor neurological outcomes. To prevent its occurrence, it is important to slowly normalize osmolarity over a period of 48 hours, paying attention to glucose and sodium levels, as well as ensuring proper hydration. Monitoring the child for symptoms such as headache, recurrent vomiting, irritability, changes in Glasgow Coma Scale (GCS), abnormal slowing of heart rate, and increasing blood pressure is crucial.

If cerebral edema does occur, it should be treated with either a hypertonic (3%) saline solution at a dosage of 3 ml/kg or a mannitol infusion at a dosage of 250-500 mg/kg over a 20-minute period.

In addition to cerebral edema, there are other complications associated with DKA in children, including cardiac arrhythmias, pulmonary edema, and acute renal failure.

Legionella pneumophila, a Gram-negative bacterium, can be found in natural water supplies and soil. It is responsible for causing Legionnaires’ disease, a serious illness. Outbreaks of this disease have been associated with poorly maintained air conditioning systems, whirlpool spas, and hot tubs.

The pneumonic form of Legionnaires’ disease presents with specific clinical features. Initially, there may be a mild flu-like prodrome lasting for 1-3 days. A non-productive cough, occurring in approximately 90% of cases, is also common. Pleuritic chest pain, haemoptysis, headache, nausea, vomiting, diarrhoea, and anorexia are other symptoms that may be experienced.

Fortunately, Legionella pneumophila infections can be effectively treated with macrolide antibiotics like erythromycin, or quinolones such as ciprofloxacin. Tetracyclines, including doxycycline, can also be used as a treatment option.

While the majority of Legionnaires’ disease cases are caused by Legionella pneumophila, there are several other species of Legionella that have been identified. One such species is Legionella longbeachae, which is less commonly encountered. It is primarily found in soil and potting compost and has been associated with outbreaks of Pontiac fever, a milder variant of Legionnaires’ disease that does not primarily affect the respiratory system.

In cases of delirium with challenging behavior, short-term low-dose haloperidol is typically the preferred medication. This patient is likely experiencing delirium due to a urinary tract infection. If the patient’s behavior becomes aggressive or poses a risk to themselves or others, pharmacological intervention may be necessary if non-verbal and verbal de-escalation techniques are ineffective or inappropriate. It is important to note that antipsychotics should be avoided in patients with Parkinson’s disease. Low-dose haloperidol can be administered orally or through an intramuscular injection. However, if the patient refuses oral medication, alternative methods may need to be considered.

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, pressure sores.

Activated charcoal is a commonly utilized substance for decontamination in cases of poisoning. Its main function is to attract and bind molecules of the ingested toxin onto its surface.

Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. This powder is created by subjecting carbonaceous matter to high heat, a process known as pyrolysis, and then concentrating it with a solution of zinc chloride. Through this process, the activated charcoal develops a complex network of pores, providing it with a large surface area of approximately 3,000 m2/g. This extensive surface area allows it to effectively hinder the absorption of the harmful toxin by up to 50%.

The typical dosage for adults is 50 grams, while children are usually given 1 gram per kilogram of body weight. Activated charcoal can be administered orally or through a nasogastric tube. It is crucial to administer it within one hour of ingestion, and if necessary, a second dose may be repeated after one hour.

Wolff-Parkinson-White (WPW) syndrome is a condition that affects the electrical system of the heart. It occurs when there is an abnormal pathway, known as the bundle of Kent, between the atria and the ventricles. This pathway can cause premature contractions of the ventricles, leading to a type of rapid heartbeat called atrioventricular re-entrant tachycardia (AVRT).

In a normal heart rhythm, the electrical signals travel through the bundle of Kent and stimulate the ventricles. However, in WPW syndrome, these signals can cause the ventricles to contract prematurely. This can be seen on an electrocardiogram (ECG) as a shortened PR interval, a slurring of the initial rise in the QRS complex (known as a delta wave), and a widening of the QRS complex.

