Parental responsibility encompasses the legal rights, duties, powers, responsibilities, and authority that a parent holds for their child. This includes the ability to provide consent for medical treatment on behalf of the child. Any individual with parental responsibility has the authority to give consent for their child. If a father meets any of the aforementioned criteria, he is considered to have parental responsibility. On the other hand, a mother is automatically granted parental responsibility for her child from the moment of birth.

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.

This patient has presented with an Addisonian crisis, which is a rare but potentially catastrophic condition if not diagnosed promptly. The most likely underlying rheumatological diagnosis in this case is polymyalgia rheumatica, and it is likely that the GP started the patient on prednisolone medication.

Addison’s disease occurs when the adrenal glands underproduce steroid hormones, affecting the production of glucocorticoids, mineralocorticoids, and sex steroids. The main causes of Addison’s disease include autoimmune adrenalitis (accounting for 80% of cases), bilateral adrenalectomy, Waterhouse-Friderichsen syndrome (hemorrhage into the adrenal glands), and tuberculosis.

An Addisonian crisis is most commonly triggered by the deliberate or accidental withdrawal of steroid therapy in patients with Addison’s disease. Other factors that can precipitate a crisis include infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

The clinical features of Addison’s disease include weakness, lethargy, hypotension (especially orthostatic hypotension), nausea, vomiting, weight loss, reduced axillary and pubic hair, depression, and hyperpigmentation (particularly in palmar creases, buccal mucosa, and exposed areas). In an Addisonian crisis, the main features are usually hypoglycemia and shock, characterized by tachycardia, peripheral vasoconstriction, hypotension, altered consciousness, and coma.

Biochemically, Addison’s disease is characterized by increased ACTH levels (as a compensatory response to stimulate the adrenal glands), elevated serum renin levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Diagnostic investigations may include the Synacthen test, plasma ACTH level, plasma renin level, and adrenocortical antibodies.

Management of Addison’s disease should be overseen by an Endocrinologist. Typically, patients require hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also need thyroxine if there is hypothalamic-pituitary disease present. Treatment is lifelong, and patients should carry a steroid card and a MedicAlert bracelet, being aware of the possibility of an Addisonian crisis.

The three sites most frequently used for IO access are the proximal tibia, distal tibia, and distal femur. The proximal tibia is located 2 cm below the tibial tuberosity, while the distal tibia is just above the medial malleolus. The distal femur site is situated 2 cm above the condyle in the midline. These sites are commonly chosen for IO access. However, there are also less commonly used sites such as the proximal humerus (above the surgical neck) and the iliac crest. It is important to note that the proximal humerus may be challenging to palpate in children and is typically not used in those under 5 years of age. Additionally, accessing the sternum requires a specialist device.

Further Reading:

Intraosseous (IO) cannulation is a technique used to gain urgent intravenous (IV) access in patients where traditional IV access is difficult to obtain. It involves injecting fluid or drugs directly into the medullary cavity of the bone. This procedure can be performed in both adult and pediatric patients and is commonly used in emergency situations.

There are different types of IO needles available, including manual IO needles and device-powered IO needles such as the EZ-IO. These tools allow healthcare professionals to access the bone and administer necessary medications or fluids quickly and efficiently.

The most commonly used sites for IO cannulation are the tibia (shinbone) and the femur (thighbone). In some cases, the proximal humerus (upper arm bone) may also be used. However, there are certain contraindications to IO cannulation that should be considered. These include fractures of the bone to be cannulated, overlying skin infections or a high risk of infection (such as burns), conditions like osteogenesis imperfecta or osteoporosis, ipsilateral vascular injury, and coagulopathy.

While IO cannulation is a valuable technique, there are potential complications that healthcare professionals should be aware of. These include superficial skin infections, osteomyelitis (infection of the bone), skin necrosis, growth plate injury (in pediatric patients), fractures, failure to access or position the needle correctly, extravasation (leakage of fluid or medication into surrounding tissues), and compartment syndrome (a rare but serious condition that can occur if there is an undiagnosed fracture).

Overall, IO cannulation is a useful method for gaining urgent IV access in patients when traditional methods are challenging. However, it is important for healthcare professionals to be aware of the potential complications and contraindications associated with this procedure.

