The recommended daily oral dose for adults is 900 mg, which should be taken in 2-3 divided doses. For severe asthma or COPD, the initial intravenous dose is 5 mg/kg and should be administered over 10-20 minutes. This can be followed by a continuous infusion of 0.5 mg/kg/hour. In the case of a 60 kg patient, the appropriate infusion rate would be 30 mg/hour. It is important to note that the therapeutic range for aminophylline is narrow, ranging from 10-20 microgram/ml. Therefore, it is beneficial to estimate the plasma concentration of aminophylline during long-term treatment.

This patient is experiencing a breast abscess that has developed as a result of lactational mastitis. When milk is not properly drained, it can lead to an overgrowth of bacteria and subsequently cause an infection in the breast. If left untreated, this infection can lead to the accumulation of pus in a specific area of the breast. It is estimated that around 5-10% of women with infectious mastitis will develop a breast abscess. The recommended treatment involves a combination of antibiotics, such as flucloxacillin or co-amoxiclav, along with either aspiration or incision and drainage of the abscess.

When treating adults with bradycardia, a maximum of 6 doses of atropine 500 mcg can be administered. Each dose is given intravenously every 3-5 minutes. The total dose should not exceed 3mg.

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

Harmful drinking is when a person consumes at least 35 units of alcohol per week if they are a woman, or at least 50 units per week if they are a man. This level of drinking can lead to negative consequences for their mental and physical health.

Hazardous drinking, also known as increasing risk drinking, refers to a pattern of alcohol consumption that raises the likelihood of harm. For women, this means drinking more than 14 units but less than 35 units per week, while for men it means drinking more than 14 units but less than 50 units per week.

High-risk drinking, or harmful drinking, is a pattern of alcohol consumption that causes mental or physical damage. This occurs when a woman drinks 35 units or more per week, or when a man drinks 50 units or more per week.

Further Reading:

Alcoholic liver disease (ALD) is a spectrum of disease that ranges from fatty liver at one end to alcoholic cirrhosis at the other. Fatty liver is generally benign and reversible with alcohol abstinence, while alcoholic cirrhosis is a more advanced and irreversible form of the disease. Alcoholic hepatitis, which involves inflammation of the liver, can lead to the development of fibrotic tissue and cirrhosis.

Several factors can increase the risk of progression of ALD, including female sex, genetics, advanced age, induction of liver enzymes by drugs, and co-existent viral hepatitis, especially hepatitis C.

The development of ALD is multifactorial and involves the metabolism of alcohol in the liver. Alcohol is metabolized to acetaldehyde and then acetate, which can result in the production of damaging reactive oxygen species. Genetic polymorphisms and co-existing hepatitis C infection can enhance the pathological effects of alcohol metabolism.

Patients with ALD may be asymptomatic or present with non-specific symptoms such as abdominal discomfort, vomiting, or anxiety. Those with alcoholic hepatitis may have fever, anorexia, and deranged liver function tests. Advanced liver disease can manifest with signs of portal hypertension and cirrhosis, such as ascites, varices, jaundice, and encephalopathy.

Screening tools such as the AUDIT questionnaire can be used to assess alcohol consumption and identify hazardous or harmful drinking patterns. Liver function tests, FBC, and imaging studies such as ultrasound or liver biopsy may be performed to evaluate liver damage.

Management of ALD involves providing advice on reducing alcohol intake, administering thiamine to prevent Wernicke’s encephalopathy, and addressing withdrawal symptoms with benzodiazepines. Complications of ALD, such as intoxication, encephalopathy, variceal bleeding, ascites, hypoglycemia, and coagulopathy, require specialized interventions.

Heavy alcohol use can also lead to thiamine deficiency and the development of Wernicke Korsakoff’s syndrome, characterized by confusion, ataxia, hypothermia, hypotension, nystagmus, and vomiting. Prompt treatment is necessary to prevent progression to Korsakoff’s psychosis.

In summary, alcoholic liver disease is a spectrum of disease that can range from benign fatty liver to irreversible cirrhosis. Risk factors for progression include female sex, genetics, advanced age, drug-induced liver enzyme induction, and co-existing liver conditions.