There are two distinct types of WPW syndrome that can be identified on an ECG. Type A is characterized by predominantly positive delta waves and QRS complexes in the praecordial leads, with a dominant R wave in V1. This can sometimes be mistaken for right bundle branch block (RBBB). Type B, on the other hand, shows predominantly negative delta waves and QRS complexes in leads V1 and V2, and positive in the other praecordial leads, resembling left bundle branch block (LBBB).

Overall, WPW syndrome is a condition that affects the electrical conduction system of the heart, leading to abnormal heart rhythms. It can be identified on an ECG by specific features such as shortened PR interval, delta waves, and widened QRS complex.

To insert an IJV line, the patient should be positioned in the Trendelenburg position. This means that the patient should lie on their back with their head tilted down by at least 15 degrees. Additionally, the patient’s head should be turned away or laterally rotated from the side where the cannulation will take place. This positioning helps to distend the neck veins, making it easier to access them for the procedure.

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.

This patient’s clinical presentation is consistent with a diagnosis of idiopathic pulmonary fibrosis. The typical symptoms of idiopathic pulmonary fibrosis include a dry cough, progressive breathlessness, arthralgia and muscle pain, finger clubbing (seen in 50% of cases), cyanosis, fine end-expiratory bibasal crepitations, and right heart failure and cor pulmonale in later stages.

Finger clubbing, which is prominent in this patient, can also be caused by bronchiectasis and tuberculosis. However, these conditions would not result in a raised FEV1/FVC ratio, which is a characteristic feature of a restrictive lung disorder.

In restrictive lung disease, the FEV1/FVC ratio is typically normal, around 70% predicted, while the FVC is reduced to less than 80% predicted. Both the FVC and FEV1 are generally reduced in this condition. The ratio can also be elevated if the FVC is reduced to a greater extent.

It is important to note that smoking is a risk factor for developing idiopathic pulmonary fibrosis, particularly in individuals with a history of smoking greater than 20 pack-years.

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.

Congenital adrenal hyperplasia (CAH) is a group of inherited disorders that are caused by autosomal recessive genes. The majority of affected patients, over 90%, have a deficiency of the enzyme 21-hydroxylase. This enzyme is encoded by the 21-hydroxylase gene, which is located on chromosome 6p21 within the HLA histocompatibility complex. The second most common cause of CAH is a deficiency of the enzyme 11-beta-hydroxylase. The condition is rare, with an incidence of approximately 1 in 500 births in the UK. It is more prevalent in the offspring of consanguineous marriages.

The deficiency of 21-hydroxylase leads to a deficiency of cortisol and/or aldosterone, as well as an excess of precursor steroids. As a result, there is an increased secretion of ACTH from the anterior pituitary, leading to adrenocortical hyperplasia.

The severity of CAH varies depending on the degree of 21-hydroxylase deficiency. Female infants often exhibit ambiguous genitalia, such as clitoral hypertrophy and labial fusion. Male infants may have an enlarged scrotum and/or scrotal pigmentation. Hirsutism, or excessive hair growth, occurs in 10% of cases.

Boys with CAH often experience a salt-losing adrenal crisis at around 1-3 weeks of age. This crisis is characterized by symptoms such as vomiting, weight loss, floppiness, and circulatory collapse.

The diagnosis of CAH can be made by detecting markedly elevated levels of the metabolic precursor 17-hydroxyprogesterone. Neonatal screening is possible, primarily through the identification of persistently elevated 17-hydroxyprogesterone levels.

In infants presenting with a salt-losing crisis, the following biochemical abnormalities are observed: hyponatremia (low sodium levels), hyperkalemia (high potassium levels), metabolic acidosis, and hypoglycemia.

Boys experiencing a salt-losing crisis will require fluid resuscitation, intravenous dextrose, and intravenous hydrocortisone.

Affected females will require corrective surgery for their external genitalia. However, they have an intact uterus and ovaries and are capable of having children.

The long-term management of both sexes involves lifelong replacement of hydrocortisone (to suppress ACTH levels).

Paracetamol poisoning occurs when the liver is unable to metabolize paracetamol properly, leading to the production of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is conjugated by glutathione into a non-toxic form. However, during an overdose, the liver’s conjugation systems become overwhelmed, resulting in increased production of NAPQI and depletion of glutathione stores. This leads to the formation of covalent bonds between NAPQI and cell proteins, causing cell death in the liver and kidneys.

