The patient in this scenario is exhibiting a clinical sign known as paradoxical breathing. This is characterized by an abnormal movement of the chest wall during respiration. Normally, the chest expands during inhalation and contracts during exhalation. However, in paradoxical breathing, the opposite occurs. The chest wall moves inward during inhalation and outward during exhalation. This can be seen in cases of chest trauma or injury, where there is a disruption in the normal mechanics of breathing.

Further Reading:

Flail chest is a serious condition that occurs when multiple ribs are fractured in two or more places, causing a segment of the ribcage to no longer expand properly. This condition is typically caused by high-impact thoracic blunt trauma and is often accompanied by other significant injuries to the chest.

The main symptom of flail chest is a chest deformity, where the affected area moves in a paradoxical manner compared to the rest of the ribcage. This can cause chest pain and difficulty breathing, known as dyspnea. X-rays may also show evidence of lung contusion, indicating further damage to the chest.

In terms of management, conservative treatment is usually the first approach. This involves providing adequate pain relief and respiratory support to the patient. However, if there are associated injuries such as a pneumothorax or hemothorax, specific interventions like thoracostomy or surgery may be necessary.

Positive pressure ventilation can be used to provide internal splinting of the airways, helping to prevent atelectasis, a condition where the lungs collapse. Overall, prompt and appropriate management is crucial in order to prevent further complications and improve the patient’s outcome.

Cardiac arrest during pregnancy is a rare occurrence, happening in approximately 16 out of every 100,000 live births. It is crucial to consider both the mother and the fetus when dealing with cardiac arrest in pregnancy, as the best way to ensure a positive outcome for the fetus is by effectively resuscitating the mother.

The main causes of cardiac arrest during pregnancy include pre-existing cardiac disease, pulmonary embolism, hemorrhage, ectopic pregnancy, hypertensive disorders of pregnancy, amniotic fluid embolism, and suicide. Many cardiovascular problems associated with pregnancy are caused by compression of the inferior vena cava.

To prevent decompensation or potential cardiac arrest during pregnancy, it is important to follow these steps when dealing with a distressed or compromised pregnant patient:

– Place the patient in the left lateral position or manually displace the uterus to the left.
– Administer high-flow oxygen, guided by pulse oximetry.
– Give a fluid bolus if there is low blood pressure or signs of hypovolemia.
– Re-evaluate the need for any medications currently being administered.
– Seek expert help and involve obstetric and neonatal specialists early.
– Identify and treat the underlying cause.

In the event of cardiac arrest during pregnancy, in addition to following the standard guidelines for basic and advanced life support, the following modifications should be made:

– Immediately call for expert help, including an obstetrician, anesthetist, and neonatologist.
– Start CPR according to the standard ALS guidelines, but adjust the hand position slightly higher on the sternum.
– Ideally establish IV or IO access above the diaphragm to account for potential compression of the inferior vena cava.
– Manually displace the uterus to the left to relieve caval compression.
– Tilt the table to the left side (around 15-30 degrees of tilt).
– Perform early tracheal intubation to reduce the risk of aspiration (seek assistance from an expert anesthetist).
– Begin preparations for an emergency Caesarean section.

A perimortem Caesarean section should be performed within 5 minutes of the onset of cardiac arrest. This delivery will alleviate caval compression and increase the chances of successful resuscitation by improving venous return during CPR. It will also maximize the chances of the infant’s survival, as the best survival rate occurs when delivery is achieved within 5 minutes of the mother’s cardiac arrest.

For the treatment of men with lower urinary tract infection (UTI), it is recommended to offer an immediate prescription of antibiotics. However, certain factors should be taken into account. This includes considering previous urine culture and susceptibility results, as well as any history of antibiotic use that may have led to the development of resistant bacteria.

Before starting antibiotics, it is important to obtain a midstream urine sample from men and send it for culture and susceptibility testing. This will help determine the most appropriate choice of antibiotic.

Once the microbiological results are available, it is necessary to review the initial choice of antibiotic. If the bacteria are found to be resistant and symptoms are not improving, it is recommended to switch to a narrow-spectrum antibiotic whenever possible.

The first-choice antibiotics for men with lower UTI are trimethoprim 200 mg taken orally twice daily for 7 days, or nitrofurantoin 100 mg modified-release taken orally twice daily for 7 days if the estimated glomerular filtration rate (eGFR) is above 45 ml/minute.

If there is no improvement in lower UTI symptoms after at least 48 hours on the first-choice antibiotics, or if the first-choice is not suitable, it is important to consider alternative diagnoses and follow the recommendations in the NICE guidelines on pyelonephritis (acute): antimicrobial prescribing or prostatitis (acute): antimicrobial prescribing. The choice of antibiotic should be based on recent culture and susceptibility results.

A tension pneumothorax occurs when there is an air leak from the lung or chest wall that acts like a one-way valve. This causes air to build up in the pleural space without any way to escape. As a result, pressure in the pleural space increases and pushes the mediastinum into the opposite hemithorax. If left untreated, this can lead to cardiovascular instability, shock, and cardiac arrest.

The clinical features of tension pneumothorax include respiratory distress and cardiovascular instability. Tracheal deviation away from the side of the injury, unilateral absence of breath sounds on the affected side, and a hyper-resonant percussion note are also characteristic. Other signs include distended neck veins and cyanosis, which is a late sign. It’s important to note that both tension pneumothorax and massive haemothorax can cause decreased breath sounds on auscultation. However, percussion can help differentiate between the two conditions. Hyper-resonance suggests tension pneumothorax, while dullness suggests a massive haemothorax.

Tension pneumothorax is a clinical diagnosis and should not be delayed for radiological confirmation. Requesting a chest X-ray in this situation can delay treatment and put the patient at risk. Immediate decompression through needle thoracocentesis is the recommended treatment. Traditionally, a large-bore needle or cannula is inserted into the 2nd intercostal space in the midclavicular line of the affected hemithorax. However, studies on cadavers have shown better success in reaching the thoracic cavity when the 4th or 5th intercostal space in the midaxillary line is used in adult patients. ATLS now recommends this location for needle decompression in adults. The site for needle thoracocentesis in children remains the same, using the 2nd intercostal space in the midclavicular line. It’s important to remember that needle thoracocentesis is a temporary measure, and the insertion of a chest drain is the definitive treatment.

To ensure prompt response in case of an adverse reaction, it is important to have adrenaline, antihistamine, and steroid readily available when administering Zagreb antivenom.

Further Reading:

Snake bites in the UK are primarily caused by the adder, which is the only venomous snake species native to the country. While most adder bites result in minor symptoms such as pain, swelling, and inflammation, there have been cases of life-threatening illness and fatalities. Additionally, there are instances where venomous snakes that are kept legally or illegally also cause bites in the UK.