The majority of treatments provided to individuals with sickle cell disease are supportive measures that have limited impact on the underlying pathophysiology of the condition.

Currently, the only approved therapy that can modify the disease is Hydroxyurea. This medication is believed to function by increasing the levels of fetal hemoglobin, which in turn decreases the concentration of HbS within the cells and reduces the abnormal hemoglobin tendency to form polymers.

Hydroxyurea is currently authorized for use in adult patients who experience recurrent moderate-to-severe painful crises (at least three in the past 12 months). Its approval is specifically for reducing the frequency of these painful episodes and the need for blood transfusions.

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

Significant toxicity can occur with the ingestion of more than 10 tablets of verapamil (160 mg or 240 mg immediate or sustained-release capsules) or diltiazem (180 mg, 240 mg or 360 mg immediate or sustained-release capsules). In children, even 1-2 tablets of immediate or sustained-release verapamil or diltiazem can be harmful. Symptoms usually appear within 1-2 hours of taking standard preparations, but with slow-release versions, the onset of severe toxicity may be delayed by 12-16 hours, with peak effects occurring after 24 hours.

The main clinical manifestations of calcium-channel blocker overdose include nausea and vomiting, low blood pressure, slow heart rate and first-degree heart block, heart muscle ischemia and stroke, kidney failure, pulmonary edema, and high blood sugar levels.

When managing a patient with calcium-channel blocker overdose, certain bedside investigations are crucial. These include checking blood glucose levels, performing an electrocardiogram (ECG), and obtaining an arterial blood gas sample. Additional investigations that can provide helpful information include assessing urea and electrolyte levels, conducting a chest X-ray to check for pulmonary edema, and performing an echocardiography.

Two types of tapeworms, Taenia solium and Taenia saginata, can infest humans. Infestation occurs when people consume meat from intermediate hosts that contain the parasite’s tissue stages. Tapeworms compete for nutrients and infestation is often without symptoms. However, in more severe cases, individuals may experience epigastric pain, diarrhea, and vomiting. Diagnosis involves identifying characteristic eggs in the patient’s stool.

Taenia solium infestation can also lead to a condition called cysticercosis. This occurs when larval cysts infiltrate and spread throughout the lung, liver, eye, or brain. Cysticercosis presents with neurological symptoms, seizures, and impaired vision. Confirmation of cysticercosis involves the presence of antibodies and imaging tests such as chest X-rays and CT brain scans.

The treatment for tapeworm infestation is highly effective and involves the use of medications like niclosamide or praziquantel. However, it is important to seek specialist advice when managing Taenia infections in the central nervous system, as severe inflammatory reactions can occur.

Borderline personality disorder is characterized by a range of clinical features. These include having unstable relationships, experiencing undue anger, and having variable moods. Individuals with this disorder often struggle with chronic boredom and may have doubts about their personal identity. They also tend to have an intolerance of being left alone and may engage in self-injury. Additionally, they exhibit impulsive behavior that can be damaging to themselves.

This patient exhibits signs of potentially life-threatening asthma. In adults, acute severe asthma is characterized by a peak expiratory flow (PEF) of 33-50% of the best or predicted value, a respiratory rate exceeding 25 breaths per minute, a heart rate over 110 beats per minute, and an inability to complete sentences in one breath. On the other hand, life-threatening asthma is indicated by a PEF below 33% of the best or predicted value, a blood oxygen saturation (SpO2) below 92%, a partial pressure of oxygen (PaO2) below 8 kPA, a normal partial pressure of carbon dioxide (PaCO2) within the range of 4.6-6.0 kPa, a silent chest, cyanosis, poor respiratory effort, exhaustion, altered consciousness, and hypotension.

To address acute asthma in adults, the recommended drug doses include administering 5 mg of salbutamol through an oxygen-driven nebulizer, delivering 500 mcg of ipratropium bromide via an oxygen-driven nebulizer, providing 40-50 mg of prednisolone orally, administering 100 mg of hydrocortisone intravenously, and infusing 1.2-2 g of magnesium sulfate intravenously over a period of 20 minutes.