Symptoms of paracetamol poisoning may not appear for the first 24 hours or may include abdominal symptoms such as nausea and vomiting. After 24 hours, hepatic necrosis may develop, leading to elevated liver enzymes, right upper quadrant pain, and jaundice. Other complications can include encephalopathy, oliguria, hypoglycemia, renal failure, and lactic acidosis.

The management of paracetamol overdose depends on the timing and amount of ingestion. Activated charcoal may be given if the patient presents within 1 hour of ingesting a significant amount of paracetamol. N-acetylcysteine (NAC) is used to increase hepatic glutathione production and is given to patients who meet specific criteria. Blood tests are taken to assess paracetamol levels, liver function, and other parameters. Referral to a medical or liver unit may be necessary, and psychiatric follow-up should be considered for deliberate overdoses.

In cases of staggered ingestion, all patients should be treated with NAC without delay. Blood tests are also taken, and if certain criteria are met, NAC can be discontinued. Adverse reactions to NAC are common and may include anaphylactoid reactions, rash, hypotension, and nausea. Treatment for adverse reactions involves medications such as chlorpheniramine and salbutamol, and the infusion may be stopped if necessary.

The prognosis for paracetamol poisoning can be poor, especially in cases of severe liver injury. Fulminant liver failure may occur, and liver transplant may be necessary. Poor prognostic indicators include low arterial pH, prolonged prothrombin time, high plasma creatinine, and hepatic encephalopathy.

Patients typically initiate dialysis when their glomerular filtration rate (GFR) drops to 10 ml/min. However, if the patient has diabetes, dialysis may be recommended when their GFR reaches 15 ml/min. The GFR is a measure of kidney function and indicates how well the kidneys are able to filter waste products from the blood. Dialysis is a medical procedure that helps perform the function of the kidneys by removing waste and excess fluid from the body.

An Addisonian crisis is characterized by several distinct features. These include experiencing pain in the legs and abdomen, as well as symptoms of vomiting and dehydration. Hypotension, or low blood pressure, is also commonly observed during an Addisonian crisis. Confusion and psychosis may also occur, along with the presence of a fever. In some cases, convulsions may be present as well. Additionally, individuals experiencing an Addisonian crisis may also exhibit hypoglycemia, hyponatremia, hyperkalemia, hypercalcemia, eosinophilia, and metabolic acidosis.

The patient in this case has been diagnosed with type 1 autoimmune hepatitis, also known as classic type autoimmune hepatitis. This condition is characterized by inflammation of the liver due to reduced levels of regulatory T-cells (Treg cells), leading to the production of autoantibodies against hepatocyte surface antigens. It primarily affects women (70%) between the ages of 15 and 40.

Autoimmune hepatitis causes chronic and progressive hepatitis, which eventually progresses to cirrhosis. Patients typically experience non-specific symptoms of malaise, but in some cases, the disease may present in its later stages with jaundice and severe illness. During this stage, liver function tests often show significantly elevated transaminases (ALT and AST), usually more than ten times the normal levels, and a normal or slightly elevated alkaline phosphatase (ALP). Around 80% of cases show positive antinuclear antibodies (ANA), while approximately 70% show positive smooth muscle antibodies (SMA). Antimitochondrial antibodies are usually low or absent.

There are four recognized subtypes of autoimmune hepatitis:
1. Type 1 (Classic type): Positive ANA and SMA, and grossly elevated IgG
2. Type 2: Positive liver kidney microsomal antibodies (affects children)
3. Type 3: Positive soluble liver antigen antibodies
4. Type 4: Seronegative

Treatment for autoimmune hepatitis involves the use of corticosteroids and/or azathioprine. Remission can be achieved in approximately 70% of cases. In some cases where drug therapy is not effective, liver transplantation may be necessary.