For adults and children over the age of 12 who are suspected to have glandular fever and have a normal immune system, it is recommended to conduct a Full Blood Count (FBC) and a monospot test during the second week of the illness. The timing and choice of investigations for glandular fever vary depending on the patient’s age, immune system status, and duration of symptoms. For children under the age of 12 and individuals with compromised immune systems, it is advised to perform a blood test for Epstein-Barr virus (EBV) viral serology after at least 7 days of illness. However, for immunocompetent adults and children older than 12, a FBC with differential white cell count and a monospot test (heterophile antibodies) should be conducted during the second week of the illness.

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.

Eye movement desensitization and reprocessing (EMDR) and trauma-focused cognitive-behavioral therapy (CBT) are the primary treatment options for post-traumatic stress disorder (PTSD). These therapies should be provided to individuals of all ages, including children, adolescents, and adults, regardless of the time that has passed since the traumatic event. The recommended number of sessions is typically 8-12, although additional sessions may be necessary in cases involving multiple traumas, chronic disability, comorbidities, or social difficulties.

There is a significant link between methotrexate and the development of pulmonary fibrosis. While there have been instances of pulmonary fibrosis occurring as a result of infliximab, this particular side effect is more commonly associated with methotrexate use.

Methotrexate can also cause other side effects such as nausea and vomiting, abdominal pain, gastrointestinal bleeding, dizziness, stomatitis, hepatotoxicity, neutropenia, and pneumonitis.

Inspired oxygen primarily works by removing nitrogen from the lungs, which would otherwise take up a significant portion of the lung capacity. This nitrogen is replaced with oxygen, leading to improved oxygenation of the tissues and an increased oxygen reserve. As a result, the patient can safely hold their breath for a longer period of time. It is recommended to preoxygenate the patient for at least 3 minutes.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

This patient’s medical history suggests a diagnosis of acute coronary syndrome. It is important to provide pain relief as soon as possible. This can be achieved by administering GTN (sublingual or buccal), but if there is suspicion of an acute myocardial infarction (MI), intravenous opioids such as morphine should be offered.

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

For patients without a high risk of bleeding and no planned coronary angiography within 24 hours of admission, fondaparinux should be administered. However, if coronary angiography is planned within 24 hours, unfractionated heparin can be offered as an alternative to fondaparinux. For patients with significant renal impairment (creatinine above 265 micromoles per litre), unfractionated heparin should 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 given to individuals with an oxygen saturation (SpO2) below 94% who are not at risk of hypercapnic respiratory failure, aiming for an 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 potential 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.

Atropine acts as a blocker for muscarinic acetylcholine receptors, making it an antagonist. It is commonly administered during peri-arrest bradycardia. In adults, a dose of 500 mcg is given every 3-5 minutes, with a maximum total dose of 3mg. On the other hand, the initial intravenous dose of amiodarone is 300 mg. Amiodarone works by prolonging repolarization and decreasing myocardial excitability. Additionally, lidocaine functions by blocking sodium channels.

Further Reading:

In the management of respiratory and cardiac arrest, several drugs are commonly used to help restore normal function and improve outcomes. Adrenaline is a non-selective agonist of adrenergic receptors and is administered intravenously at a dose of 1 mg every 3-5 minutes. It works by causing vasoconstriction, increasing systemic vascular resistance (SVR), and improving cardiac output by increasing the force of heart contraction. Adrenaline also has bronchodilatory effects.

Amiodarone is another drug used in cardiac arrest situations. It blocks voltage-gated potassium channels, which prolongs repolarization and reduces myocardial excitability. The initial dose of amiodarone is 300 mg intravenously after 3 shocks, followed by a dose of 150 mg after 5 shocks.

Lidocaine is an alternative to amiodarone in cardiac arrest situations. It works by blocking sodium channels and decreasing heart rate. The recommended dose is 1 mg/kg by slow intravenous injection, with a repeat half of the initial dose after 5 minutes. The maximum total dose of lidocaine is 3 mg/kg.

Magnesium sulfate is used to reverse myocardial hyperexcitability associated with hypomagnesemia. It is administered intravenously at a dose of 2 g over 10-15 minutes. An additional dose may be given if necessary, but the maximum total dose should not exceed 3 g.

Atropine is an antagonist of muscarinic acetylcholine receptors and is used to counteract the slowing of heart rate caused by the parasympathetic nervous system. It is administered intravenously at a dose of 500 mcg every 3-5 minutes, with a maximum dose of 3 mg.