Adder bites typically occur from early spring to late autumn, with the hand being the most common site of the bite. Symptoms can be local or systemic, with local symptoms including sharp pain, tingling or numbness, and swelling that spreads proximally. Systemic symptoms may include spreading pain, tenderness, inflammation, regional lymph node enlargement, and bruising. In severe cases, anaphylaxis can occur, leading to symptoms such as nausea, vomiting, abdominal pain, diarrhea, and shock.

It is important for clinicians to be aware of the potential complications and complications associated with adder bites. These can include acute renal failure, pulmonary and cerebral edema, acute gastric dilatation, paralytic ileus, acute pancreatitis, and coma and seizures. Anaphylaxis symptoms can appear within minutes or be delayed for hours, and hypotension is a critical sign to monitor.

Initial investigations for adder bites include blood tests, ECG, and vital sign monitoring. Further investigations such as chest X-ray may be necessary based on clinical signs. Blood tests may reveal abnormalities such as leukocytosis, raised hematocrit, anemia, thrombocytopenia, and abnormal clotting profile. ECG changes may include tachyarrhythmias, bradyarrhythmias, atrial fibrillation, and ST segment changes.

First aid measures at the scene include immobilizing the patient and the bitten limb, avoiding aspirin and ibuprofen, and cleaning the wound site in the hospital. Tetanus prophylaxis should be considered. In cases of anaphylaxis, prompt administration of IM adrenaline is necessary. In the hospital, rapid assessment and appropriate resuscitation with intravenous fluids are required.

Antivenom may be indicated in cases of hypotension, systemic envenoming, ECG abnormalities, peripheral neutrophil leucocytosis, elevated serum creatine kinase or metabolic acidosis, and extensive or rapidly spreading local swelling. Zagreb antivenom is commonly used in the UK, with an initial dose of 8 mL.

The current algorithm for the treatment of a convulsing child, known as APLS, is as follows:

Step 1 (5 minutes after the start of convulsion):
If a child has been convulsing for 5 minutes or more, the initial dose of benzodiazepine should be administered. This can be done by giving Lorazepam at a dose of 0.1 mg/kg intravenously (IV) or intraosseously (IO) if vascular access is available. Alternatively, buccal midazolam at a dose of 0.5 mg/kg or rectal diazepam at a dose of 0.5 mg/kg can be given if vascular access is not available.

Step 2 (10 minutes after the start of Step 1):
If the convulsion continues for a further 10 minutes, a second dose of benzodiazepine should be given. It is also important to summon senior help at this point.

Step 3 (10 minutes after the start of Step 2):
At this stage, it is necessary to involve senior help to reassess the child and provide guidance on further management. The recommended approach is as follows:
– If the child is not already on phenytoin, a phenytoin infusion should be initiated. This involves administering 20 mg/kg of phenytoin intravenously over a period of 20 minutes.
– If the child is already taking phenytoin, phenobarbitone can be used as an alternative. The recommended dose is 20 mg/kg administered intravenously over 20 minutes.
– In the meantime, rectal paraldehyde can be considered at a dose of 0.8 ml/kg of the 50:50 mixture while preparing the infusion.

Step 4 (20 minutes after the start of Step 3):
If the child is still experiencing convulsions at this stage, it is crucial to have an anaesthetist present. A rapid sequence induction with thiopental is recommended for further management.

Please note that this algorithm is subject to change based on individual patient circumstances and the guidance of medical professionals.

The PaO2/FiO2 ratio is a measurement used to determine the severity of Acute Respiratory Distress Syndrome (ARDS). It is calculated by dividing the arterial oxygen partial pressure (PaO2) by the fraction of inspired oxygen (FiO2). However, it is important to note that this calculation should only be done when the patient is receiving a minimum positive end-expiratory pressure (PEEP) of 5 cm water. The resulting ratio is then used to classify the severity of ARDS, with specific thresholds provided below.

Further Reading:

ARDS is a severe form of lung injury that occurs in patients with a predisposing risk factor. It is characterized by the onset of respiratory symptoms within 7 days of a known clinical insult, bilateral opacities on chest X-ray, and respiratory failure that cannot be fully explained by cardiac failure or fluid overload. Hypoxemia is also present, as indicated by a specific threshold of the PaO2/FiO2 ratio measured with a minimum requirement of positive end-expiratory pressure (PEEP) ≥5 cm H2O. The severity of ARDS is classified based on the PaO2/FiO2 ratio, with mild, moderate, and severe categories.

Lung protective ventilation is a set of measures aimed at reducing lung damage that may occur as a result of mechanical ventilation. Mechanical ventilation can cause lung damage through various mechanisms, including high air pressure exerted on lung tissues (barotrauma), over distending the lung (volutrauma), repeated opening and closing of lung units (atelectrauma), and the release of inflammatory mediators that can induce lung injury (biotrauma). These mechanisms collectively contribute to ventilator-induced lung injury (VILI).

The key components of lung protective ventilation include using low tidal volumes (5-8 ml/kg), maintaining inspiratory pressures (plateau pressure) below 30 cm of water, and allowing for permissible hypercapnia. However, there are some contraindications to lung protective ventilation, such as an unacceptable level of hypercapnia, acidosis, and hypoxemia. These factors need to be carefully considered when implementing lung protective ventilation strategies in patients with ARDS.

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.

Amiodarone is a medication that can have numerous harmful side effects, making it crucial to conduct a comprehensive clinical assessment before starting treatment with it. Some of the side effects associated with amiodarone include corneal microdeposits, photosensitivity, nausea, sleep disturbance, hyperthyroidism, hypothyroidism, acute hepatitis and jaundice, peripheral neuropathy, lung fibrosis, QT prolongation, and optic neuritis (although this is very rare). If optic neuritis occurs, immediate discontinuation of amiodarone is necessary to prevent the risk of blindness.

The majority of patients taking amiodarone experience corneal microdeposits, but these typically resolve after treatment is stopped and rarely affect vision. Amiodarone has a chemical structure similar to thyroxine and can bind to the nuclear thyroid receptor, leading to both hypothyroidism and hyperthyroidism. However, hypothyroidism is more commonly observed, affecting around 5-10% of patients.

A surgical cricothyroidotomy is a procedure performed in emergency situations to secure the airway by making an incision in the cricothyroid membrane. It is also known as an emergency surgical airway (ESA) and is typically done when intubation and oxygenation are not possible.

There are certain conditions in which a surgical cricothyroidotomy should not be performed. These include patients who are under 12 years old, those with laryngeal fractures or pre-existing or acute laryngeal pathology, individuals with tracheal transection and retraction of the trachea into the mediastinum, and cases where the anatomical landmarks are obscured due to trauma.