Primary sclerosing cholangitis (PSC) is a condition that affects the bile ducts, causing progressive inflammation and obstruction. It is characterized by recurrent episodes of cholangitis and progressive scarring of the bile ducts. PSC can ultimately lead to liver cirrhosis, liver failure, and hepatocellular carcinoma. There is a known association between PSC and ulcerative colitis, with more than 80% of PSC patients also having ulcerative colitis.

Primary biliary cirrhosis (PBC) is an autoimmune disease that results in the progressive destruction of the small bile ducts in the liver, primarily affecting the intralobular ducts. This leads to cholestatic jaundice, liver fibrosis, and eventually cirrhosis. PBC is more common in females (90%)

The term renal colic is commonly used to describe a sudden and intense pain in the lower back caused by a blockage in the ureter, which is the tube that carries urine from the kidney to the bladder. However, a more accurate term is ureteric colic, as the pain usually arises from a blockage in the ureter itself.

Renal or ureteric colic typically presents with a sudden onset of severe abdominal pain on one side, starting in the lower back or flank and radiating to the genital area in women or to the groin or testicle in men.

The pain usually:
– Lasts for minutes to hours and comes in spasms, with periods of no pain or a dull ache
– Is often accompanied by nausea, vomiting, and blood in the urine
– Is often described as the most intense pain a person has ever experienced (many women describe it as worse than childbirth).

People with renal or ureteric colic:
– Are restless and unable to find relief by lying still (which helps distinguish it from peritonitis)
– May have a history of previous episodes
– May have a fever and sweating if there is a urinary tract infection present
– May complain of painful urination, frequent urination, and straining when the stone reaches the junction between the ureter and bladder (due to irritation of the bladder muscle).

If possible, a urine dipstick test should be done to support the diagnosis and check for signs of a urinary tract infection.

Checking for blood in the urine can also support the diagnosis of renal or ureteric colic. However, the absence of blood does not rule out the diagnosis and other causes of pain should be considered.

Checking for nitrite and leukocyte esterase in the urine can indicate an infection.

Pain management:
– Non-steroidal anti-inflammatory drugs (NSAIDs) are the first-line treatment for adults, children, and young people with suspected renal colic.
– Intravenous paracetamol can be given to adults, children, and young people if NSAIDs are not suitable or not providing enough pain relief.
– Opioids may be considered if both NSAIDs and intravenous paracetamol are not suitable or not providing enough pain relief.
– Antispasmodics should not be given to adults, children, and young people with suspected renal colic.

Alzheimer’s disease is characterized by various clinical features. These include memory loss, mood swings, apathy, and the presence of depressive or paranoid symptoms. Additionally, individuals with Alzheimer’s may experience Parkinsonism, a condition that affects movement, as well as a syndrome associated with the parietal lobe. Other symptoms may include difficulties with tasks such as copying 2D drawings, dressing properly, and carrying out a sequence of actions. Furthermore, individuals may struggle with copying gestures and may exhibit denial of their disorder, known as anosognosia. Topographical agnosia, or getting lost in familiar surroundings, may also be present, along with sensory inattention and astereognosis, which is the inability to identify objects when placed in the hand. Ultimately, Alzheimer’s disease is characterized by a relentless progression of personality and intellectual deterioration.

Calcium-channel blocker overdose is a serious condition that can be life-threatening. The most dangerous types of calcium channel blockers in overdose are verapamil and diltiazem. These medications work by binding to the alpha-1 subunit of L-type calcium channels, which prevents the entry of calcium into cells. These channels are important for the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

When managing a patient with calcium-channel blocker overdose, it is crucial to follow the standard ABC approach for resuscitation. If there is a risk of life-threatening toxicity, early intubation and ventilation should be considered. Invasive blood pressure monitoring is also necessary if hypotension and shock are developing.

The specific treatments for calcium-channel blocker overdose primarily focus on supporting the cardiovascular system. These treatments include:

1. Fluid resuscitation: Administer up to 20 mL/kg of crystalloid solution.

2. Calcium administration: This can temporarily increase blood pressure and heart rate. Options include 10% calcium gluconate (60 mL IV) or 10% calcium chloride (20 mL IV) via central venous access. Repeat boluses can be given up to three times, and a calcium infusion may be necessary to maintain serum calcium levels above 2.0 mEq/L.