Naloxone is a competitive antagonist for opioid receptors and is used in cases of respiratory arrest caused by opioid overdose. It has a short duration of action, so careful monitoring is necessary. The initial dose of naloxone is 400 micrograms, followed by 800 mcg after 1 minute. The dose can be gradually escalated up to 2 mg per dose if there is no response to the preceding dose.

It is important for healthcare professionals to have knowledge of the pharmacology and dosing schedules of these drugs in order to effectively manage respiratory and cardiac arrest situations.

During the examination, the child is observed to be grunting and has had an episode of urinary incontinence. The question asks about the likely complication that has developed.

The most likely complication in this case is cerebral edema. Cerebral edema refers to the swelling of the brain due to an increase in fluid accumulation. It is a severe and potentially life-threatening complication of diabetic ketoacidosis, particularly in children. The symptoms observed, such as headaches, increasing drowsiness, grunting, and urinary incontinence, are indicative of cerebral edema.

Cerebral edema can occur due to various factors, including the rapid correction of hyperglycemia and dehydration, as well as the release of inflammatory mediators. It is crucial to recognize and manage cerebral edema promptly as it can lead to increased intracranial pressure and neurological deterioration.

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.

The diving reflex occurs when the face comes into contact with cold water, leading to apnoea, bradycardia, and peripheral vasoconstriction. This response helps decrease the workload on the heart, lower oxygen demand in the heart muscle, and ensure adequate blood flow to the brain and vital organs. The trigeminal nerve (CN V) is responsible for transmitting sensory information, while the vagus nerve (CN X) primarily controls the motor response. This reflex is more prominent in young children and is believed to contribute to their improved survival rates in prolonged submersion in cold water.

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.

Blood transfusion is a crucial medical treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion use, errors and adverse reactions still occur. One common adverse reaction is febrile transfusion reactions, which present as an unexpected rise in temperature during or after transfusion. This can be caused by cytokine accumulation or recipient antibodies reacting to donor antigens. Treatment for febrile transfusion reactions is supportive, and other potential causes should be ruled out.

Another serious complication is acute haemolytic reaction, which is often caused by ABO incompatibility due to administration errors. This reaction requires the transfusion to be stopped and IV fluids to be administered. Delayed haemolytic reactions can occur several days after a transfusion and may require monitoring and treatment for anaemia and renal function. Allergic reactions, TRALI (Transfusion Related Acute Lung Injury), TACO (Transfusion Associated Circulatory Overload), and GVHD (Graft-vs-Host Disease) are other potential complications that require specific management approaches.

In summary, blood transfusion carries risks and potential complications, but efforts have been made to improve safety procedures. It is important to be aware of these complications and to promptly address any adverse reactions that may occur during or after a transfusion.

Drug-induced acute dystonic reactions are frequently seen in the Emergency Department. These reactions occur in approximately 0.5% to 1% of patients who have been administered metoclopramide or prochlorperazine. Procyclidine, an anticholinergic medication, has proven to be effective in treating drug-induced parkinsonism, akathisia, and acute dystonia. In emergency situations, a dose of 10 mg IV of procyclidine can be administered to promptly treat acute drug-induced dystonic reactions.

Hepatitis B surface antigen (HBsAg) is a protein found on the surface of the hepatitis B virus. It can be detected in high levels in the blood during both acute and chronic hepatitis B virus infections. The presence of HBsAg indicates that the person is capable of spreading the infection to others. Normally, the body produces antibodies to HBsAg as part of the immune response to the infection. HBsAg is also used to create the hepatitis B vaccine.

Hepatitis B surface antibody (anti-HBs) indicates that a person has recovered from the hepatitis B virus infection and is now immune to it. This antibody can also develop in individuals who have been successfully vaccinated against hepatitis B.

Total hepatitis B core antibody (anti-HBc) appears when symptoms of acute hepatitis B begin and remains present for life. The presence of anti-HBc indicates that a person has either had a previous or ongoing infection with the hepatitis B virus, although the exact time frame cannot be determined. This antibody is not present in individuals who have received the hepatitis B vaccine.

IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicates a recent infection or acute hepatitis B. If this antibody is present, it suggests that the infection occurred within the past six months.

Benzodiazepines are helpful in reducing shivering and improving the effectiveness of active cooling techniques. They are particularly useful in controlling seizures and making cooling more tolerable for patients. By administering small doses of intravenous benzodiazepines like diazepam or midazolam, shivering can be reduced, which in turn prevents heat gain and enhances the cooling process. On the other hand, dantrolene does not currently have any role in managing heat stroke. Additionally, antipyretics are not effective in reducing high body temperature caused by excessive heat. They only work when the core body temperature is elevated due to pyrogens.