The procedure is carried out in the following steps:
1. Gathering and preparing the necessary equipment.
2. Positioning the patient on their back with the neck in a neutral position.
3. Sterilizing the patient’s neck using antiseptic swabs.
4. Administering local anesthesia, if time permits.
5. Locating the cricothyroid membrane, which is situated between the thyroid and cricoid cartilage.
6. Stabilizing the trachea with the left hand until it can be intubated.
7. Making a transverse incision through the cricothyroid membrane.
8. Inserting the scalpel handle into the incision and rotating it 90°. Alternatively, a haemostat can be used to open the airway.
9. Placing a properly-sized, cuffed endotracheal tube (usually a size 5 or 6) into the incision, directing it into the trachea.
10. Inflating the cuff and providing ventilation.
11. Monitoring for chest rise and auscultating the chest to ensure adequate ventilation.
12. Securing the airway to prevent displacement.

Potential complications of a surgical cricothyroidotomy include aspiration of blood, creation of a false passage into the tissues, subglottic stenosis or edema, laryngeal stenosis, hemorrhage or hematoma formation, laceration of the esophagus or trachea, mediastinal emphysema, and vocal cord paralysis or hoarseness.

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.

When patients are exposed to the inhalation of combustion byproducts, they face the danger of being poisoned by carbon monoxide and cyanide. In situations where hydrocarbons and substances containing carbon and nitrogen are incompletely burned, the formation of both carbon monoxide and cyanide gas can occur. Individuals who inhale smoke are particularly vulnerable to this type of poisoning.

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 initial stage of SJS is characterized by a rash on the skin, specifically on the macular area. As the condition progresses, the rash transforms into blisters, known as bullae, which eventually detach from the skin.

Further Reading:

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe mucocutaneous immune reactions characterized by blistering skin rash and erosions/ulceration of mucous membranes. SJS has less than 10% total body surface area (TBSA) involvement, SJS/TEN overlap has 10% to 30% TBSA involvement, and TEN has more than 30% TBSA involvement. The exact cause of SJS and TEN is not well understood, but it is believed to be a T-cell–mediated cytotoxic reaction triggered by drugs, infections, or vaccinations. Drugs are responsible for 50% of SJS cases and up to 95% of TEN cases, with antibiotics and anticonvulsants being the most common culprits.

The clinical features of SJS and TEN include a prodrome of malaise, fever, headache, and cough, followed by the appearance of small pink-red macules with darker centers. These macules can coalesce and develop into larger blisters (bullae) that eventually break and cause the epidermis to slough off. Painful mucosal erosions can also occur, affecting various parts of the body and leading to complications such as renal failure, hepatitis, pneumonia, and urethritis. Nikolsky’s sign, which refers to the easy sloughing off of the epidermal layer with pressure, is a characteristic feature of SJS and TEN.

The diagnosis of SJS, SJS/TEN overlap, and TEN can be confirmed through a skin biopsy, which typically shows desquamation at the epidermal-papillary dermal junction and the presence of necrotic epithelium and lymphocytes. Management of SJS and TEN involves supportive care, withdrawal of the causative agent if drug-related, monitoring for metabolic derangement and infection, maintaining the airway, treating respiratory function and pneumonia, fluid resuscitation, wound care, analgesia, and nutritional support. Ophthalmology consultation is also recommended. Intravenous immunoglobulin, ciclosporin, corticosteroids, and plasmapheresis may be used in treatment, but there is limited evidence supporting their effectiveness.

The prognosis of SJS and TEN can be assessed using the SCORTEN score, which comprises of 7 clinical and biological parameters, with the predicted probability of mortality ranging from 3.2% to 90.0%.

The traffic light system is a useful tool for evaluating the potential risk of serious illness in children. This system categorizes clinical features into three groups based on severity: red (high-risk), amber (intermediate-risk), and green (low-risk).

Children displaying any of the following symptoms or signs fall into the high-risk group for serious illness: pale/mottled/ashen/blue skin, lips or tongue; lack of response to social cues; appearing unwell to a healthcare professional; inability to wake or stay awake when roused; weak, high-pitched, or continuous cry; grunting; respiratory rate exceeding 60 breaths per minute; moderate or severe chest indrawing; reduced skin turgor; and bulging fontanelle.

Children exhibiting any of the following symptoms or signs are considered at least intermediate-risk for serious illness: pallor of skin, lips or tongue reported by parent or caregiver; abnormal response to social cues; absence of a smile; waking only with prolonged stimulation; decreased activity; nasal flaring; dry mucous membranes; poor feeding in infants; reduced urine output; and rigors.

Children displaying any of the following symptoms or signs are classified as low-risk for serious illness: normal color of skin, lips, and tongue; normal response to social cues; contentment and smiles; staying awake or quickly awakening; strong normal cry or absence of crying; normal skin and eyes; and moist mucous membranes.

To summarize, children with fever and any symptoms or signs in the red column are considered high-risk, while those with fever and any symptoms or signs in the amber column (but none in the red column) are considered intermediate-risk. Children with symptoms and signs in the green column (and none in the amber or red columns) are classified as low-risk.

For more information, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

Differentiating between the various causes of vertigo can be challenging, but there are several clues in the question that can help determine the most likely cause. The sudden onset of severe fixed vertigo, not related to position, following a sinus infection suggests vestibular neuronitis rather than labyrinthitis. Vestibular neuronitis is typically characterized by severe vertigo without hearing loss or tinnitus.

Here are the key clinical features of the different causes of vertigo mentioned in the question:

Vestibular neuronitis:
– Infection of the 8th cranial nerve, which can be viral or bacterial
– Often preceded by a sinus infection or upper respiratory tract infection
– Severe vertigo
– Vertigo is not related to position
– No hearing loss or tinnitus
– Nausea and vomiting are common
– Nystagmus (involuntary eye movement) away from the side of the lesion
– Episodes may recur over an 18-month period

Labyrinthitis:
– Usually caused by a viral infection
– Can affect the entire inner ear and 8th cranial nerve
– Severe vertigo
– Vertigo can be related to position
– May be accompanied by sensorineural hearing loss and tinnitus
– Nausea and vomiting are common
– Nystagmus away from the side of the lesion

Benign positional vertigo:
– Often idiopathic (no known cause)
– Can be secondary to trauma or other inner ear disorders
– Triggered by head movement, rolling over, or looking upward
– Brief episodes lasting less than 5 minutes
– No hearing loss or tinnitus
– Nausea is common, vomiting is rare
– Positive Hallpike maneuver (a diagnostic test)

Meniere’s disease:
– Idiopathic (no known cause)
– Sensorineural hearing loss
– Hearing loss usually gradually progressive and affects one ear
– Associated with tinnitus
– Vertigo attacks typically last 2-3 hours
– Attacks of vertigo last less than 24 hours
– Sensation of fullness or pressure in the ear(s)
– Nausea and vomiting are common
– Nystagmus away from the side of the lesion
– More common in individuals with migraines

Acoustic neuroma:
– Benign tumor of the 8th cranial nerve in the brain
– Gradually worsening unilateral sensorineural hearing loss
– Facial numbness and tingling

In order to achieve satisfactory bronchodilation, most individuals require a plasma theophylline concentration of 10-20 mg/litre (55-110 micromol/litre). However, it is possible for a lower concentration to still be effective. Adverse effects can occur within the range of 10-20 mg/litre, and their frequency and severity increase when concentrations exceed 20 mg/litre.