3. Atropine: Consider administering 0.6 mg every 2 minutes, up to a total of 1.8 mg. However, atropine is often ineffective in these cases.

4. High dose insulin – euglycemic therapy (HIET): The use of HIET in managing cardiovascular toxicity has evolved. It used to be a last-resort measure, but early administration is now increasingly recommended. This involves giving a bolus of short-acting insulin (1 U/kg) and 50 mL of 50% glucose IV (unless there is marked hyperglycemia). Therapy should be continued with a short-acting insulin/dextrose infusion. Glucose levels should be monitored frequently, and potassium should be replaced if levels drop below 2.5 mmol/L.

5. Vasoactive infusions: Catecholamines such as dopamine, adrenaline, and/or noradrenaline can be titrated to achieve the desired inotropic and chronotropic effects.

6. Sodium bicarbonate: Consider using sodium bicarbonate in cases where a severe metabolic acidosis develops.

Gastroenteritis is a common condition in children, particularly those under the age of 5. It is characterized by the sudden onset of diarrhea, with or without vomiting. The most common cause of gastroenteritis in infants and young children is rotavirus, although other viruses, bacteria, and parasites can also be responsible. Prior to the introduction of the rotavirus vaccine in 2013, rotavirus was the leading cause of gastroenteritis in children under 5 in the UK. However, the vaccine has led to a significant decrease in cases, with a drop of over 70% in subsequent years.

Norovirus is the most common cause of gastroenteritis in adults, but it also accounts for a significant number of cases in children. In England & Wales, there are approximately 8,000 cases of norovirus each year, with 15-20% of these cases occurring in children under 9.

When assessing a child with gastroenteritis, it is important to consider whether there may be another more serious underlying cause for their symptoms. Dehydration assessment is also crucial, as some children may require intravenous fluids. The NICE traffic light system can be used to identify the risk of serious illness in children under 5.

In terms of investigations, stool microbiological testing may be indicated in certain cases, such as when the patient has been abroad, if diarrhea lasts for more than 7 days, or if there is uncertainty over the diagnosis. U&Es may be necessary if intravenous fluid therapy is required or if there are symptoms and/or signs suggestive of hypernatremia. Blood cultures may be indicated if sepsis is suspected or if antibiotic therapy is planned.

Fluid management is a key aspect of treating children with gastroenteritis. In children without clinical dehydration, normal oral fluid intake should be encouraged, and oral rehydration solution (ORS) supplements may be considered. For children with dehydration, ORS solution is the preferred method of rehydration, unless intravenous fluid therapy is necessary. Intravenous fluids may be required for children with shock or those who are unable to tolerate ORS solution.

Antibiotics are generally not required for gastroenteritis in children, as most cases are viral or self-limiting. However, there are some exceptions, such as suspected or confirmed sepsis, Extraintestinal spread of bacterial infection, or specific infections like Clostridium difficile-associated pseudomembranous enterocolitis or giardiasis.

Abducens nerve palsy is often linked to extradural hematoma. When there is a mass effect, downward brain herniation can occur, leading to the involvement of the 6th cranial nerve (abducens nerve, CN VI). This nerve controls the lateral rectus muscle, which is responsible for eye abduction. When the abducens nerve is affected, the lateral rectus muscle is unable to function properly, resulting in an inward turning of the affected eye towards the nose (esotropia).

Further Reading:

Extradural haematoma (EDH) is a collection of blood that forms between the inner surface of the skull and the outer layer of the dura, the dura mater. It is typically caused by head trauma and is often associated with a skull fracture, with the pterion being the most common site of injury. The middle meningeal artery is the most common source of bleeding in EDH.

Clinical features of EDH include a history of head injury with transient loss of consciousness, followed by a lucid interval and gradual loss of consciousness. Other symptoms may include severe headache, sixth cranial nerve palsies, nausea and vomiting, seizures, signs of raised intracranial pressure, and focal neurological deficits.