Further Reading:

Heat Stroke:
– Core temperature >40°C with central nervous system dysfunction
– Classified into classic/non-exertional heat stroke and exertional heat stroke
– Classic heat stroke due to passive exposure to severe environmental heat
– Exertional heat stroke due to strenuous physical activity in combination with excessive environmental heat
– Mechanisms to reduce core temperature overwhelmed, leading to tissue damage
– Symptoms include high body temperature, vascular endothelial surface damage, inflammation, dehydration, and renal failure
– Management includes cooling methods and supportive care
– Target core temperature for cooling is 38.5°C

Heat Exhaustion:
– Mild to moderate heat illness that can progress to heat stroke if untreated
– Core temperature elevated but <40°C
– Symptoms include nausea, vomiting, dizziness, and mild neurological symptoms
– Normal thermoregulation is disrupted
– Management includes moving patient to a cooler environment, rehydration, and rest

Other Heat-Related Illnesses:
– Heat oedema: transitory swelling of hands and feet, resolves spontaneously
– Heat syncope: results from volume depletion and peripheral vasodilatation, managed by moving patient to a cooler environment and rehydration
– Heat cramps: painful muscle contractions associated with exertion, managed with cooling, rest, analgesia, and rehydration

Risk Factors for Severe Heat-Related Illness:
– Old age, very young age, chronic disease and debility, mental illness, certain medications, housing issues, occupational factors

Management:
– Cooling methods include spraying with tepid water, fanning, administering cooled IV fluids, cold or ice water immersion, and ice packs
– Benzodiazepines may be used to control shivering
– Rapid cooling to achieve rapid normothermia should be avoided to prevent overcooling and hypothermia
– Supportive care includes intravenous fluid replacement, seizure treatment if required, and consideration of haemofiltration
– Some patients may require liver transplant due to significant liver damage
– Patients with heat stroke should ideally be managed in a HDU/ICU setting with CVP and urinary catheter output measurements

When someone takes too much paracetamol, it can harm their liver cells and the tubules in their kidneys. This is because paracetamol produces a harmful substance called NAPQI, which is normally combined with glutathione. However, when there is too much NAPQI, it can cause damage and death to liver and kidney cells.

Further Reading:

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.

The interpretation of facial X-rays is often assisted by the use of McGrigor-Campbell lines and Dolan lines. These lines, along with accompanying notes and images, provide additional information for a more accurate analysis.

Further Reading:

Facial X-rays are commonly used to assess and diagnose facial fractures. Two standard views are typically performed: the Occipitomental view and the Occipitomental 30º view. The Occipitomental view provides a comprehensive look at the upper and middle thirds of the face, including the orbital margins, frontal sinuses, zygomatic arches, and maxillary antra. On the other hand, the Occipitomental 30º view uses a 30-degree caudal angulation to better visualize the zygomatic arches and walls of the maxillary antra, although it may compromise the clear view of the orbital margins.

To assist in the interpretation of facial X-rays, imaginary lines are often drawn across the images to highlight any asymmetry or disruption. Two commonly used sets of lines are the McGrigor-Campbell lines and Dolan’s lines. McGrigor-Campbell lines are used to aid in the interpretation of both the Occipitomental and Occipitomental 30º views. These lines include an upper line that passes through the zygomatico-frontal sutures and the upper edge of the orbits, a middle line that follows the zygomatic arch and crosses the zygomatic bone, and a lower line that passes through the condyle and coronoid process of the mandible and the walls of the maxillary antra.

Dolan’s lines, described by Dolan and Jacoby, are often used in conjunction with McGrigor-Campbell lines. These lines include the orbital line, which traces the inner margins of the orbital walls and the nasal arch, the zygomatic line, which traces the superior margin of the zygomatic arch and body, and the maxillary line, which traces the inferior margin of the zygomatic arch, body, and buttress, as well as the lateral wall of the maxillary sinus. Together, the zygomatic and maxillary lines resemble the profile of an elephant’s head and are referred to as Dolan’s elephant. These lines help provide additional information and aid in the interpretation of facial X-rays.