To measure plasma theophylline concentration, a blood sample should be taken five days after starting oral treatment and at least three days after any dose adjustment. For modified-release preparations, the blood sample should typically be taken 4-6 hours after an oral dose (specific sampling times may vary, so it is advisable to consult local guidelines). If aminophylline is administered intravenously, a blood sample should be taken 4-6 hours after initiating treatment.

An elevated pH (normal range 7.34-7.45) suggests alkalosis. A low pCO2 (normal range 4.4-6.0 Kpa) indicates that the respiratory system is causing the alkalosis. The metabolic system, on the other hand, is not contributing to either alkalosis or acidosis as both the bicarbonate and base excess levels are within the normal ranges.

Further Reading:

Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.

The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.

When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.

To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.

Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.

In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.

Pregnant women who contract chickenpox for the first time are more likely to develop pneumonitis, a condition characterized by inflammation of the lungs. Additionally, these women face a five-fold increased risk of pneumonitis compared to non-pregnant individuals. Furthermore, the fetus is at risk of developing fetal varicella syndrome, a condition associated with chickenpox infection during pregnancy.

Further Reading:

Chickenpox exposure during pregnancy poses risks to both the mother and the fetus. The mother has a 5 times greater risk of developing pneumonitis, a potentially serious complication. The fetus is at risk of developing fetal varicella syndrome (FVS) if the maternal exposure occurs before 20 weeks gestation. The risk of FVS is around 1% in these cases and includes features such as skin scarring, eye defects, limb hypoplasia, microcephaly, and learning disabilities. There have been very few cases of FVS reported between 20-28 weeks gestation and none following 28 weeks.

Other risks to the fetus include the development of shingles in infancy, which has a 1-2% risk if the maternal exposure occurs in the second or third trimester. There is also a risk of severe neonatal varicella if the mother develops a rash between 5 days before and 2 days after birth. This condition can be fatal to the newborn child in around 20% of cases.

In the management of chickenpox exposure during pregnancy, it is important to determine if the mother is immune to varicella. If there is any doubt, maternal blood should be urgently checked for varicella antibodies. If the pregnant woman is not immune, she should be given varicella zoster immunoglobulin (VZIG) as soon as possible. VZIG is considered effective up to 10 days post-exposure. Consensus guidelines also recommend the use of oral aciclovir if the pregnant woman presents with chickenpox within 24 hours of the rash onset.

Rhabdomyolysis leads to an increase in phosphate levels in the blood, which in turn causes a decrease in the levels of ionized calcium. On the other hand, conditions such as Addison’s disease, hyperthyroidism, the use of thiazide diuretics, and lithium can all contribute to an elevation in calcium levels. There are also other factors that can result in low calcium levels, including hypoparathyroidism, a deficiency of vitamin D, sepsis, fluoride poisoning, a lack of magnesium, renal failure, tumor lysis syndrome, pancreatitis, and the administration of EDTA infusions.

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 temperatures, a process known as pyrolysis, and then concentrating it with a zinc chloride solution. This creates a network of pores within the charcoal, giving it a large absorptive area of approximately 3,000 m2/g. This porous structure helps prevent the absorption of the harmful toxin by up to 50%.

The usual dosage 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 give the charcoal 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. If the patient is unconscious or in a coma, there is a risk of aspiration, so the charcoal should not be given. Similarly, if seizures are likely to occur, there is a risk of aspiration and the charcoal should be avoided. Additionally, if there is reduced gastrointestinal motility, there is a risk of obstruction, so activated charcoal should not be used in such cases.

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

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

The supraspinatus muscle is a small muscle located in the upper back. It extends from the supraspinatus fossa of the scapula to the greater tubercle of the humerus. This muscle is part of the rotator cuff, along with three other muscles. The supraspinatus muscle is innervated by the suprascapular nerve, which also innervates the infraspinatus muscle. The suprascapular nerve originates from the upper trunk of the brachial plexus.

The main function of the supraspinatus muscle is to assist the deltoid muscle in abducting the arm at the shoulder joint. Specifically, it is responsible for the initial 15 degrees of arm abduction. Beyond this range, the deltoid muscle takes over as the primary abductor.

In addition to its role in arm movement, the supraspinatus muscle works together with the other rotator cuff muscles to stabilize the shoulder joint. It helps keep the humeral head in the glenoid fossa and counteracts the downward gravitational forces exerted on the shoulder joint by the weight of the arm.

One common test used to assess the supraspinatus muscle is called the empty can test. During this test, the patient is positioned either standing or sitting, with their arms raised parallel to the ground in the scapular plane. The arm is then internally rotated fully, with the thumb facing downward. The clinician applies downward pressure on either the wrists or the elbow, while the patient resists this pressure. If the patient experiences weakness, pain, or both during this resistance, it indicates a possible tear in the supraspinatus tendon or muscle, or a suprascapular nerve neuropathy.

Spironolactone, a potassium sparing diuretic, is the preferred initial treatment for ascites. Ascites triggers the renin-angiotensin-aldosterone system (RAAS), causing sodium retention (Hypernatraemia) and potassium excretion (Hypokalaemia). By blocking aldosterone, spironolactone helps to counteract these effects. Other diuretics can worsen potassium deficiency, so close monitoring of electrolyte levels is necessary if they are used instead.

Further Reading:

Cirrhosis is a condition where the liver undergoes structural changes, resulting in dysfunction of its normal functions. It can be classified as either compensated or decompensated. Compensated cirrhosis refers to a stage where the liver can still function effectively with minimal symptoms, while decompensated cirrhosis is when the liver damage is severe and clinical complications are present.

Cirrhosis develops over a period of several years due to repeated insults to the liver. Risk factors for cirrhosis include alcohol misuse, hepatitis B and C infection, obesity, type 2 diabetes, autoimmune liver disease, genetic conditions, certain medications, and other rare conditions.