According to the current Advanced Life Support (ALS) guidelines, it is advisable to seek senior advice before considering the use of intravenous aminophylline in cases of severe or life-threatening asthma. If used, a loading dose of 5 mg/kg should be given over 20 minutes, followed by a continuous infusion of 500-700 mcg/kg/hour. To prevent toxicity, it is important to maintain serum theophylline levels below 20 mcg/ml.

In situations where inhaled therapy is not feasible, intravenous salbutamol can be considered, with a slow administration of 250 mcg. However, it should only be used when a patient is receiving bag-mask ventilation.

It is worth noting that there is currently no evidence supporting the use of leukotriene receptor antagonists, such as montelukast, or Heliox in the management of acute severe or life-threatening asthma.

During the second and third trimesters of pregnancy, exposure to ACE inhibitors can lead to hypoperfusion, renal failure, and the oligohydramnios sequence. This sequence refers to the abnormal physical appearance of a fetus or newborn due to low levels of amniotic fluid in the uterus. It is also associated with malformations of the patient ductus arteriosus and aortic arch. These defects are believed to be caused by the inhibitory effects of ACE inhibitors on the renin-angiotensin-aldosterone system. To avoid these risks, it is recommended to discontinue ACE inhibitors before the second trimester.

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

Drug: ACE inhibitors
Adverse effects: If given in the second and third trimesters, can cause hypoperfusion, renal failure, and the oligohydramnios sequence.

Drug: Aminoglycosides
Adverse effects: Ototoxicity (damage to the ear) and deafness.

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

Drug: Benzodiazepines
Adverse effects: When given late in pregnancy, respiratory depression and a neonatal withdrawal syndrome can occur.

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

Epidemic keratoconjunctivitis is a type of viral conjunctivitis that is primarily caused by adenoviruses. This highly contagious condition tends to occur in outbreaks. It is a common cause of acute conjunctivitis and has distinct clinical features. These include the sudden onset of acute follicular conjunctivitis, severe pain in the affected eye, a significant amount of watery discharge, the presence of subconjunctival hemorrhages, potential visual changes, hyperemia and chemosis, and the possibility of membranes and pseudomembranes forming. Additionally, ipsilateral preauricular lymphadenopathy may be observed.

This patient is diagnosed with Krukenberg tumors, also known as carcinoma microcellulare. These tumors are ovarian malignancies that have spread from a primary site. The most common source of these tumors is gastric adenocarcinoma, which aligns with the patient’s history of weight loss, dysphagia, and intermittent vomiting.

Other primary cancers that can serve as the origin for Krukenberg tumors include colorectal carcinoma, breast cancer, lung cancer, contralateral ovarian carcinoma, and cholangiocarcinoma.

During an ultrasound, a solid and well-defined ovarian mass is typically observed, often affecting both ovaries. Further evaluation through a CT scan or MRI can provide additional helpful information. A biopsy is necessary to confirm the diagnosis, and histological examination will reveal the presence of mucin-secreting signet-rings.

Graphorrhoea is a communication disorder characterized by an excessive use of words and a tendency to ramble in written work. It is similar to word salad, but specifically occurs in written form. This condition is often observed in individuals with schizophrenia.

ATLS guidelines now suggest administering only 1 liter of crystalloid fluid during the initial assessment. If patients do not respond to the crystalloid, it is recommended to quickly transition to blood products. Studies have shown that infusing more than 1.5 liters of crystalloid fluid is associated with higher mortality rates in trauma cases. Therefore, it is advised to prioritize the early use of blood products and avoid large volumes of crystalloid fluid in trauma patients. In cases where it is necessary, massive transfusion should be considered, defined as the transfusion of more than 10 units of blood in 24 hours or more than 4 units of blood in one hour. For patients with evidence of Class III and IV hemorrhage, early resuscitation with blood and blood products in low ratios is recommended.