Imaging of EDH typically shows a biconvex shape and may cause mass effect with brain herniation. It can be differentiated from subdural haematoma by its appearance on imaging.

Management of EDH involves prompt referral to neurosurgery for evacuation of the haematoma. In some cases with a small EDH, conservative management may be considered. With prompt evacuation, the prognosis for EDH is generally good.

In order for a patient to be considered to have capacity, they must meet four criteria. Firstly, they must be able to comprehend the decision that needs to be made and understand the information that has been provided to them. Secondly, they should be able to retain the information in order to make an informed decision. Thirdly, they must demonstrate the ability to evaluate the advantages and disadvantages of the decision at hand. Lastly, they should be able to effectively communicate their decision.

Further Reading:

Patients have the right to determine what happens to their own bodies, and for consent to be valid, certain criteria must be met. These criteria include the person being informed about the intervention, having the capacity to consent, and giving consent voluntarily and freely without any pressure or undue influence.

In order for a person to be deemed to have capacity to make a decision on a medical intervention, they must be able to understand the decision and the information provided, retain that information, weigh up the pros and cons, and communicate their decision.

Valid consent can only be provided by adults, either by the patient themselves, a person authorized under a Lasting Power of Attorney, or someone with the authority to make treatment decisions, such as a court-appointed deputy or a guardian with welfare powers.

In the UK, patients aged 16 and over are assumed to have the capacity to consent. If a patient is under 18 and appears to lack capacity, parental consent may be accepted. However, a young person of any age may consent to treatment if they are considered competent to make the decision, known as Gillick competence. Parental consent may also be given by those with parental responsibility.

The Fraser guidelines apply to the prescription of contraception to under 16’s without parental involvement. These guidelines allow doctors to provide contraceptive advice and treatment without parental consent if certain criteria are met, including the young person understanding the advice, being unable to be persuaded to inform their parents, and their best interests requiring them to receive contraceptive advice or treatment.

Competent adults have the right to refuse consent, even if it is deemed unwise or likely to result in harm. However, there are exceptions to this, such as compulsory treatment authorized by the mental health act or if the patient is under 18 and refusing treatment would put their health at serious risk.

In emergency situations where a patient is unable to give consent, treatment may be provided without consent if it is immediately necessary to save their life or prevent a serious deterioration of their condition. Any treatment decision made without consent must be in the patient’s best interests, and if a decision is time-critical and the patient is unlikely to regain capacity in time, a best interest decision should be made. The treatment provided should be the least restrictive on the patient’s future choices.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on the bundle of nerves in the lower back and sacrum. As a result, individuals may experience loss of control over their bladder and bowel functions.

There are certain red flags that may indicate the presence of CES. These include experiencing sciatica on both sides of the body, having severe or worsening neurological issues in both legs (such as significant weakness in knee extension, ankle eversion, or foot dorsiflexion), difficulty starting urination or a decreased sensation of urinary flow, loss of sensation in the rectum, experiencing numbness or tingling in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and having a lax anal sphincter.

Conus medullaris syndrome (CMS) is a condition that affects the conus medullaris, which is located above the cauda equina at the T12-L2 level. Unlike CES, CMS primarily causes back pain and may have less noticeable nerve root pain. The main symptoms of CMS are urinary retention and constipation.

To confirm a diagnosis of CES and determine the level of compression and any underlying causes, an MRI scan is considered the gold-standard investigation. In cases where an MRI is not possible or contraindicated, a CT myelogram or standard CT scans can be helpful. However, plain radiographs have limited value and may only show significant degenerative or traumatic bone diseases.

There are two scoring systems that NICE recommends for assessing sore throat: the Centor Clinical Prediction Score and the FeverPAIN Score.

The Centor Clinical Prediction Score was initially developed as a tool to determine the likelihood of a group A beta-haemolytic Streptococcus (GABHS) infection in adults with a sore throat. It was created and tested in US Emergency Departments, specifically for adults.

The Centor score evaluates patients based on several criteria, with one point given for each positive criterion. These criteria include a history of fever (temperature above 38°C), the presence of exudate or swelling on the tonsils, tender or swollen anterior cervical lymph nodes, and the absence of cough.