The prognosis of cirrhosis can be assessed using the Child-Pugh score, which predicts mortality based on parameters such as bilirubin levels, albumin levels, INR, ascites, and encephalopathy. The score ranges from A to C, with higher scores indicating a poorer prognosis.

Complications of cirrhosis include portal hypertension, ascites, hepatic encephalopathy, variceal hemorrhage, increased infection risk, hepatocellular carcinoma, and cardiovascular complications.

Diagnosis of cirrhosis is typically done through liver function tests, blood tests, viral hepatitis screening, and imaging techniques such as transient elastography or acoustic radiation force impulse imaging. Liver biopsy may also be performed in some cases.

Management of cirrhosis involves treating the underlying cause, controlling risk factors, and monitoring for complications. Complications such as ascites, spontaneous bacterial peritonitis, oesophageal varices, and hepatic encephalopathy require specific management strategies.

Overall, cirrhosis is a progressive condition that requires ongoing monitoring and management to prevent further complications and improve outcomes for patients.

In infants who are less than 4 weeks old, it is recommended to measure their body temperature using an electronic thermometer placed in the armpit.

For children between the ages of 4 weeks and 5 years, there are several methods that can be used to measure body temperature. These include using an electronic thermometer in the armpit, a chemical dot thermometer in the armpit, or an infra-red tympanic thermometer.

It is important to note that measuring temperature orally or rectally should be avoided in this age group. Additionally, forehead chemical thermometers are not reliable and should not be used.

Propofol, also known as 2,6-diisopropylphenol, is commonly used to induce anesthesia due to its short-acting properties. The exact way in which it works is not fully understood, but it is believed to enhance the effects of the inhibitory neurotransmitters GABA and glycine. This, in turn, strengthens spinal inhibition during the anesthesia process.

Intussusception occurs when a section of the bowel folds into another section, causing a blockage. This can be due to a specific underlying issue, like a Meckel’s diverticulum, or it can happen without any specific cause. The condition is most commonly seen in boys between the ages of 5 and 10 months. Symptoms include sudden vomiting and episodes of abdominal pain that come and go. The vomit quickly becomes greenish-yellow in color. Dance’s sign, which is the absence of bowel in the lower right part of the abdomen, may be observed. Redcurrant jelly-like stools are a late indication of the condition. It is believed that more than 90% of cases are caused by a non-specific underlying issue, often viral infections like rotavirus, adenovirus, and human herpesvirus 6.

Prolongation of the QT interval can lead to a dangerous ventricular arrhythmia called torsades de pointes, which can result in sudden cardiac death. There are several commonly used medications that are known to cause QT prolongation.

Low levels of potassium (hypokalaemia) and magnesium (hypomagnesaemia) can increase the risk of QT prolongation. For example, diuretics can interact with QT-prolonging drugs by causing hypokalaemia.

The QT interval varies with heart rate, and formulas are used to correct the QT interval for heart rate. Once corrected, it is referred to as the QTc interval. The QTc interval is typically reported on the ECG printout. A normal QTc interval is less than 440 ms.

If the QTc interval is greater than 440 ms but less than 500 ms, it is considered borderline. Although there may be some variation in the literature, a QTc interval within these values is generally considered borderline prolonged. In such cases, it is important to consider reducing the dose of QT-prolonging drugs or switching to an alternative medication that does not prolong the QT interval.

A prolonged QTc interval exceeding 500 ms is clinically significant and is likely to increase the risk of arrhythmia. Any medications that prolong the QT interval should be reviewed immediately.

Here are some commonly encountered drugs that are known to prolong the QT interval:

Antimicrobials:
– Erythromycin
– Clarithromycin
– Moxifloxacin
– Fluconazole
– Ketoconazole

Antiarrhythmics:
– Dronedarone
– Sotalol
– Quinidine
– Amiodarone
– Flecainide

Antipsychotics:
– Risperidone
– Fluphenazine
– Haloperidol
– Pimozide
– Chlorpromazine
– Quetiapine
– Clozapine

Antidepressants:
– Citalopram/escitalopram
– Amitriptyline
– Clomipramine
– Dosulepin
– Doxepin
– Imipramine
– Lofepramine

Antiemetics:
– Domperidone
– Droperidol
– Ondansetron/Granisetron

Others:
– Methadone
– Protein kinase inhibitors (e.g. sunitinib)

The use of NSAIDs during the third trimester of pregnancy is associated with several risks. These risks include delayed onset of labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus, which is a condition characterized by bilirubin-induced brain dysfunction. Additionally, there is a slight increase in the risk of first-trimester abortion if NSAIDs are used early in pregnancy.

Below is a list outlining the most commonly encountered drugs that have adverse effects during pregnancy:

Drug: ACE inhibitors (e.g. ramipril)
Adverse effects: If given in the second and third trimester, ACE inhibitors can cause hypoperfusion, renal failure, and the oligohydramnios sequence.

Drug: Aminoglycosides (e.g. gentamicin)
Adverse effects: Aminoglycosides can cause ototoxicity, leading to deafness in the fetus.

Drug: Aspirin
Adverse effects: High doses of aspirin can cause first-trimester abortions, delayed onset of labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g. 75 mg) have no significant associated risk.

Drug: Benzodiazepines (e.g. diazepam)
Adverse effects: When given late in pregnancy, benzodiazepines can cause respiratory depression and a neonatal withdrawal syndrome.

Drug: Calcium-channel blockers
Adverse effects: If given in the first trimester, calcium-channel blockers can cause phalangeal abnormalities. If given in the second and third trimester, they can cause fetal growth retardation.

Chancroid is a sexually transmitted infection caused by the bacteria Haemophilus ducreyi. It is not very common in the UK but is prevalent in Africa, Asia, and South America. HIV is often associated with chancroid, particularly in Africa where there is a 60% correlation.

The main symptom of chancroid is the development of painful ulcers on the genitalia. In women, these ulcers typically appear on the labia majora. Sometimes, kissing ulcers can form when ulcers are located on opposing surfaces of the labia. Painful swelling of the lymph nodes occurs in 30-60% of patients, and in some cases, these swollen nodes can turn into abscesses known as buboes.

The CDC recommends treating chancroid with a single oral dose of 1 gram of azithromycin or a single intramuscular dose of ceftriaxone. Alternatively, a 7-day course of oral erythromycin can be used. It’s important to note that Haemophilus ducreyi is resistant to several antibiotics, including penicillins, tetracyclines, trimethoprim, ciprofloxacin, aminoglycosides, and sulfonamides.