The first-line treatment for Addisonian (adrenal) crisis is hydrocortisone. This patient displays symptoms that indicate an Addisonian crisis, and the main components of their management involve administering hydrocortisone and providing intravenous fluids for resuscitation.

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

Vascular dementia is the second most common form of dementia, accounting for approximately 25% of all cases. It occurs when the brain is damaged due to various factors, such as major strokes, multiple smaller strokes that go unnoticed (known as multi-infarct), or chronic changes in smaller blood vessels (referred to as subcortical dementia). The term vascular cognitive impairment (VCI) is increasingly used to encompass this range of diseases.

Unlike Alzheimer’s disease, which has a gradual and subtle onset, vascular dementia can occur suddenly and typically shows a series of stepwise increases in symptom severity. The presentation and progression of the disease can vary significantly.

There are certain features that suggest a vascular cause of dementia. These include a history of transient ischemic attacks (TIAs) or cardiovascular disease, the presence of focal neurological abnormalities, prominent memory impairment in the early stages of the disease, early onset of gait disturbance and unsteadiness, frequent unprovoked falls in the early stages, bladder symptoms (such as incontinence) without any identifiable urological condition in the early stages, and seizures.

Renal colic, also known as ureteric colic, refers to 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. This condition is commonly associated with the presence of a urinary tract stone.

The main symptoms of renal or ureteric colic include severe abdominal pain on one side, starting in the lower back or flank and radiating to the groin or genital area in men, or to the labia in women. The pain comes and goes in spasms, lasting for minutes to hours, with periods of no pain or a dull ache. Nausea, vomiting, and the presence of blood in the urine are often accompanying symptoms.

People experiencing renal or ureteric colic are usually restless and unable to find relief by lying still, which helps to distinguish this condition from peritonitis. They may have a history of previous episodes and may also present with fever and sweating if there is an associated urinary infection. Some individuals may complain of painful urination, frequent urination, and straining when the stone reaches the junction between the ureter and the bladder, as the stone irritates the detrusor muscle.

In terms of pain management, the first-line treatment for adults, children, and young people with suspected renal colic is a non-steroidal anti-inflammatory drug (NSAID), which can be administered through various routes. If NSAIDs are contraindicated or not providing sufficient pain relief, intravenous paracetamol can be offered as an alternative. Opioids may be considered if both NSAIDs and intravenous paracetamol are contraindicated or not effective in relieving pain. Antispasmodics should not be given to individuals with suspected renal colic.

For more detailed information, you can refer to the NICE guidelines on the assessment and management of renal and ureteric stones.

Amiodarone is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) while performing chest compressions. The prescribed dose is 300 mg, which should be given as an intravenous bolus. To ensure proper administration, the medication should be diluted in 20 mL of 5% dextrose solution.

In cases where VF/pVT continues after five defibrillation attempts, an additional dose of 150 mg of Amiodarone should be administered. It is important to note that Amiodarone is not suitable for treating PEA or asystole, and its use is specifically indicated for shockable cardiac arrest situations.

Spondylolysis refers to a flaw or fracture caused by stress in the pars interarticularis of the vertebral arch. While it can occur in the cervical vertebrae, it is most commonly found in the lower lumbar vertebrae, specifically L5. This injury is frequently seen in children and adolescents who engage in sports activities that place repetitive strain on the lower back, such as gymnastics, football, and weightlifting.

Nelson’s syndrome is a rare condition that occurs many years after a bilateral adrenalectomy for Cushing’s syndrome. It is believed to develop due to the loss of the normal negative feedback control that suppresses high cortisol levels. As a result, the hypothalamus starts producing CRH again, which stimulates the growth of a pituitary adenoma that produces adrenocorticotropic hormone (ACTH).

Only 15-20% of patients who undergo bilateral adrenalectomy will develop this condition, and it is now rarely seen as the procedure is no longer commonly performed.

The symptoms and signs of Nelson’s syndrome are related to the growth of the pituitary adenoma and the increased production of ACTH and melanocyte-stimulating hormone (MSH) from the adenoma. These may include headaches, visual field defects (up to 50% of cases), increased skin pigmentation, and the possibility of hypopituitarism.

ACTH levels will be significantly elevated (usually >500 ng/L). Thyroxine, TSH, gonadotrophin, and sex hormone levels may be low. Prolactin levels may be high, but not as high as with a prolactin-producing tumor. MRI or CT scanning can be helpful in identifying the presence of an expanding pituitary mass.