According to the current NICE guidance, the Centor score can be used to guide management in the following way:
– A score of 0 to 2 indicates a 3-17% likelihood of streptococcus isolation, and antibiotics are not recommended.
– A score of 3 to 4 suggests a 32-56% likelihood of streptococcus isolation, and immediate treatment with empirical antibiotics or a ‘backup prescription’ should be considered.

An advance decision, also known as an advance directive in Scotland, is a statement made by a patient expressing their desire to refuse certain types of medical treatment or care in the event that they become unable to make or communicate decisions for themselves. These statements serve as a means of effectively communicating the patient’s wishes to healthcare professionals and family members, helping to avoid any confusion that may arise. If a patient reaches a point where they are no longer capable of making informed decisions about their care, an advance decision can provide clarity and guidance.

An advance decision can typically be utilized in the following situations: making decisions regarding CPR, determining the use of IV fluids and parenteral nutrition, deciding on specific procedures, and addressing the use of blood products for Jehovah’s Witnesses. However, it is important to note that advance decisions have their limitations and cannot be used to grant a relative lasting power of attorney, appoint a spokesperson to make decisions on the patient’s behalf, request a specific medical treatment, advocate for something illegal (such as assisted suicide), refuse treatment for a mental health condition, or authorize treatments that are not in the patient’s best interests.

A doctor is legally obligated to adhere to an advance decision unless certain circumstances arise. These circumstances include changes that invalidate the decision, advances or changes in treatment that alter the circumstances, ambiguity in the wording of the decision, or if the decision is unsigned or its authenticity is in doubt. If there are any doubts about the validity of an advance decision, it is advisable to seek legal advice. Unfortunately, there have been instances where advance decisions have been forged or signed under duress, and any suspicions of this nature should be raised.

It is important to note that there is no specific time period for which an advance decision remains valid.

A recent audit conducted by the Royal College of Emergency Medicine (RCEM) in 2018 revealed a concerning decline in the standards of pain management for children with fractured limbs in Emergency Departments (EDs). The audit found that the majority of patients experienced longer waiting times for pain relief compared to previous years. Shockingly, more than 1 in 10 children who presented with significant pain due to a limb fracture did not receive any pain relief at all.

To address this issue, the Agency for Health Care Policy and Research (AHCPR) in the USA recommends following the ABCs of pain management for all patients, including children. This approach involves regularly asking about pain, systematically assessing it, believing the patient and their family in their reports of pain and what relieves it, choosing appropriate pain control options, delivering interventions in a timely and coordinated manner, and empowering patients and their families to have control over their pain management.

The RCEM has established standards that require a child’s pain to be assessed within 15 minutes of their arrival at the ED. This is considered a fundamental standard. Various rating scales are available for assessing pain in children, with the choice depending on the child’s age and ability to use the scale. These scales include the Wong-Baker Faces Pain Rating Scale, Numeric rating scale, and Behavioural scale.

To ensure timely administration of analgesia to children in acute pain, the RCEM has set specific standards. These standards state that 100% of patients in severe pain should receive appropriate analgesia within 60 minutes of their arrival or triage, whichever comes first. Additionally, 75% should receive analgesia within 30 minutes, and 50% within 20 minutes.

Diabetes insipidus is characterized by low urine osmolality and high serum osmolality. This occurs because the kidneys are unable to properly reabsorb water and sodium, resulting in diluted urine with low osmolality. On the other hand, the loss of water and sodium leads to dehydration and concentration of the serum, causing a rise in serum osmolality. Hypernatremia is a common finding in patients with diabetes insipidus. In cases of nephrogenic diabetes insipidus, hypokalemia and hypercalcemia may also be observed. Glucose levels are typically normal, unless the patient also has diabetes mellitus.

Further Reading:

Diabetes insipidus (DI) is a condition characterized by either a decrease in the secretion of antidiuretic hormone (cranial DI) or insensitivity to antidiuretic hormone (nephrogenic DI). Antidiuretic hormone, also known as arginine vasopressin, is produced in the hypothalamus and released from the posterior pituitary. The typical biochemical disturbances seen in DI include elevated plasma osmolality, low urine osmolality, polyuria, and hypernatraemia.