Possible complications of chancroid include extensive swelling of the lymph nodes, large abscesses and sinuses in the groin area, phimosis (a condition where the foreskin cannot be retracted), and superinfection with Fusarium spp. or Bacteroides spp.

Syphilis, caused by Treponema pallidum, presents with a painless ulcer called a chancre during its primary stage. This is different from chancroid, which causes painful ulcers. Chlamydia trachomatis can lead to lymphogranuloma venereum, where a painless genital ulcer may develop initially and go unnoticed. Granuloma inguinale, caused by Klebsiella granulomatis, causes painless nodules and ulcers on the genitals that eventually burst and create open, oozing lesions. Neisseria gonorrhoeae, on the other hand, typically causes vaginal or urethral discharge and is often asymptomatic, rather than causing genital ulceration.

According to the ALS algorithm, the main drugs used during CPR are oxygen, adrenaline, and amiodarone. Adrenaline is administered every 3-5 minutes as per the 2021 UK ALS algorithm. Amiodarone is given after 3 shocks.

Further Reading:

In the event of an adult experiencing cardiorespiratory arrest, it is crucial for doctors to be familiar with the Advanced Life Support (ALS) algorithm. They should also be knowledgeable about the proper technique for chest compressions, the appropriate rhythms for defibrillation, the reversible causes of arrest, and the drugs used in advanced life support.

During chest compressions, the rate should be between 100-120 compressions per minute, with a depth of compression of 5-6 cm. The ratio of chest compressions to rescue breaths should be 30:2. It is important to change the person giving compressions regularly to prevent fatigue.

There are two shockable ECG rhythms that doctors should be aware of: ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT). These rhythms require defibrillation.

There are four reversible causes of cardiorespiratory arrest, known as the 4 H’s and 4 T’s. The 4 H’s include hypoxia, hypovolemia, hypo or hyperkalemia or metabolic abnormalities, and hypothermia. The 4 T’s include thrombosis (coronary or pulmonary), tension pneumothorax, tamponade, and toxins. Identifying and treating these reversible causes is crucial for successful resuscitation.

When it comes to resus drugs, they are considered of secondary importance during CPR due to the lack of high-quality evidence for their efficacy. However, adrenaline (epinephrine) and amiodarone are the two drugs included in the ALS algorithm. Doctors should be familiar with the dosing, route, and timing of administration for both drugs.

Adrenaline should be administered intravenously at a concentration of 1 in 10,000 (100 micrograms/mL). It should be repeated every 3-5 minutes. Amiodarone is initially given at a dose of 300 mg, either from a pre-filled syringe or diluted in 20 mL of Glucose 5%. If required, an additional dose of 150 mg can be given by intravenous injection. This is followed by an intravenous infusion of 900 mg over 24 hours. The first dose of amiodarone is given after 3 shocks.

Some reversible metabolic causes of bradycardia include hypothyroidism, hyperkalaemia, hypermagnesemia, and hypothermia. These conditions can lead to a slow heart rate and can be treated or reversed.

Further Reading:

Causes of Bradycardia:
– Physiological: Athletes, sleeping
– Cardiac conduction dysfunction: Atrioventricular block, sinus node disease
– Vasovagal & autonomic mediated: Vasovagal episodes, carotid sinus hypersensitivity
– Hypothermia
– Metabolic & electrolyte disturbances: Hypothyroidism, hyperkalaemia, hypermagnesemia
– Drugs: Beta-blockers, calcium channel blockers, digoxin, amiodarone
– Head injury: Cushing’s response
– Infections: Endocarditis
– Other: Sarcoidosis, amyloidosis

Presenting symptoms of Bradycardia:
– Presyncope (dizziness, lightheadedness)
– Syncope
– Breathlessness
– Weakness
– Chest pain
– Nausea

Management of Bradycardia:
– Assess and monitor for adverse features (shock, syncope, myocardial ischaemia, heart failure)
– Treat reversible causes of bradycardia
– Pharmacological treatment: Atropine is first-line, adrenaline and isoprenaline are second-line
– Transcutaneous pacing if atropine is ineffective
– Other drugs that may be used: Aminophylline, dopamine, glucagon, glycopyrrolate

Bradycardia Algorithm:
– Follow the algorithm for management of bradycardia, which includes assessing and monitoring for adverse features, treating reversible causes, and using appropriate medications or pacing as needed.
https://acls-algorithms.com/wp-content/uploads/2020/12/Website-Bradycardia-Algorithm-Diagram.pdf

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.

Fractures that extend into the calcaneocuboid joint are commonly intra-articular. It is recommended to refer patients to orthopaedics for further evaluation and treatment. Conservative management usually involves keeping the patient non-weight bearing for a period of 6-12 weeks.

Further Reading:

Calcaneus fractures are a common type of lower limb and joint injury. The calcaneus, or heel bone, is the most frequently fractured tarsal bone. These fractures are often intra-articular, meaning they involve the joint. The most common cause of calcaneus fractures is a fall or jump from a height.

When assessing calcaneus fractures, X-rays are used to visualize the fracture lines. Two angles are commonly assessed to determine the severity of the fracture. Böhler’s angle, which measures the angle between two tangent lines drawn across the anterior and posterior borders of the calcaneus, should be between 20-40 degrees. If it is less than 20 degrees, it indicates a calcaneal fracture with flattening. The angle of Gissane, which measures the depression of the posterior facet of the subtalar joint, should be between 120-145 degrees. An increased angle of Gissane suggests a calcaneal fracture.

In the emergency department, the management of a fractured calcaneus involves identifying the injury and any associated injuries, providing pain relief, elevating the affected limb(s), and referring the patient to an orthopedic specialist. It is important to be aware that calcaneus fractures are often accompanied by other injuries, such as bilateral fractures of vertebral fractures.

The definitive management of a fractured calcaneus can be done conservatively or through surgery, specifically open reduction internal fixation (ORIF). The orthopedic team will typically order a CT or MRI scan to classify the fracture and determine the most appropriate treatment. However, a recent UK heel fracture trial suggests that in most cases, ORIF does not improve fracture outcomes.

The therapeutic range for theophylline is quite limited, ranging from 10 to 20 micrograms per milliliter (10-20 mg/L). It is important to estimate the plasma concentration of aminophylline during long-term treatment as it can provide valuable information.

Hyperkalaemia can be identified by certain signs, such as muscle weakness, cramps, and delayed deep tendon reflexes. Additionally, there are neurological signs that may be present, including flaccid paralysis, twitching, peripheral paresthesia, weakness, and hypo-reflexia.

Further Reading:

Vasoactive drugs can be classified into three categories: inotropes, vasopressors, and unclassified. Inotropes are drugs that alter the force of muscular contraction, particularly in the heart. They primarily stimulate adrenergic receptors and increase myocardial contractility. Commonly used inotropes include adrenaline, dobutamine, dopamine, isoprenaline, and ephedrine.