Based on the findings of significant trials, such as the CRASH-2 study, the use of tranexamic acid is now recommended within 3 hours. This involves administering a loading dose of 1 gram intravenously over 10 minutes, followed by an infusion of 1 gram over eight hours. In some regions, tranexamic acid is also being utilized in the prehospital setting.

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

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

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

Symptoms of urinary tract infection (UTI) can be difficult to detect in elderly patients, especially those with dementia. Common signs like painful urination and abdominal discomfort may be absent. Instead, these patients often experience increased confusion, restlessness, and a decline in cognitive abilities. Therefore, if an elderly patient suddenly develops urinary incontinence and experiences a rapid deterioration in cognitive function, it is highly likely that they have a UTI.

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)

Pabrinex is a supplement that includes a combination of essential vitamins. These vitamins are Thiamine (also known as vitamin B1), Riboflavin (commonly referred to as vitamin B2), Nicotinamide (which encompasses Vitamin B3, niacin, and nicotinic acid), Pyridoxine (known as vitamin B6), and Ascorbic acid (which is vitamin C). Each of these vitamins plays a crucial role in maintaining our overall health and well-being. By incorporating Pabrinex into our daily routine, we can ensure that our bodies receive the necessary nutrients to support various bodily functions.

To insert a femoral line, the patient should be lying on their back with a pillow placed under their buttocks to elevate the groin area. The thigh should be slightly moved away from the body and rotated outward.

Further Reading:

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

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

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

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

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

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

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In such cases, it is important to address any low blood glucose levels urgently by administering intravenous glucose. While the patient may require additional antiepileptic drug (AED) therapy, the management of status epilepticus involves several general measures.

During the early stage of status epilepticus (0-10 minutes), the airway should be secured and resuscitation measures should be taken. Oxygen should be administered and the cardiorespiratory function should be assessed. It is also important to establish intravenous access. In the second stage (0-30 minutes), regular monitoring should be instituted and the possibility of non-epileptic status should be considered. Emergency AED therapy should be initiated and emergency investigations should be conducted. If there are indications of alcohol abuse or impaired nutrition, glucose and/or intravenous thiamine may be administered. Acidosis should be treated if severe.

In the third stage (0-60 minutes), the underlying cause of status epilepticus should be identified. The anaesthetist and intensive care unit (ITU) should be alerted. Any medical complications should be identified and treated, and pressor therapy may be considered if appropriate. In the fourth stage (30-90 minutes), the patient should be transferred to intensive care. Intensive care and EEG monitoring should be established, and intracranial pressure monitoring may be initiated if necessary. Initial long-term, maintenance AED therapy should also be initiated.

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

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

Suxamethonium is a medication that can cause an increase in serum potassium levels by causing potassium to leave muscle cells. This can be a problem in patients who already have high levels of potassium, such as those with crush injuries. Therefore, suxamethonium should not be used in these cases.

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.

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.

When evaluating a disturbed or violent patient, your own safety should be the top priority. It is essential that the room you use for the examination has certain features to ensure your well-being. Firstly, there should be an internal inspection window that allows the staff to regularly check on both you and the patient. Additionally, the room should have an unimpeded exit, preferably with an outward opening door that is easy to exit through. It is also crucial to choose a room that is close to well-staffed areas, as this can provide immediate assistance if needed.

It is highly recommended to avoid examining patients in isolated areas, as it significantly increases the risk of harm to the assessor. While the room should be comfortable, it is unnecessary to have excessive furnishings. In fact, having too much furniture and unnecessary equipment can pose a threat, as they can be used as weapons by the patient. Therefore, it is ideal to remove any excess furniture and unnecessary equipment from the room. In this case, an examination couch is not required and should be avoided, as it could potentially be used as a weapon.

A secure locking mechanism is not necessary for the room, and it should be easily accessible to other staff members during the assessment. It is important to note that the room should not be used as a detainment area for the patient, and they should never be locked inside. By following these guidelines and ensuring the room has the recommended features, you can prioritize your safety while examining disturbed or violent patients.