Cranial DI can be caused by various factors such as head injury, CNS infections, pituitary tumors, and pituitary surgery. Nephrogenic DI, on the other hand, can be genetic or result from electrolyte disturbances or the use of certain drugs. Symptoms of DI include polyuria, polydipsia, nocturia, signs of dehydration, and in children, irritability, failure to thrive, and fatigue.

To diagnose DI, a 24-hour urine collection is done to confirm polyuria, and U&Es will typically show hypernatraemia. High plasma osmolality with low urine osmolality is also observed. Imaging studies such as MRI of the pituitary, hypothalamus, and surrounding tissues may be done, as well as a fluid deprivation test to evaluate the response to desmopressin.

Management of cranial DI involves supplementation with desmopressin, a synthetic form of arginine vasopressin. However, hyponatraemia is a common side effect that needs to be monitored. In nephrogenic DI, desmopressin supplementation is usually not effective, and management focuses on ensuring adequate fluid intake to offset water loss and monitoring electrolyte levels. Causative drugs need to be stopped, and there is a risk of developing complications such as hydroureteronephrosis and an overdistended bladder.

Second degree frostbite is characterized by tissue necrosis that affects both the epidermis and a variable depth of the dermis. However, there is still some healthy dermis present, which allows for regeneration and recovery of the skin. This type of frostbite is often referred to as partial thickness. Clinically, it is observed as the formation of blisters filled with clear or milky fluid on the surface of the skin, accompanied by redness and swelling.

Further Reading:

Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in decreased myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

According to the 2011 recommendations from the World Health Organization (WHO), the following criteria are used to diagnose diabetes mellitus:

– A random venous plasma glucose concentration that exceeds 11.1 mmol/l.
– A fasting plasma glucose concentration that is higher than 7.0 mmol/l.
– A two-hour plasma glucose concentration that exceeds 11.1 mmol/l, measured two hours after consuming 75g of anhydrous glucose during an oral glucose tolerance test (OGTT).
– An HbA1c level that is greater than 48 mmol/mol (equivalent to 6.5%).

These guidelines provide specific thresholds for diagnosing diabetes mellitus based on various glucose measurements and HbA1c levels. It is important for healthcare professionals to consider these criteria when evaluating individuals for diabetes mellitus.

Otoliths are commonly found in the inferior semicircular canal of patients, while their presence in the anterior semicircular canal is extremely uncommon.

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.

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.

The current recommendations from NICE for managing warfarin in the presence of bleeding or an abnormal INR are as follows:

In cases of major active bleeding, regardless of the INR level, the first step is to stop administering warfarin. Next, 5 mg of vitamin K (phytomenadione) should be given intravenously. Additionally, dried prothrombin complex concentrate, which contains factors II, VII, IX, and X, should be administered. If dried prothrombin complex is not available, fresh frozen plasma can be given at a dose of 15 ml/kg.

If the INR is greater than 8.0 and there is minor bleeding, warfarin should be stopped. Slow injection of 1-3 mg of vitamin K can be given, and this dose can be repeated after 24 hours if the INR remains high. Warfarin can be restarted once the INR is less than 5.0.

If the INR is greater than 8.0 with no bleeding, warfarin should be stopped. Oral administration of 1-5 mg of vitamin K can be given, and this dose can be repeated after 24 hours if the INR remains high. Warfarin can be restarted once the INR is less than 5.0.

If the INR is between 5.0-8.0 with minor bleeding, warfarin should be stopped. Slow injection of 1-3 mg of vitamin K can be given, and warfarin can be restarted once the INR is less than 5.0.

If the INR is between 5.0-8.0 with no bleeding, one or two doses of warfarin should be withheld, and the subsequent maintenance dose should be reduced.

For more information, please refer to the NICE Clinical Knowledge Summary on the management of warfarin therapy and the BNF guidance on the use of phytomenadione.

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.