Vasopressors, on the other hand, increase systemic vascular resistance (SVR) by stimulating alpha-1 receptors, causing vasoconstriction. This leads to an increase in blood pressure. Commonly used vasopressors include norepinephrine, metaraminol, phenylephrine, and vasopressin.

Electrolytes, such as potassium, are essential for proper bodily function. Solutions containing potassium are often given to patients to prevent or treat hypokalemia (low potassium levels). However, administering too much potassium can lead to hyperkalemia (high potassium levels), which can cause dangerous arrhythmias. It is important to monitor potassium levels and administer it at a controlled rate to avoid complications.

Hyperkalemia can be caused by various factors, including excessive potassium intake, decreased renal excretion, endocrine disorders, certain medications, metabolic acidosis, tissue destruction, and massive blood transfusion. It can present with cardiovascular, respiratory, gastrointestinal, and neuromuscular symptoms. ECG changes, such as tall tented T-waves, prolonged PR interval, flat P-waves, widened QRS complex, and sine wave, are also characteristic of hyperkalemia.

In summary, vasoactive drugs can be categorized as inotropes, vasopressors, or unclassified. Inotropes increase myocardial contractility, while vasopressors increase systemic vascular resistance. Electrolytes, particularly potassium, are important for bodily function, but administering too much can lead to hyperkalemia. Monitoring potassium levels and ECG changes is crucial in managing hyperkalemia.

The Seidel test is a method used to assess ocular trauma. The procedure involves applying a 10% fluorescein strip to the affected area and examining it using a cobalt blue filter. If there is a corneal laceration with leakage of aqueous fluid, the dye will be diluted by the fluid, resulting in a visible stream.

In addition to the Seidel test, there are several other important steps to be taken during an eye examination for trauma. These include inspecting the overall appearance of the eye, examining the lids and peri-orbital bones, assessing visual acuity in both eyes, testing visual fields by confrontation, evaluating eye movements, measuring pupil size and response to light and accommodation, checking for foreign bodies using a slit lamp, performing fundoscopy and assessing the red reflex.

The Amsler grid test is a useful tool for detecting central visual field defects and aiding in the diagnosis of age-related macular degeneration. A positive Amsler test is indicated by the appearance of curved or wavy lines on the grid.

Tonometry is a technique used to measure intraocular pressure (IOP), which is helpful in diagnosing glaucoma.

Retinal photography is a sophisticated imaging process that involves using a digital camera to capture detailed pictures of the retina. It is primarily used to document the health of various structures in the eye, such as the optic nerve, posterior pole, macula, retina, and its blood vessels. However, it is not typically used as part of the initial evaluation for trauma.

Eye pH measurement is a valuable tool in evaluating chemical eye injuries.

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 explanation states that the increased activity of the enzyme kininogenase is caused by hormonal factors, specifically oestrogen, as well as genetic factors.

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.

To minimize the risk of infection and promote proper healing, the best approach for preparing the skin would be to clean it for 30 seconds with 2% chlorhexidine gluconate in 70% alcohol. This solution has been shown to effectively kill bacteria and reduce the risk of infection. Other options such as povidone-iodine, 90% isopropyl alcohol, and 30% isopropyl alcohol may also have some antimicrobial properties, but they are not as effective as chlorhexidine gluconate.

Further Reading:

Peripheral venous cannulation is a procedure that should be performed following established guidelines to minimize the risk of infection, injury, extravasation, and early failure of the cannula. It is important to maintain good hand hygiene, use personal protective equipment, ensure sharps safety, and employ an aseptic non-touch technique during the procedure.

According to the National Institute for Health and Care Excellence (NICE), the skin should be disinfected with a solution of 2% chlorhexidine gluconate and 70% alcohol before inserting the catheter. It is crucial to allow the disinfectant to completely dry before inserting the cannula.

The flow rates of IV cannulas can vary depending on factors such as the gauge, color, type of fluid used, presence of a bio-connector, length of the cannula, and whether the fluid is drained under gravity or pumped under pressure. However, the following are typical flow rates for different gauge sizes: 14 gauge (orange) has a flow rate of 270 ml/minute, 16 gauge (grey) has a flow rate of 180 ml/minute, 18 gauge (green) has a flow rate of 90 ml/minute, 20 gauge (pink) has a flow rate of 60 ml/minute, and 22 gauge (blue) has a flow rate of 36 ml/minute. These flow rates are based on infusing 1000 ml of normal saline under ideal circumstances, but they may vary in practice.

Cardiac enzymes do not increase in unstable angina. However, if cardiac markers do rise, it is classified as a non-ST elevation myocardial infarction (NSTEMI). Both unstable angina and NSTEMI can have a normal ECG. An extended ventricular activation time indicates damage to the heart muscle. This occurs because infarcting myocardium conducts electrical impulses at a slower pace, resulting in a prolonged interval between the start of the QRS complex and the apex of the R wave. A positive troponin test indicates the presence of necrosis in cardiac myocytes.

Summary:
Marker | Initial Rise | Peak | Normal at
Creatine kinase | 4-8 hours | 18 hours 2-3 days | CK-MB = main cardiac isoenzyme
Myoglobin | 1-4 hours | 6-7 hours | 24 hours | Low specificity due to skeletal muscle damage
Troponin I | 3-12 hours | 24 hours | 3-10 days | Appears to be the most sensitive and specific
HFABP | 1-2 hours | 5-10 hours | 24 hours | HFABP = heart fatty acid binding protein
LDH | 10 hours | 24-48 hours | 14 days | Cardiac muscle mainly contains LDH

Gout is a form of arthritis that causes a swollen, tender, red, and hot joint. Initially, it was believed to primarily affect wealthy individuals due to dietary connections, but it is now becoming more prevalent and is estimated to impact around 1-2% of the Western population. This increase may be attributed to longer lifespans and changes in our eating habits. Additionally, there is a positive correlation between the rising rates of metabolic disease and gout.

While gout commonly affects the metatarsal-phalangeal joint of the big toe (approximately 50% of cases), it can also impact other joints such as the fingers, wrists, knees, and ankles. The pain experienced during an episode is often excruciating, and these episodes typically last about a week. Approximately half of the patients experience a recurrence within a year.

Hyperuricemia is the underlying cause of gout. Uric acid, a byproduct of purine metabolism, is typically eliminated through the kidneys. However, in about 90% of cases, hyperuricemia occurs due to the under-excretion of urate, while the remaining 10% is caused by overproduction. Elevated urate levels increase the likelihood of crystal formation. Measuring uric acid levels in the blood can be misleading, as some individuals with high levels do not develop gout, and levels can be normal during an attack. The crystallization process is complex and more likely to occur in cooler temperatures (which is why the feet are often affected, and symptoms worsen at night), during acidosis, and when there are rapid fluctuations in uric acid levels.