For the treatment of pregnant women with lower urinary tract infections (UTIs), it is recommended to provide them with an immediate prescription for antibiotics. It is important to consider their previous urine culture and susceptibility results, as well as any prior use of antibiotics that may have contributed to the development of resistant bacteria. Before starting antibiotics, it is advised to obtain a midstream urine sample from pregnant women and send it for culture and susceptibility testing.

Once the microbiological results are available, it is necessary to review the choice of antibiotic. If the bacteria are found to be resistant, it is recommended to switch to a narrow-spectrum antibiotic whenever possible. The choice of antibiotics for pregnant women aged 12 years and over is summarized below:

First-choice:
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days, if the estimated glomerular filtration rate (eGFR) is above 45 ml/minute.

Second-choice (if there is no improvement in lower UTI symptoms with the first-choice antibiotic for at least 48 hours, or if the first-choice is not suitable):
– Amoxicillin 500 mg taken orally three times daily for 7 days (only if culture results are available and show susceptibility).
– Cefalexin 500 mg taken twice daily for 7 days.

For alternative second-choice antibiotics, it is recommended to consult a local microbiologist and choose the appropriate antibiotics based on the culture and sensitivity results.

Lidocaine works by blocking voltage-gated sodium channels. These channels are responsible for the propagation of action potentials in nerve fibers. By blocking these channels, lidocaine prevents the influx of sodium ions into the nerve cells, thereby inhibiting the generation and conduction of nerve impulses. This results in local anesthesia, as the transmission of pain signals from the skin to the brain is effectively blocked.

Further Reading:

Local anaesthetics, such as lidocaine, bupivacaine, and prilocaine, are commonly used in the emergency department for topical or local infiltration to establish a field block. Lidocaine is often the first choice for field block prior to central line insertion. These anaesthetics work by blocking sodium channels, preventing the propagation of action potentials.

However, local anaesthetics can enter the systemic circulation and cause toxic side effects if administered in high doses. Clinicians must be aware of the signs and symptoms of local anaesthetic systemic toxicity (LAST) and know how to respond. Early signs of LAST include numbness around the mouth or tongue, metallic taste, dizziness, visual and auditory disturbances, disorientation, and drowsiness. If not addressed, LAST can progress to more severe symptoms such as seizures, coma, respiratory depression, and cardiovascular dysfunction.

The management of LAST is largely supportive. Immediate steps include stopping the administration of local anaesthetic, calling for help, providing 100% oxygen and securing the airway, establishing IV access, and controlling seizures with benzodiazepines or other medications. Cardiovascular status should be continuously assessed, and conventional therapies may be used to treat hypotension or arrhythmias. Intravenous lipid emulsion (intralipid) may also be considered as a treatment option.

If the patient goes into cardiac arrest, CPR should be initiated following ALS arrest algorithms, but lidocaine should not be used as an anti-arrhythmic therapy. Prolonged resuscitation may be necessary, and intravenous lipid emulsion should be administered. After the acute episode, the patient should be transferred to a clinical area with appropriate equipment and staff for further monitoring and care.

It is important to report cases of local anaesthetic toxicity to the appropriate authorities, such as the National Patient Safety Agency in the UK or the Irish Medicines Board in the Republic of Ireland. Additionally, regular clinical review should be conducted to exclude pancreatitis, as intravenous lipid emulsion can interfere with amylase or lipase assays.

If IV methylene blue is obtained, it is typically used to treat a specific cause. However, if there is no response to methylene blue, alternative treatments such as hyperbaric oxygen or exchange transfusion may be considered. In cases where the cause is NADH-methaemoglobinaemia reductase deficiency, ascorbic acid can be used as a potential treatment.

Further Reading:

Methaemoglobinaemia is a condition where haemoglobin is oxidised from Fe2+ to Fe3+. This process is normally regulated by NADH methaemoglobin reductase, which transfers electrons from NADH to methaemoglobin, converting it back to haemoglobin. In healthy individuals, methaemoglobin levels are typically less than 1% of total haemoglobin. However, an increase in methaemoglobin can lead to tissue hypoxia as Fe3+ cannot bind oxygen effectively.