The treatment of choice for Nelson’s syndrome is trans-sphenoidal surgery.

The second heart sound (S2) is created by vibrations produced when the aortic and pulmonary valves close. It marks the end of systole. It is normal to hear a split in the sound during inspiration.

A loud S2 can be associated with certain conditions such as systemic hypertension (resulting in a loud A2), pulmonary hypertension (resulting in a loud P2), hyperdynamic states (like tachycardia, fever, or thyrotoxicosis), and atrial septal defect (which causes a loud P2).

On the other hand, a soft S2 can be linked to decreased aortic diastolic pressure (as seen in aortic regurgitation), poorly mobile cusps (such as calcification of the aortic valve), aortic root dilatation, and pulmonary stenosis (which causes a soft P2).

A widely split S2 can occur during deep inspiration, right bundle branch block, prolonged right ventricular systole (seen in conditions like pulmonary stenosis or pulmonary embolism), and severe mitral regurgitation. However, in the case of atrial septal defect, the splitting is fixed and does not vary with respiration.

Reversed splitting of S2, where P2 occurs before A2 (paradoxical splitting), can occur during deep expiration, left bundle branch block, prolonged left ventricular systole (as seen in hypertrophic cardiomyopathy), severe aortic stenosis, and right ventricular pacing.

The NICE recommendations for managing patients with suspected TIA are as follows:

– Offer aspirin (300 mg daily) to individuals who have experienced a suspected TIA, unless there are contraindications. This treatment should be started immediately.
– Immediately refer individuals who have had a suspected TIA for specialist assessment and investigation. They should be seen within 24 hours of the onset of symptoms.
– Avoid using scoring systems, such as ABCD2, to assess the risk of subsequent stroke or determine the urgency of referral for individuals with suspected or confirmed TIA.
– Provide secondary prevention measures, in addition to aspirin, as soon as possible after confirming the diagnosis of TIA.

The NICE recommendations for imaging in individuals with suspected TIA or acute non-disabling stroke are as follows:

– Do not offer CT brain scanning to individuals with suspected TIA, unless there is clinical suspicion of an alternative diagnosis that CT could detect.
– After a specialist assessment in the TIA clinic, consider performing an MRI (including diffusion-weighted and blood-sensitive sequences) to determine the area of ischemia, detect hemorrhage, or identify alternative pathologies. If an MRI is conducted, it should be done on the same day as the assessment.
– Carotid imaging is necessary for all individuals with TIA who, after specialist assessment, are considered candidates for carotid endarterectomy. This imaging should be done urgently.

For more information, refer to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old: diagnosis and initial management.

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.

Blood transfusion is a crucial medical treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion usage, errors and adverse reactions still occur.

One serious complication is acute haemolytic transfusion reactions, which happen when incompatible red cells are transfused and react with the patient’s own antibodies. This usually occurs due to human error, such as mislabelling sample tubes or request forms. Symptoms of this reaction include a feeling of impending doom, fever, chills, pain and warmth at the transfusion site, nausea, vomiting, and back, joint, and chest pain. Immediate action should be taken to stop the transfusion, replace the donor blood with normal saline or another suitable crystalloid, and check the blood to confirm the intended recipient. IV diuretics may be administered to increase renal blood flow, and urine output should be maintained.

Another common complication is febrile transfusion reaction, which presents with a 1-degree rise in temperature from baseline, along with chills and malaise. This reaction is usually caused by cytokines from leukocytes in the transfused blood components. Supportive treatment is typically sufficient, and paracetamol can be helpful.

Allergic reactions can also occur, usually due to foreign plasma proteins or anti-IgA. These reactions often present with urticaria, pruritus, and hives, and in severe cases, laryngeal edema or bronchospasm may occur. Symptomatic treatment with antihistamines is usually enough, and there is usually no need to stop the transfusion. However, if anaphylaxis occurs, the transfusion should be stopped, and the patient should be administered adrenaline and treated according to the ALS protocol.

Transfusion-related acute lung injury (TRALI) is a severe complication characterized by non-cardiogenic pulmonary edema within 6 hours of transfusion. It is associated with antibodies in the donor blood reacting with recipient leukocyte antigens. This is the most common cause of death related to transfusion reactions. Treatment involves stopping the transfusion, administering oxygen, and providing aggressive respiratory support in approximately 75% of patients. Diuretic usage should be avoided.