Diagnosing gout is primarily based on clinical evaluation. If there is a rapid onset of severe pain, swelling, and tenderness that reaches its peak within 6-12 hours, accompanied by redness, it strongly suggests crystal inflammation. The presence of monosodium urate crystals in synovial fluid or tophi confirms the diagnosis. When these crystals are examined under polarized light, they exhibit negative birefringence. Since gout symptoms can be mistaken for septic arthritis, if there is uncertainty in the diagnosis and the joint has been aspirated, it should also be sent for gram-staining.

Tophi are painless, hard lumps that develop when hyperuricemia persists for an extended period. They often appear on the elbows and ears.

The upper part of the nose receives blood supply from the anterior and posterior ethmoidal arteries, which are derived from the internal carotid artery. On the other hand, the remaining parts of the nose and sinuses are nourished by the greater palatine, sphenopalatine, and superior labial arteries. These arteries are branches of the external carotid arteries.

In the front part of the nasal septum, there exists a network of blood vessels where the branches of the internal and external carotid artery connect. This network is known as Kiesselbach’s plexus, also referred to as Little’s area. It is worth noting that Kiesselbach’s plexus is the most common location for anterior bleeding.

Urinary alkalinisation aims to achieve a urinary pH of 7.5-8.5. This process helps enhance the elimination of salicylates. It is important to regularly monitor urinary pH, ideally on an hourly basis.

Further Reading:

Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.

The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.

When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.

To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.

Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.

In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.

If someone consumes at least 75 mg of paracetamol per kilogram of body weight within a 24-hour period, it is considered to be a significant ingestion. Ingesting more than 150 mg of paracetamol per kilogram of body weight within 24 hours poses a serious risk of harm.

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.

If an adult with a head injury experiences more than one episode of vomiting, it is recommended to undergo a CT scan of the head. There are several criteria for an urgent CT scan in individuals with a head injury, including a Glasgow Coma Scale (GCS) score of less than 13 on initial assessment in the emergency department (ED), a GCS score of less than 15 at 2 hours after the injury on assessment in the ED, suspected open or depressed skull fracture, any sign of basal skull fracture (such as haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, or Battle’s sign), post-traumatic seizure, new focal neurological deficit, and being on anticoagulation medication. If any of these signs are present, a CT scan should be performed within 1 hour, except for patients on anticoagulation medication who should undergo a CT scan within 8 hours if none of the other signs are present. However, if a patient on anticoagulation medication has any of the other signs, the CT scan should be performed within 1 hour.

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.

Transfusion-related lung injury (TRALI) is responsible for about one-third of all transfusion-related deaths, making it the leading cause. On the other hand, transfusion-associated circulatory overload (TACO) accounts for approximately 20% of these fatalities, making it the second leading cause. TACO occurs when a large volume of blood is rapidly infused, particularly in patients with limited cardiac reserve or chronic anemia. Elderly individuals, infants, and severely anemic patients are especially vulnerable to this reaction.

The typical signs of TACO include acute respiratory distress, rapid heart rate, high blood pressure, the appearance of acute or worsening pulmonary edema on a chest X-ray, and evidence of excessive fluid accumulation. In many cases, simply reducing the transfusion rate, positioning the patient upright, and administering diuretics will be sufficient to manage the condition. However, in more severe cases, it is necessary to halt the transfusion and consider non-invasive ventilation.

Transfusion-related acute lung injury (TRALI) is defined as new acute lung injury (ALI) that occurs during or within six hours of transfusion, not explained by another ALI risk factor. Transfusion of part of one unit of any blood product can cause TRALI.

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.

The scalp is composed of five layers, starting from the outermost layer, which is the skin, and moving towards the deepest layer, which is the periosteum of the skull. These layers can be remembered using the mnemonic: SCALP – Skin, Connective tissue, Aponeurosis, Loose areolar connective tissue, and Periosteum.

Further Reading:

The scalp is the area of the head that is bordered by the face in the front and the neck on the sides and back. It consists of several layers, including the skin, connective tissue, aponeurosis, loose connective tissue, and periosteum of the skull. These layers provide protection and support to the underlying structures of the head.

The blood supply to the scalp primarily comes from branches of the external carotid artery and the ophthalmic artery, which is a branch of the internal carotid artery. These arteries provide oxygen and nutrients to the scalp tissues.

The scalp also has a complex venous drainage system, which is divided into superficial and deep networks. The superficial veins correspond to the arterial branches and are responsible for draining blood from the scalp. The deep venous network is drained by the pterygoid venous plexus.

In terms of innervation, the scalp receives sensory input from branches of the trigeminal nerve and the cervical nerves. These nerves transmit sensory information from the scalp to the brain, allowing us to perceive touch, pain, and temperature in this area.

In certain scenarios, it may not be possible to obtain consent for emergency treatment. This is particularly true when dealing with individuals who have severe learning difficulties. In such cases, there is no one who can provide or deny consent on their behalf. It becomes the responsibility of the clinicians responsible for the patient’s care to make a decision that is in the patient’s best interests. If the treatment is urgently required to save the patient’s life, it can be administered without obtaining consent.

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.

There are various specific remedies available for different types of poisons and overdoses. The following list provides an outline of some of these antidotes:

Poison: Benzodiazepines
Antidote: Flumazenil

Poison: Beta-blockers
Antidotes: Atropine, Glucagon, Insulin

Poison: Carbon monoxide
Antidote: Oxygen

Poison: Cyanide
Antidotes: Hydroxocobalamin, Sodium nitrite, Sodium thiosulphate

Poison: Ethylene glycol
Antidotes: Ethanol, Fomepizole

Poison: Heparin
Antidote: Protamine sulphate

Poison: Iron salts
Antidote: Desferrioxamine

Poison: Isoniazid
Antidote: Pyridoxine

Poison: Methanol
Antidotes: Ethanol, Fomepizole

Poison: Opioids
Antidote: Naloxone

Poison: Organophosphates
Antidotes: Atropine, Pralidoxime

Poison: Paracetamol
Antidotes: Acetylcysteine, Methionine

Poison: Sulphonylureas
Antidotes: Glucose, Octreotide

Poison: Thallium
Antidote: Prussian blue

Poison: Warfarin
Antidote: Vitamin K, Fresh frozen plasma (FFP)

By utilizing these specific antidotes, medical professionals can effectively counteract the harmful effects of various poisons and overdoses.