Methaemoglobinaemia can be congenital or acquired. Congenital causes include haemoglobin chain variants (HbM, HbH) and NADH methaemoglobin reductase deficiency. Acquired causes can be due to exposure to certain drugs or chemicals, such as sulphonamides, local anaesthetics (especially prilocaine), nitrates, chloroquine, dapsone, primaquine, and phenytoin. Aniline dyes are also known to cause methaemoglobinaemia.

Clinical features of methaemoglobinaemia include slate grey cyanosis (blue to grey skin coloration), chocolate blood or chocolate cyanosis (brown color of blood), dyspnoea, low SpO2 on pulse oximetry (which often does not improve with supplemental oxygen), and normal PaO2 on arterial blood gas (ABG) but low SaO2. Patients may tolerate hypoxia better than expected. Severe cases can present with acidosis, arrhythmias, seizures, and coma.

Diagnosis of methaemoglobinaemia is made by directly measuring the level of methaemoglobin using a co-oximeter, which is present in most modern blood gas analysers. Other investigations, such as a full blood count (FBC), electrocardiogram (ECG), chest X-ray (CXR), and beta-human chorionic gonadotropin (bHCG) levels (in pregnancy), may be done to assess the extent of the condition and rule out other contributing factors.

Active treatment is required if the methaemoglobin level is above 30% or if it is below 30% but the patient is symptomatic or shows evidence of tissue hypoxia. Treatment involves maintaining the airway and delivering high-flow oxygen, removing the causative agents, treating toxidromes and consider giving IV dextrose 5%.

Sexually transmitted eye infections can be quite severe and are often characterized by prolonged mucopurulent discharge. There are two main causes of these infections: Chlamydia trachomatis and Neisseria gonorrhoea. Differentiating between the two can be done by considering certain features.

Chlamydia trachomatis infection typically presents with chronic low-grade irritation and mucous discharge that lasts for more than two weeks in sexually active individuals. It may also be accompanied by pre-auricular lymphadenopathy. This type of infection is usually unilateral but can sometimes affect both eyes.

On the other hand, Neisseria gonorrhoea infection tends to develop rapidly, usually within 12 to 24 hours. It is characterized by copious mucopurulent discharge, eyelid swelling, and tender preauricular lymphadenopathy. This type of infection carries a higher risk of complications, such as uveitis, severe keratitis, and corneal perforation.

Based on the patient’s symptoms, it appears that they are more consistent with a Neisseria gonorrhoea infection. The rapid onset, copious discharge, and tender preauricular lymphadenopathy are indicative of this type of infection.

Treatment for gonococcal conjunctivitis in adults is typically based on limited research. However, a study has shown that all 12 patients responded well to a single 1 g intramuscular injection of ceftriaxone, along with a single episode of ocular lavage with saline.

In summary, sexually transmitted eye infections can be caused by either Chlamydia trachomatis or Neisseria gonorrhoea. Differentiating between the two is important in order to provide appropriate treatment. The patient in this case exhibits symptoms that align more closely with a Neisseria gonorrhoea infection, which carries a higher risk of complications. Treatment options for gonococcal conjunctivitis are limited, but a single injection of ceftriaxone has shown positive results in previous studies.

Ulcerative colitis is a condition that is less common among smokers, as around 70-80% of individuals affected by this disease are non-smokers. There are several recognized associations of ulcerative colitis, including aphthous ulcers, uveitis and episcleritis, seronegative spondyloarthropathies, sacroiliitis, erythema nodosum, pyoderma gangrenosum, finger clubbing, autoimmune hemolytic anemia, primary biliary cirrhosis, primary sclerosing cholangitis, and chronic active hepatitis. These conditions often coexist with ulcerative colitis and can provide additional insight into the disease.

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.

Warfarin has been found to elevate the likelihood of bleeding events when taken in conjunction with NSAIDs like ibuprofen. Consequently, it is advisable to refrain from co-prescribing warfarin with ibuprofen. For more information on this topic, please refer to the BNF section on warfarin interactions.