Blunt abdominal trauma often results in injury to the liver and spleen, which are the two organs most commonly affected. The liver, being the largest and located in a vulnerable position, is particularly prone to injury in such cases.

Further Reading:

Abdominal trauma can be classified into two categories: blunt trauma and penetrating trauma. Blunt trauma occurs when compressive or deceleration forces are applied to the abdomen, often resulting from road traffic accidents or direct blows during sports. The spleen and liver are the organs most commonly injured in blunt abdominal trauma. On the other hand, penetrating trauma involves injuries that pierce the skin and enter the abdominal cavity, such as stabbings, gunshot wounds, or industrial accidents. The bowel and liver are the organs most commonly affected in penetrating injuries.

When it comes to imaging in blunt abdominal trauma, there are three main modalities that are commonly used: focused assessment with sonography in trauma (FAST), diagnostic peritoneal lavage (DPL), and computed tomography (CT). FAST is a non-invasive and quick method used to detect free intraperitoneal fluid, aiding in the decision on whether a laparotomy is needed. DPL is also used to detect intraperitoneal blood and can be used in both unstable blunt abdominal trauma and penetrating abdominal trauma. However, it is more invasive and time-consuming compared to FAST and has largely been replaced by it. CT, on the other hand, is the gold standard for diagnosing intra-abdominal pathology and is used in stable abdominal trauma patients. It offers high sensitivity and specificity but requires a stable and cooperative patient. It also involves radiation and may have delays in availability.

In the case of penetrating trauma, it is important to assess these injuries with the help of a surgical team. Penetrating objects should not be removed in the emergency department as they may be tamponading underlying vessels. Ideally, these injuries should be explored in the operating theater.

In summary, abdominal trauma can be classified into blunt trauma and penetrating trauma. Blunt trauma is caused by compressive or deceleration forces and commonly affects the spleen and liver. Penetrating trauma involves injuries that pierce the skin and commonly affect the bowel and liver. Imaging modalities such as FAST, DPL, and CT are used to assess and diagnose abdominal trauma, with CT being the gold standard. Penetrating injuries should be assessed by a surgical team and should ideally be explored in the operating theater.

Migraine without aura typically needs to meet the specific criteria set by the International Headache Society. These criteria include experiencing at least five attacks that meet the requirements outlined in criteria 2-4. The duration of these headache attacks should last between 4 to 72 hours. Additionally, the headache should exhibit at least two of the following characteristics: unilateral location, pulsating quality, moderate or severe pain intensity, and aggravation or avoidance of routine physical activity. Furthermore, during the headache, individuals should experience at least one of the following symptoms: nausea and/or vomiting, photophobia, and phonophobia. For more detailed information, you can refer to the guidelines provided by The British Association for the Study of Headache.

When a patient is semi-conscious, it is less likely for the nasopharyngeal airway adjuncts (NPA’s) to trigger the gag reflex compared to oropharyngeal airways. Therefore, NPA’s are typically the preferred option in these cases.

Further Reading:

Techniques to keep the airway open:

1. Suction: Used to remove obstructing material such as blood, vomit, secretions, and food debris from the oral cavity.

2. Chin lift manoeuvres: Involves lifting the head off the floor and lifting the chin to extend the head in relation to the neck. Improves alignment of the pharyngeal, laryngeal, and oral axes.

3. Jaw thrust: Used in trauma patients with cervical spine injury concerns. Fingers are placed under the mandible and gently pushed upward.

Airway adjuncts:

1. Oropharyngeal airway (OPA): Prevents the tongue from occluding the airway. Sized according to the patient by measuring from the incisor teeth to the angle of the mandible. Inserted with the tip facing backwards and rotated 180 degrees once it touches the back of the palate or oropharynx.

2. Nasopharyngeal airway (NPA): Useful when it is difficult to open the mouth or in semi-conscious patients. Sized by length (distance between nostril and tragus of the ear) and diameter (roughly that of the patient’s little finger). Contraindicated in basal skull and midface fractures.

Laryngeal mask airway (LMA):

– Supraglottic airway device used as a first line or rescue airway.
– Easy to insert, sized according to patient’s bodyweight.
– Advantages: Easy insertion, effective ventilation, some protection from aspiration.
– Disadvantages: Risk of hypoventilation, greater gastric inflation than endotracheal tube (ETT), risk of aspiration and laryngospasm.

Note: Proper training and assessment of the patient’s condition are essential for airway management.